Many different types of water. In these species, the three pure water,
distilled water, mineral water, most people choose. That in the end the three
water are what? What are the benefits to drink water on the human body? Or what
harm? Drink water is the best? Friends of these questions is certainly not
unusual, Next, we specifically talk about.
A. Pure water
Pure water is what water
Pure water, also known as water purification or pure water, pure water,
relatively high purity, without nutrients, free of pollutants, salts and
additives of any harmful substances and bacteria, is a weak acid water. Pure
water effective way to avoid all kinds of bacteria invade the body, can be an
effective and safe to add water to the human body, has a strong solubility, and
therefore a strong affinity with the human cells, can effectively promote the
body's metabolism.
Pure water should not be long-term consumption
Removal of suspended solids in water bacteria and other harmful substances,
while pure water in the process, will also be required for the body of water
contains minerals in conjunction addition. Processing natural water after the
dozen Road filtering layer water treatment, purification and purification. After
a lot of drinking, the original human body necessary trace elements and
nutrients are quickly dissolved in pure water is excreted, it is difficult to be
assured of the mass balance of the human body, in other words, no grocery, no
human body pure water to be trace elements in fact do not have any nutritional
value. Trace elements lack long-term drinking can cause, causing stunted
children, adults will cause limb weakness and lack of energy, the elderly will
also suffer from a variety of trace elements deficiency.
B. Distilled water
1. Distilled water is what water
Distilled water by distillation the water was heated to boiling was vaporized
state, and then the steam is condensed into distilled water.
2. Distilled water should not be long-term consumption
Distilled water is pure water areas, the same is not suitable for long-term
consumption. Distilled water can not be removed water than a substance with low
boiling point of water, such as organics, artificial composites, chlorides,
algae, and other harmful substances, acidity phase for pure water is even
higher. Long-term consumption, also lost electrolytes and certain minerals,
which is likely to cause high blood pressure and heart problems. If you use
distilled water for cooking, it will also reduce the nutritional value of food.
Europe and the United States law does not allow the sale of distilled water as
drinking water, long-term consumption of distilled water acidic the body will
lead to the occurrence of the disease.
C. mineral water
1.What is mineral water
Mineral water from deep underground natural spring or artificial, unpolluted
water underground mine development. Mineral water contains a certain amount of
mineral salts, trace elements, or carbon dioxide gas. In the underlying deep
loop is formed, containing the national standards for minerals and defining
indicators, in normal circumstances, and its chemical composition, flow,
temperature and other relatively stable under natural fluctuation. Most of the
mineral water was slightly alkaline, suitable for the physiological environment
of the human body, help to promote the metabolism, help to recuperate.
2. Mineral water should not be long-term consumption
Some mineral water contains more sodium element sodium is the main component
of salt, drinking mineral water may lead to excessive salt intake per day
(dietary guidelines: 6g salt per day per person), if you can not redundant the
sodium excreted also a potential threat to the body, high blood pressure, kidney
disease, patients may also lead to the exacerbation. And mineral water, lack of
fluoride, the teeth at a disadvantage, such as the long-term only drink mineral
water, greatly increasing the possibility of suffering from dental problems.
Warm Tips:
Drinking mineral water should not boil drinking mineral water generally
contains calcium, magnesium more ionic state at room temperature, easily
absorbed by the body. But when the mineral water after boiling, calcium,
magnesium easily generated carbonate scale deposition, which lost nutrients.
Therefore, the mineral water is best to not heat, cold or slightly warm
appropriate.
D. boiled water
Boiled water is calorie-free and contains calcium, does not stimulate the
stomach, do not digest directly absorbed by the body can make use of the best
drinks. Generally recommended to drink warm water below 30 ℃ best, so not too
much to stimulate gastrointestinal motility, and is not easy to cause
vasoconstriction.
From a nutritional point of view, the boiled water is the most beneficial to
the body. Pure drinking water is the best thirst-quenching, can be carried out
immediately after it enters the body metabolism, can play a role to regulate
body temperature, transport nutrients and clean the inside of the body. Cold
water after boiling natural cooling is most easily through the cell membrane to
promote the body's metabolism, increasing the hemoglobin content of the blood,
enhance immune function, improve the body's resistance to disease. Often people
drink cool white open is not easy to produce fatigue.
Once again, we fell in love with boiled water!
Learn more knowledge of kidney disease, early found early treatment, prevention of dialysis, improve the quality of life. http://www.nephritiscn.com
Monday, August 20, 2012
What is the cause of the formation of hypertensive nephropathy factors
The the hypertensive nephropathy serious injury to the public health, and the
occurrence of hypertensive nephropathy seriously disrupting the lives of the
public, coupled with the high incidence of kidney disease in recent years,
attracted the attention of a lot of people, the treatment of kidney disease must
authority, so as soon as possible out of the entanglement, current treatment
methods to get rid of but clearly the cause of hypertension, renal disease, the
following factors on the formation of the etiology of hypertension, renal
disease what?
Hypertensive nephropathy causes formation factors? The hypertensive nephropathy etiology performance many necessary wise to cure, the best current treatment of nephrotic which hospital?
1, renal vascular disease: small renal artery or its branches caused by a variety of causes of atherosclerosis, the most common muscle fiber hyperplasia, non-specific arteritis, transplant crowding fibrosis can cause renal artery ischemia, thrombosis constitute or embolism due to renal hypertension.
2 Kidney essence lesions: acute or chronic glomerulonephritis, renal pelvis nephritis is the most common, followed by congenital kidney disease (polycystic kidney disease, horseshoe kidney, renal hypoplasia), renal tuberculosis, kidney stones, kidney tumor secondary nephropathy.
3, urinary tract blockage diseases: such as urinary tract stones, kidney and urinary tract tumors. Additionally, surrounded by the kidney inflammation, abscesses, tumors, trauma, bleeding can cause high blood pressure. Domestic materials reported in a variety of kidney disease associated with hypertension accounted for half.
4 anti boosted substances reduced secretion: decrease in prostaglandin synthesis and secretion of renal parenchymal lesions occur, renin secretion extreme to both balance disorders lead to high blood pressure. Kidney disease, such as chronic nephritis, pyelonephritis, hypertension is the most common secondary cause of performance especially in young people. Some experts said that the clinic, they found that the the renal hypertension youngest only 7 years old.
Hypertensive nephropathy causes formation factors? The hypertensive nephropathy etiology performance many necessary wise to cure, the best current treatment of nephrotic which hospital?
1, renal vascular disease: small renal artery or its branches caused by a variety of causes of atherosclerosis, the most common muscle fiber hyperplasia, non-specific arteritis, transplant crowding fibrosis can cause renal artery ischemia, thrombosis constitute or embolism due to renal hypertension.
2 Kidney essence lesions: acute or chronic glomerulonephritis, renal pelvis nephritis is the most common, followed by congenital kidney disease (polycystic kidney disease, horseshoe kidney, renal hypoplasia), renal tuberculosis, kidney stones, kidney tumor secondary nephropathy.
3, urinary tract blockage diseases: such as urinary tract stones, kidney and urinary tract tumors. Additionally, surrounded by the kidney inflammation, abscesses, tumors, trauma, bleeding can cause high blood pressure. Domestic materials reported in a variety of kidney disease associated with hypertension accounted for half.
4 anti boosted substances reduced secretion: decrease in prostaglandin synthesis and secretion of renal parenchymal lesions occur, renin secretion extreme to both balance disorders lead to high blood pressure. Kidney disease, such as chronic nephritis, pyelonephritis, hypertension is the most common secondary cause of performance especially in young people. Some experts said that the clinic, they found that the the renal hypertension youngest only 7 years old.
Treatment and clinical manifestations of hypertensive nephropathy
Hypertensive nephropathy in clinical performance? Hypertensive nephropathy is
a primary hypertension caused by benign arteriolar nephrosclerosis (also known
as hypertension renal arteriosclerosis) and malignant small artery renal
sclerosis, and accompanied by the corresponding clinical manifestationsdiseases.
Life, serious injury to a public body, to bring a lot of unchanged interest of
the health for the patient, must be aware of the clinical symptoms of
hypertensive nephropathy, taken according to the symptoms of early treatment is
best.
Hypertensive nephropathy in clinical performance? Clinical symptoms of hypertensive nephropathy multifaceted, the following is a detailed introduction to both auxiliary nephropathy treatment can also be found according to the symptoms disease.
Severe edema: edema is often the first symptom was generalized edema, and acupressure with depression. Severely ill patient and pleural effusion, ascites, the Dangxiong water ascites more can cause difficulty breathing, umbilical or inguinal hernia. High degree of edema the often accompanied oliguria, hypertension, mild azotemia.
2, proteinuria: massive proteinuria is the most important manifestation of nephrotic syndrome, urine protein and more + + + + + +, adult daily urinary protein excretion ≥ 3.5 g / d, most selective proteinuria.
Hypoproteinemia: decline in plasma protein, serum albumin <30 g / L, severe cases of less than 10g / L.
Hyperlipidemia: blood cholesterol, triglycerides are significantly higher.
Presenting symptoms are also more than four points of the clinical symptoms of hypertensive nephropathy life factors cause nephrotic too much public body discomfort, hoping to stop the hands carefully check the origin of the symptoms, such as the early detection of diseases early treatment.
Hypertensive nephropathy in clinical performance? Clinical symptoms of hypertensive nephropathy multifaceted, the following is a detailed introduction to both auxiliary nephropathy treatment can also be found according to the symptoms disease.
Severe edema: edema is often the first symptom was generalized edema, and acupressure with depression. Severely ill patient and pleural effusion, ascites, the Dangxiong water ascites more can cause difficulty breathing, umbilical or inguinal hernia. High degree of edema the often accompanied oliguria, hypertension, mild azotemia.
2, proteinuria: massive proteinuria is the most important manifestation of nephrotic syndrome, urine protein and more + + + + + +, adult daily urinary protein excretion ≥ 3.5 g / d, most selective proteinuria.
Hypoproteinemia: decline in plasma protein, serum albumin <30 g / L, severe cases of less than 10g / L.
Hyperlipidemia: blood cholesterol, triglycerides are significantly higher.
Presenting symptoms are also more than four points of the clinical symptoms of hypertensive nephropathy life factors cause nephrotic too much public body discomfort, hoping to stop the hands carefully check the origin of the symptoms, such as the early detection of diseases early treatment.
Saturday, August 18, 2012
How the treatment of diabetic nephropathy syndrome
Diabetic nephropathy syndrome is a kind of a disease? Perhaps we only know a
very serious diabetic nephropathy syndrome, but in fact does not have a more
in-depth understanding of diabetic nephropathy syndrome awareness for diabetic
nephropathy syndrome just to stay in the most surface, followed by expert of
diabetic nephropathy syndrome depth of dialysis to help your understanding of
diabetic nephropathy
Direct diabetic nephropathy syndrome prevalence reason there are two ways: The first is a long time with diabetes and lead to kidney failure and thus give rise to diabetic nephropathy syndrome. The second is due to chronic kidney disease, resulting in blood sugar and diabetes rising, and therefore the formation of diabetic nephropathy syndrome. So, to say that the complex etiology of diabetic renal syndrome relative treatment more difficult.
Hypoglycemic diet to lower blood sugar. There are a lot of diet hypoglycemic effect in the Chinese pharmacopoeia, such food and hypoglycemic effect and no side effects. So is a good choice for most patients.
Diabetic nephropathy syndrome in addition to high blood sugar, high blood pressure is one of the main symptoms of diabetic nephropathy syndrome. In the treatment of diabetic nephropathy syndrome, lowering blood pressure is also one of the main indicators.
Hypertensive renal failure can promote effective antihypertensive therapy can slow the rate of decline in glomerular filtration rate, reduce urinary albumin excretion. At present, most diabetic nephropathy syndrome use western medicine to lower blood pressure, these drugs lower blood pressure fast but the side effects, long-term use will be a key resistant therapeutic buck while the use of such drugs. Diet buck slow effect, but there will not be any side effects.
Treatment of diabetic nephropathy syndrome in addition to the blood pressure, lowering blood sugar, the most important thing is to reduce urinary protein
Proteinuria can cause kidney failure, the control urinary protein treatment of diabetic nephropathy syndrome is another important indicator. Control of proteinuria control by dietary protein intake. Therapy generally use a small amount of high-quality protein intake.
The treatment of diabetic nephropathy syndrome treatment by more than three, as well as medication to solve other complications, so as to achieve the control diabetic nephropathy syndrome in stable condition.
By above Dialysis seen, high blood sugar, high blood pressure, high protein prone to lead to kidney disease, in daily life to avoid causing high blood sugar, high blood pressure, high protein variety of reasons, conservation own kidneys, thus preventing diabetes nephrotic syndrome.
Direct diabetic nephropathy syndrome prevalence reason there are two ways: The first is a long time with diabetes and lead to kidney failure and thus give rise to diabetic nephropathy syndrome. The second is due to chronic kidney disease, resulting in blood sugar and diabetes rising, and therefore the formation of diabetic nephropathy syndrome. So, to say that the complex etiology of diabetic renal syndrome relative treatment more difficult.
Hypoglycemic diet to lower blood sugar. There are a lot of diet hypoglycemic effect in the Chinese pharmacopoeia, such food and hypoglycemic effect and no side effects. So is a good choice for most patients.
Diabetic nephropathy syndrome in addition to high blood sugar, high blood pressure is one of the main symptoms of diabetic nephropathy syndrome. In the treatment of diabetic nephropathy syndrome, lowering blood pressure is also one of the main indicators.
Hypertensive renal failure can promote effective antihypertensive therapy can slow the rate of decline in glomerular filtration rate, reduce urinary albumin excretion. At present, most diabetic nephropathy syndrome use western medicine to lower blood pressure, these drugs lower blood pressure fast but the side effects, long-term use will be a key resistant therapeutic buck while the use of such drugs. Diet buck slow effect, but there will not be any side effects.
Treatment of diabetic nephropathy syndrome in addition to the blood pressure, lowering blood sugar, the most important thing is to reduce urinary protein
Proteinuria can cause kidney failure, the control urinary protein treatment of diabetic nephropathy syndrome is another important indicator. Control of proteinuria control by dietary protein intake. Therapy generally use a small amount of high-quality protein intake.
The treatment of diabetic nephropathy syndrome treatment by more than three, as well as medication to solve other complications, so as to achieve the control diabetic nephropathy syndrome in stable condition.
By above Dialysis seen, high blood sugar, high blood pressure, high protein prone to lead to kidney disease, in daily life to avoid causing high blood sugar, high blood pressure, high protein variety of reasons, conservation own kidneys, thus preventing diabetes nephrotic syndrome.
How to eat when you have kidney disease
The following are general food guidelines for people who have kidney disease.
Be sure to follow the diet your doctor or dietitian gave you.
Protein
Eating too much protein can stress the kidneys. But if you don't get enough, you can become weak, tired, and more likely to get infections. To get the right amount of protein:
· Know how much protein you can have each day. Limit high-protein foods to 5 to 7 ounces a day, or less, if your doctor or dietitian tells you to. A 3-ounce serving of protein is about the size of a deck of cards.
· Learn which foods contain protein. High-protein foods include meat, poultry, seafood, and eggs. Milk and milk products, beans, nuts, breads, pastas, cereals, and vegetables also contain protein.
Sodium
To limit sodium:
· Don't add salt to your food. Avoid foods that list salt, sodium, or monosodium glutamate (MSG) on the label. Buy foods that are labeled "no salt added," "sodium-free," or "low-sodium." Foods labeled "reduced-sodium" and "light sodium" may still have too much sodium.
· Avoid salted snacks such as pretzels, chips, and popcorn.
· Avoid smoked, cured, salted, and canned meat, fish, and poultry. This includes ham, bacon, hot dogs, and luncheon meats.
· Don't use a salt substitute or lite salt unless your doctor or dietitian says it is okay. Most salt substitutes and lite salts are high in potassium. Use lemon, herbs, and other spices to flavor your meals.
· Limit how often you eat food from restaurants. Most of the sodium we eat is hidden in processed foods and restaurant food, especially at fast-food and take-out places.
Fluids
If you need to limit fluids:
· Know how much fluid you can drink. Each day, fill a pitcher with that amount of water. If you drink another fluid during the day, such as coffee, pour an equal amount of water out of the pitcher. When the pitcher is empty, you're done drinking for the day.
· Remember that soups and foods that are liquid at room temperature, such as gelatin dessert (for example, Jell-O) and ice cream, count as fluids.
· Be aware that some fruits and vegetables contain a lot of water and will count in your fluid intake. Examples include grapes, oranges, apples, lettuce, and celery.
· Count the liquid in canned fruits and vegetables as part of your daily intake, or drain them well before serving.
Potassium
If you need to limit potassium:
· Choose low-potassium fruits such as apples, blueberries, pears, plums, and tangerines. You can also eat canned fruits, such as fruit cocktail, peaches, and pineapple.
· Choose low-potassium vegetables such as asparagus, bean sprouts, cabbage, cucumber, green beans, and lettuce.
Phosphorus
If you need to limit phosphorus:
Follow your food plan to know how much milk and milk products you can include.
· Limit nuts, peanut butter, seeds, lentils, beans, organ meats, and sardines. Also limit cured meats such as sausages, bologna, and hot dogs.
· Avoid colas and soft drinks with phosphate or phosphoric acid.
· Avoid bran breads and bran cereals.
General tips
· Don't skip meals or go for many hours without eating. If you don't feel very hungry, try to eat 4 or 5 small meals instead of 1 or 2 big meals.
· If you have trouble keeping your weight up, talk to your doctor or dietitian about ways you can add calories to your diet. Healthy fats such as olive or canola oil may be good choices. Unless you have diabetes, you can use honey and sugar to add calories and increase energy.
· Don't take any vitamins or minerals, supplements, or herbal products without talking to your doctor first.
· Check with your doctor about whether it is safe for you to drink alcohol. If you do drink alcohol, have no more than 1 drink a day. Count it as part of your fluids for the day.
Protein
Eating too much protein can stress the kidneys. But if you don't get enough, you can become weak, tired, and more likely to get infections. To get the right amount of protein:
· Know how much protein you can have each day. Limit high-protein foods to 5 to 7 ounces a day, or less, if your doctor or dietitian tells you to. A 3-ounce serving of protein is about the size of a deck of cards.
· Learn which foods contain protein. High-protein foods include meat, poultry, seafood, and eggs. Milk and milk products, beans, nuts, breads, pastas, cereals, and vegetables also contain protein.
Sodium
To limit sodium:
· Don't add salt to your food. Avoid foods that list salt, sodium, or monosodium glutamate (MSG) on the label. Buy foods that are labeled "no salt added," "sodium-free," or "low-sodium." Foods labeled "reduced-sodium" and "light sodium" may still have too much sodium.
· Avoid salted snacks such as pretzels, chips, and popcorn.
· Avoid smoked, cured, salted, and canned meat, fish, and poultry. This includes ham, bacon, hot dogs, and luncheon meats.
· Don't use a salt substitute or lite salt unless your doctor or dietitian says it is okay. Most salt substitutes and lite salts are high in potassium. Use lemon, herbs, and other spices to flavor your meals.
· Limit how often you eat food from restaurants. Most of the sodium we eat is hidden in processed foods and restaurant food, especially at fast-food and take-out places.
Fluids
If you need to limit fluids:
· Know how much fluid you can drink. Each day, fill a pitcher with that amount of water. If you drink another fluid during the day, such as coffee, pour an equal amount of water out of the pitcher. When the pitcher is empty, you're done drinking for the day.
· Remember that soups and foods that are liquid at room temperature, such as gelatin dessert (for example, Jell-O) and ice cream, count as fluids.
· Be aware that some fruits and vegetables contain a lot of water and will count in your fluid intake. Examples include grapes, oranges, apples, lettuce, and celery.
· Count the liquid in canned fruits and vegetables as part of your daily intake, or drain them well before serving.
Potassium
If you need to limit potassium:
· Choose low-potassium fruits such as apples, blueberries, pears, plums, and tangerines. You can also eat canned fruits, such as fruit cocktail, peaches, and pineapple.
· Choose low-potassium vegetables such as asparagus, bean sprouts, cabbage, cucumber, green beans, and lettuce.
Phosphorus
If you need to limit phosphorus:
Follow your food plan to know how much milk and milk products you can include.
· Limit nuts, peanut butter, seeds, lentils, beans, organ meats, and sardines. Also limit cured meats such as sausages, bologna, and hot dogs.
· Avoid colas and soft drinks with phosphate or phosphoric acid.
· Avoid bran breads and bran cereals.
General tips
· Don't skip meals or go for many hours without eating. If you don't feel very hungry, try to eat 4 or 5 small meals instead of 1 or 2 big meals.
· If you have trouble keeping your weight up, talk to your doctor or dietitian about ways you can add calories to your diet. Healthy fats such as olive or canola oil may be good choices. Unless you have diabetes, you can use honey and sugar to add calories and increase energy.
· Don't take any vitamins or minerals, supplements, or herbal products without talking to your doctor first.
· Check with your doctor about whether it is safe for you to drink alcohol. If you do drink alcohol, have no more than 1 drink a day. Count it as part of your fluids for the day.
Early treatment of diabetic nephropathy
Diabetic nephropathy is one of the most serious complications of diabetes,
early diabetic nephropathy is not terrible. If you accept a reasonable
treatment, or can alleviate or cure diabetic nephropathy. How to treat diabetic
nephropathy? Early treatment of diabetic nephropathy, what does?
The early treatment of diabetic nephropathy, including several ways: low salt, low protein diet, eat fruits, avoid high cholesterol food. Restricted movement, prohibition of strenuous exercise. Bed rest: supine in bed, help to promote kidney recharge blood flow. To protect the lower back kidney area, and to maintain its warmth. Aggressive treatment of hypertension. Medication to be fine, protect the kidneys, can not increase the burden on the kidneys, less or disable antibiotics, kidney damage, such as sulfonamides, gentamicin, streptomycin. Have a good mood, and ease of mind to promote the body's endorphin release, which is conducive to the improvement of disease.
1, diet therapy: advocate the protein intake (0.8g/kg.d,) should be limited in the early stage of diabetic nephropathy. Existing edema and renal insufficiency patients, in addition to limiting sodium intake in the diet, protein intake should be taken to the small but efficient principle (0.6g/kg.d,), when necessary, may be appropriate to lose amino acids and plasma . Insulin may be appropriate under the guarantee to increase carbohydrate intake to ensure adequate heat. Fat should use vegetable oil. However, the effect of dietary treatment is relatively slow, and difficult to adhere to, for patients with diabetes is not a good choice.
2 drug therapy: oral hypoglycemic agents. For the simple diet and oral hypoglycemic agents control is not good and there is renal insufficiency patients using insulin as early as possible. Timely adjustment of the dose of insulin when blood glucose monitoring. However, many drugs are toxic components, will the human body a great deal of side effects, this method is not very desirable.
Early treatment of diabetic nephropathy should be noted that the two measures
The first treatment of diabetic nephropathy or control diabetes, to avoid the occurrence of kidney disease. The level of blood glucose control and development has an extremely important impact on the incidence of diabetic nephropathy and diabetic retinopathy, good blood glucose control can be decreased by half the incidence of type 1 diabetic nephropathy, the incidence of type 2 diabetic nephropathy reduced by 1/3. Patients who have developed early kidney disease stage, in order to control the disease does not affect kidney function, should actively mobilize them to accept insulin therapy.
The second measure is to control blood pressure, high blood pressure is a very important factor for exacerbation of diabetic nephropathy, so patients should be eating light, eat less salt, has high blood pressure should not hesitate to insist on the use of antihypertensive drugs , so that the blood pressure remained at normal levels.
The early treatment of diabetic nephropathy, including several ways: low salt, low protein diet, eat fruits, avoid high cholesterol food. Restricted movement, prohibition of strenuous exercise. Bed rest: supine in bed, help to promote kidney recharge blood flow. To protect the lower back kidney area, and to maintain its warmth. Aggressive treatment of hypertension. Medication to be fine, protect the kidneys, can not increase the burden on the kidneys, less or disable antibiotics, kidney damage, such as sulfonamides, gentamicin, streptomycin. Have a good mood, and ease of mind to promote the body's endorphin release, which is conducive to the improvement of disease.
1, diet therapy: advocate the protein intake (0.8g/kg.d,) should be limited in the early stage of diabetic nephropathy. Existing edema and renal insufficiency patients, in addition to limiting sodium intake in the diet, protein intake should be taken to the small but efficient principle (0.6g/kg.d,), when necessary, may be appropriate to lose amino acids and plasma . Insulin may be appropriate under the guarantee to increase carbohydrate intake to ensure adequate heat. Fat should use vegetable oil. However, the effect of dietary treatment is relatively slow, and difficult to adhere to, for patients with diabetes is not a good choice.
2 drug therapy: oral hypoglycemic agents. For the simple diet and oral hypoglycemic agents control is not good and there is renal insufficiency patients using insulin as early as possible. Timely adjustment of the dose of insulin when blood glucose monitoring. However, many drugs are toxic components, will the human body a great deal of side effects, this method is not very desirable.
Early treatment of diabetic nephropathy should be noted that the two measures
The first treatment of diabetic nephropathy or control diabetes, to avoid the occurrence of kidney disease. The level of blood glucose control and development has an extremely important impact on the incidence of diabetic nephropathy and diabetic retinopathy, good blood glucose control can be decreased by half the incidence of type 1 diabetic nephropathy, the incidence of type 2 diabetic nephropathy reduced by 1/3. Patients who have developed early kidney disease stage, in order to control the disease does not affect kidney function, should actively mobilize them to accept insulin therapy.
The second measure is to control blood pressure, high blood pressure is a very important factor for exacerbation of diabetic nephropathy, so patients should be eating light, eat less salt, has high blood pressure should not hesitate to insist on the use of antihypertensive drugs , so that the blood pressure remained at normal levels.
Sugar Friends of kidney disease to healthy diet
Sugar Friends of kidney disease how a healthy diet? Now more and more not
only diabetic patients, patients with diabetic nephropathy is increasing every
year. And patients with diabetic nephropathy was not able to early treatment,
leading to disease progression, until eventually lead to kidney failure,
suffering from uremia. Sugar Friends of suffering from kidney disease should be
how healthy diet can contribute to physical health? Control is an important
factor in the development of diabetic nephropathy that is diet.
Sugar Friends of kidney disease should be how a healthy diet? Following analysis from the type of food:
An appropriate calorie low fat diabetic diet is a low-fat diet to control total calories, and diabetic nephropathy calorie supplement should be appropriate. Insufficient supply of calories and stored fat, protein degradation, allows kidney function parameters and serum creatinine, urea and other increases. Caloric intake is too high, which does not help blood glucose control. Fat provides more calories, but on the progress of renal failure, it still requires low-fat diet. The specific implementation: General to encourage the food instead of staple food yams, taro and other starch-containing high. May be appropriate to eat noodles, vermicelli, vermicelli, etc., but should pay attention to the less staple food. More so-called wheat starch (Note that different from the ordinary flour) on sale at many supermarkets in big cities, almost no protein. This wheat starch, with mashed potatoes, sweet potato noodles, yam powder, steamed buns, rolls, buns, can add heat without increasing plant protein intake does not increase the burden on the kidneys, the most suitable for patients with diabetic nephropathy consumption.
2, high fiber diet, diet high cellulose maintain defecate unobstructed, excretion of toxins and human metabolic balance to maintain. Specific implementation: should be appropriate to eat more whole grains (such as cornmeal, buckwheat noodles, etc.), taro, kelp, some fruits, vegetables. It should be noted: renal failure in patients with common electrolyte disorders, can be expressed as hyperkalemia. Eating fruits, vegetables should be noted that to avoid high potassium species. Diet therapy is the basis of diabetic nephropathy with renal insufficiency treatment.
3, high-quality low-protein diet because of excessive protein intake can increase the burden on the kidneys, so to control the total amount of protein intake. Proteins as important nutrients the body can not do without, especially the essential amino acids the human body can not synthesize from the foreign intake, so containing the necessary amino acids are more high quality protein should be guaranteed. The specific implementation: vegetable protein (including non-essential amino acids, low-quality protein) should be minimized, should generally be a fast soy products, appropriate restrictions on staple foods (flour, rice also contains a certain amount of vegetable protein) may be appropriate to add the milk, eggs, fish, lean meat and other animal protein (including essential amino acids, high quality protein). In particular, milk, egg protein is appropriate. In general: the amount of protein intake, reference should be made in patients with serum creatinine levels and endogenous creatinine clearance rate decision. The higher the level of serum creatinine, endogenous creatinine clearance rate, the lower protein intake more stringent control.
The above is an expert on if suffering from kidney disease described in detail how a healthy diet, I hope to give patients to bring help. The hazards of diabetic nephropathy, patients in treatment to maintain a good attitude, according to early signs of diabetic nephropathy, select the correct treatment, the patients as soon as possible to get rid of the disease plagued.
Sugar Friends of kidney disease should be how a healthy diet? Following analysis from the type of food:
An appropriate calorie low fat diabetic diet is a low-fat diet to control total calories, and diabetic nephropathy calorie supplement should be appropriate. Insufficient supply of calories and stored fat, protein degradation, allows kidney function parameters and serum creatinine, urea and other increases. Caloric intake is too high, which does not help blood glucose control. Fat provides more calories, but on the progress of renal failure, it still requires low-fat diet. The specific implementation: General to encourage the food instead of staple food yams, taro and other starch-containing high. May be appropriate to eat noodles, vermicelli, vermicelli, etc., but should pay attention to the less staple food. More so-called wheat starch (Note that different from the ordinary flour) on sale at many supermarkets in big cities, almost no protein. This wheat starch, with mashed potatoes, sweet potato noodles, yam powder, steamed buns, rolls, buns, can add heat without increasing plant protein intake does not increase the burden on the kidneys, the most suitable for patients with diabetic nephropathy consumption.
2, high fiber diet, diet high cellulose maintain defecate unobstructed, excretion of toxins and human metabolic balance to maintain. Specific implementation: should be appropriate to eat more whole grains (such as cornmeal, buckwheat noodles, etc.), taro, kelp, some fruits, vegetables. It should be noted: renal failure in patients with common electrolyte disorders, can be expressed as hyperkalemia. Eating fruits, vegetables should be noted that to avoid high potassium species. Diet therapy is the basis of diabetic nephropathy with renal insufficiency treatment.
3, high-quality low-protein diet because of excessive protein intake can increase the burden on the kidneys, so to control the total amount of protein intake. Proteins as important nutrients the body can not do without, especially the essential amino acids the human body can not synthesize from the foreign intake, so containing the necessary amino acids are more high quality protein should be guaranteed. The specific implementation: vegetable protein (including non-essential amino acids, low-quality protein) should be minimized, should generally be a fast soy products, appropriate restrictions on staple foods (flour, rice also contains a certain amount of vegetable protein) may be appropriate to add the milk, eggs, fish, lean meat and other animal protein (including essential amino acids, high quality protein). In particular, milk, egg protein is appropriate. In general: the amount of protein intake, reference should be made in patients with serum creatinine levels and endogenous creatinine clearance rate decision. The higher the level of serum creatinine, endogenous creatinine clearance rate, the lower protein intake more stringent control.
The above is an expert on if suffering from kidney disease described in detail how a healthy diet, I hope to give patients to bring help. The hazards of diabetic nephropathy, patients in treatment to maintain a good attitude, according to early signs of diabetic nephropathy, select the correct treatment, the patients as soon as possible to get rid of the disease plagued.
Thursday, August 16, 2012
Hypertension, high blood sugar of diabetic nephropathy
Diabetic nephropathy is one of the microvascular complications of diabetes
the most important type 2 diabetes patients with nephropathy prevalence of
34.7%. With the rapid economic development, people's living standards continue to improve, the incidence of diabetes is increasing year by year, diabetes
Patients with nephropathy have increased. In developed countries diabetic nephropathy has become the first cause of ESRD, but also has become following the second cause of primary glomerular diseases, diabetes caused by one of the main reasons for death, disability, so the effective prevention and treatment of diabetic nephropathy has become one of the major issue.
Development and staging of diabetic nephropathy
Diabetic nephropathy is one of the diabetic microangiopathy often associated with diabetic retinopathy. Egg
White urine is a sign of diabetic nephropathy progress. The sustained microalbuminuria in early diabetic nephropathy,, the prosecution
Measured urinary conventional urine protein may be negative or only trace detection of urinary albumin excretion rate (UAER)
Of 20 to 200 μg / min or of 30 ~~ 300 mg/24 h; once the development to the period of clinical diabetic nephropathy, ie, urinary protein
(+) Or more, UAER,> 200 μg / min or> 500 mg/24 h in patients with glomerular filtration rate (GFR)
Was a progressive decline in, and tend to increase in blood pressure, renal pathological damage to the irreversible stage, the most
Final development of renal failure.
Diabetic nephropathy is divided into five, one, two clinical difficult to diagnose, often sustained microalbumin
Clinical can only be diagnosed when the urine of diabetic nephropathy 3. This time after a positive and effective antihypertensive, hypoglycemic therapy,
Part of the urinary albumin excretion in patients with reduced or negative, kidney disease reversal or development delay. But if we can not
Do on a regular basis to check the urine in patients with urinary albumin excretion rate, until the patients had edema, high
Blood pressure, proteinuria, renal function abnormalities before considering the possibility of diabetic nephropathy, and more have been developed to sugar
4 of diabetes nephropathy, the lesion is irreversible. Thus, clinical guidelines suggest that diabetic patients should be regularly
(1/3 ~ 6 months) monitoring of urine and the detection of urinary albumin in order to achieve early diagnosis,
Early treatment. The occurrence and development of diabetic nephropathy follow the laws of the two intersecting curves, one for proteinuria
Curve from the negative, trace a large number of urinary protein gradually increased, and the other a curve for the glomerular filtration rate from
Higher than normal, normal to decreased, the two curves cross more than four diabetic nephropathy.
In addition, we should also pay attention to the identification,
Patients with diabetes and proteinuria, should not be diagnosed as diabetic nephropathy, history of diabetes less than five years, the sudden appearance of a large number of patients with proteinuria and normal renal function, not associated with diabetic retinopathy, basic can exclude diabetic nephropathy possible, to referral to superiors Hospital Nephrology Renal biopsy pathological diagnosis in order to give the correct treatment. If we blindly follow the treatment of diabetic nephropathy will be adversely affected by illness. The etiology of diabetic nephropathy is very complex, it is not very clear, but mainly the following risk factors: genetic, hypertension, high blood sugar and obesity, dyslipidemia, high uric acid. Including hypertension and high blood sugar is an important risk factor for the occurrence and development of diabetic nephropathy. Previous studies recognized cardiovascular and cerebrovascular diseases is diabetes the most common complications and death in the direct cause of hypertension and high blood sugar can significantly increased the incidence of cardiovascular and cerebrovascular diseases.
The relationship between hypertension and diabetic nephropathy
Hypertension to the glomerular capillary bed is passed through the systemic blood pressure, increased pressure within the ball, filtration pressure increase
High, resulting in increased glomerular sclerosis. Hypertension and diabetic nephropathy can promote each other. Hypertension can
The progressive increase in type 2 diabetic patients with normal urine albumin levels of urinary albumin and clinical diabetes
Nephropathy in patients with renal function deterioration. Antihypertensive treatment to prevent or delay a of the two is too
The occurrence and development of process. Studies have shown that the level of blood pressure control affect the prognosis of diabetes were independent risk
Factors.
Decline in glomerular filtration rate (GFR) and blood pressure levels. According to the 2007 edition of diabetes anti
Governance guidelines, patients with proteinuria <1 g/24 h the control of blood pressure should be below 130/80 mm Hg [including the 2007
American Diabetes Association (ADA) guidelines and the European Society for Cardiovascular Diseases / European Society of Hypertension (ESC /
ESH) guidelines to blood pressure control below 130/80 mm Hg given as proteinuria <1 g / d in patients with buck head
Value]; marked proteinuria> 1 g/24 h in patients, blood pressure control should be below 125/75 mm Hg, based primarily on
MDRD (The Modification of Diet in Renal Disease Study) clinical evidence-based medical research.
The study was supported by the leadership of the U.S. National Institutes of Health (NIH), 15 kidney disease center, compared different antihypertensive goals
Value of delay in patients with chronic kidney disease, kidney damage to progress. MDRD study finds that: egg
White urine> 1 g / patients of d, mean arterial pressure (MAP) should be strictly controlled to 92 mm Hg in order to effectively delay the
Kidney damage to progress. Moreover, in the same MAP level, lower systolic blood pressure and pulse pressure is heavier than lower diastolic blood pressure
Needs. The study recommended that the control of blood pressure below 125/75 mm Hg as proteinuria> 1 g / d in patients with the
Step-down target. The proteinuria <1 g / d of CKD patients blood pressure should be controlled and to what level, the MDRD study
Study is not a conclusion.
The selection and application of antihypertensive drugs
Delay in the occurrence and development of diabetic nephropathy, we choose antihypertensive drugs benefit more? First
The antihypertensive drugs selected for the angiotensin-converting enzyme inhibitors (ACEI), angiotensin II receptor antagonist
(ARB) and the new listing of a renin inhibitor, has a lot of evidence in the basic and clinical research
Implementation can improve the prognosis of early diabetic nephropathy. Of ACEI and ARB class of antihypertensive drugs because it can reduce the renal
Ball filtration pressure and improve renal blood flow dynamics, inhibit the production and secretion of inflammatory factors and cytokines, suppression
System of mesangial cells, fibroblasts and macrophage activation and proliferation, to improve the permeability of the filtration membrane, reduce urinary
Protein excretion and so on to become the first choice for diabetic nephropathy. Therefore, in clinical practice, when patients with micro egg
White urine, with or without hypertension, should be given ACEI or ARB treatment. The recommended start small dose,
One dose every 1 to 2 weeks, patients able to tolerate the maximum dose is appropriate, that is not symptomatic low
Elevated blood pressure, drug-free serum creatinine, and hyperkalemia is appropriate. For trace, or a small amount of proteinuria the risk of
Usually the application of drugs, a dose of 1 to 2 times, the exclusion of other interfering factors,
A few months later the majority of patients with urinary protein standards. For patients with massive proteinuria, should first check 24
Urinary protein, and then gradually increase to a single drug dose can ACEI the ARB, based on each
Months urinary protein quantification check, and patients on drug tolerance of plus or minus dose (not yet
More and better evidence-based medicine evidence that combination therapy is better than single drug treatment). If the application of ACEI
Or ARB blood pressure can not be achieved and can be combined calcium antagonists. If accompanied by edema, can be combined diuretic
Agent.
beta blockers as first choice, but for the young, and rapid heart rate, history of ischemic heart disease
Patients can be applied. In addition, in the step-down at the same time, also need to limit sodium intake, increasing exercise, quitting smoking
Adjusting lifestyles treatment.
The relationship between hyperglycemia and diabetic nephropathy
High blood sugar can cause kidney a series of pathophysiological changes, including: non-enzymatic glycation end products increase, sorbitol increased production, enhanced oxidative stress, protein kinase C and transforming growth factor (TGF) beta activity increased, resulting in glomerular increased extracellular matrix, cell injury and proteinuria increased. Another long-term high blood sugar so that the glomerulus in a hyperfiltration state, resulting in glomerular hyperperfusion and ball pressure, so that the glomerular hypertrophy, basement membrane thickening, increased capillary permeability, proteinuria formation , eventually leading to glomerulosclerosis.
DCCT study conducted in 1441 patients with type 1 diabetes patients from 29 medical centers in the United States and Canada in 1993, with its strict design, large-scale observation for a long time been recognized as the most convincing studies that strict control high blood sugar can effectively delay the onset and development of diabetic nephropathy. Studies have shown that strict control of blood sugar can make of microalbuminuria in type 1 diabetes incidence decreased by 39%, the incidence of clinical proteinuria decreased by 54%. The United Kingdom Prospective Diabetes Study (UKPDS) is so far the longest Prospective Diabetes Study, intensive therapy group intervention on selected newly diagnosed patients with type 2 diabetes for more than 10 years, mean HbA1c was 7.0%, the conventional therapy group was 7.9%. Intensive treatment of the relative risk of any diabetes-related endpoint by 12%, mainly due to reduced risk of microvascular complications. Intensive glucose control can make the occurrence of microalbuminuria in patients with type 2 diabetes by 30 percent. Analysis found that intensive treatment HbA1c decreasing by 1%, 21% lower relative risk of any diabetes-related endpoint, the risk of microvascular complications can be reduced by 37%. For blood sugar control, with HbA1c as a blood glucose target value method. According to Chinese Medical Association in August 2010 Ninth National Endocrine Conference released the "China Adult 2
Diabetes, HbA1c control goal of the expert consensus, it is recommended that the HbA 1c monitoring the condition of patients every 3 to 6 months
OK time, blood glucose control targets must be individualized, individualized. For elderly patients with diabetes,
Existing cardiovascular disease or risk, the blood glucose target should be relaxed, to avoid the occurrence of hypoglycemia and
Increased risk of death.
The choice of antidiabetic drugs sulfonylureas mouth medication, insulin is the preferred biguanide drugs in renal function is
Often can be applied to the α-glucosidase inhibitors have fewer side effects, regardless of renal function can take. To
Insulin sensitizers current debate, the United States has been under the city, it is not recommended.
Expert tips
Diabetes is a disease of serious harm to human health. Closely related to the occurrence of diabetic nephropathy, development and high blood pressure, high blood sugar. Control of blood pressure and blood sugar levels were independent risk factors affecting the prognosis of diabetic nephropathy. Strict blood pressure, blood glucose control is of great significance to reduce proteinuria and protect renal function and prevention of cardiovascular and cerebrovascular complications, In addition, we should also pay attention to the regulation of lipid levels to statin cholesterol lowering agents, should be to control high uric acid hyperlipidemia, appropriate restrictions on the amount of protein intake, avoiding use of nephrotoxic drugs. Regular monitoring of urine, urinary protein excretion, renal function and blood sugar levels, in order to adjust the treatment plan, and strive to make the indicators achieved and delay the development of diabetic nephropathy, while reducing the occurrence of cardiovascular complications and fatal complications, improve quality of life of patients with diabetes.
34.7%. With the rapid economic development, people's living standards continue to improve, the incidence of diabetes is increasing year by year, diabetes
Patients with nephropathy have increased. In developed countries diabetic nephropathy has become the first cause of ESRD, but also has become following the second cause of primary glomerular diseases, diabetes caused by one of the main reasons for death, disability, so the effective prevention and treatment of diabetic nephropathy has become one of the major issue.
Development and staging of diabetic nephropathy
Diabetic nephropathy is one of the diabetic microangiopathy often associated with diabetic retinopathy. Egg
White urine is a sign of diabetic nephropathy progress. The sustained microalbuminuria in early diabetic nephropathy,, the prosecution
Measured urinary conventional urine protein may be negative or only trace detection of urinary albumin excretion rate (UAER)
Of 20 to 200 μg / min or of 30 ~~ 300 mg/24 h; once the development to the period of clinical diabetic nephropathy, ie, urinary protein
(+) Or more, UAER,> 200 μg / min or> 500 mg/24 h in patients with glomerular filtration rate (GFR)
Was a progressive decline in, and tend to increase in blood pressure, renal pathological damage to the irreversible stage, the most
Final development of renal failure.
Diabetic nephropathy is divided into five, one, two clinical difficult to diagnose, often sustained microalbumin
Clinical can only be diagnosed when the urine of diabetic nephropathy 3. This time after a positive and effective antihypertensive, hypoglycemic therapy,
Part of the urinary albumin excretion in patients with reduced or negative, kidney disease reversal or development delay. But if we can not
Do on a regular basis to check the urine in patients with urinary albumin excretion rate, until the patients had edema, high
Blood pressure, proteinuria, renal function abnormalities before considering the possibility of diabetic nephropathy, and more have been developed to sugar
4 of diabetes nephropathy, the lesion is irreversible. Thus, clinical guidelines suggest that diabetic patients should be regularly
(1/3 ~ 6 months) monitoring of urine and the detection of urinary albumin in order to achieve early diagnosis,
Early treatment. The occurrence and development of diabetic nephropathy follow the laws of the two intersecting curves, one for proteinuria
Curve from the negative, trace a large number of urinary protein gradually increased, and the other a curve for the glomerular filtration rate from
Higher than normal, normal to decreased, the two curves cross more than four diabetic nephropathy.
In addition, we should also pay attention to the identification,
Patients with diabetes and proteinuria, should not be diagnosed as diabetic nephropathy, history of diabetes less than five years, the sudden appearance of a large number of patients with proteinuria and normal renal function, not associated with diabetic retinopathy, basic can exclude diabetic nephropathy possible, to referral to superiors Hospital Nephrology Renal biopsy pathological diagnosis in order to give the correct treatment. If we blindly follow the treatment of diabetic nephropathy will be adversely affected by illness. The etiology of diabetic nephropathy is very complex, it is not very clear, but mainly the following risk factors: genetic, hypertension, high blood sugar and obesity, dyslipidemia, high uric acid. Including hypertension and high blood sugar is an important risk factor for the occurrence and development of diabetic nephropathy. Previous studies recognized cardiovascular and cerebrovascular diseases is diabetes the most common complications and death in the direct cause of hypertension and high blood sugar can significantly increased the incidence of cardiovascular and cerebrovascular diseases.
The relationship between hypertension and diabetic nephropathy
Hypertension to the glomerular capillary bed is passed through the systemic blood pressure, increased pressure within the ball, filtration pressure increase
High, resulting in increased glomerular sclerosis. Hypertension and diabetic nephropathy can promote each other. Hypertension can
The progressive increase in type 2 diabetic patients with normal urine albumin levels of urinary albumin and clinical diabetes
Nephropathy in patients with renal function deterioration. Antihypertensive treatment to prevent or delay a of the two is too
The occurrence and development of process. Studies have shown that the level of blood pressure control affect the prognosis of diabetes were independent risk
Factors.
Decline in glomerular filtration rate (GFR) and blood pressure levels. According to the 2007 edition of diabetes anti
Governance guidelines, patients with proteinuria <1 g/24 h the control of blood pressure should be below 130/80 mm Hg [including the 2007
American Diabetes Association (ADA) guidelines and the European Society for Cardiovascular Diseases / European Society of Hypertension (ESC /
ESH) guidelines to blood pressure control below 130/80 mm Hg given as proteinuria <1 g / d in patients with buck head
Value]; marked proteinuria> 1 g/24 h in patients, blood pressure control should be below 125/75 mm Hg, based primarily on
MDRD (The Modification of Diet in Renal Disease Study) clinical evidence-based medical research.
The study was supported by the leadership of the U.S. National Institutes of Health (NIH), 15 kidney disease center, compared different antihypertensive goals
Value of delay in patients with chronic kidney disease, kidney damage to progress. MDRD study finds that: egg
White urine> 1 g / patients of d, mean arterial pressure (MAP) should be strictly controlled to 92 mm Hg in order to effectively delay the
Kidney damage to progress. Moreover, in the same MAP level, lower systolic blood pressure and pulse pressure is heavier than lower diastolic blood pressure
Needs. The study recommended that the control of blood pressure below 125/75 mm Hg as proteinuria> 1 g / d in patients with the
Step-down target. The proteinuria <1 g / d of CKD patients blood pressure should be controlled and to what level, the MDRD study
Study is not a conclusion.
The selection and application of antihypertensive drugs
Delay in the occurrence and development of diabetic nephropathy, we choose antihypertensive drugs benefit more? First
The antihypertensive drugs selected for the angiotensin-converting enzyme inhibitors (ACEI), angiotensin II receptor antagonist
(ARB) and the new listing of a renin inhibitor, has a lot of evidence in the basic and clinical research
Implementation can improve the prognosis of early diabetic nephropathy. Of ACEI and ARB class of antihypertensive drugs because it can reduce the renal
Ball filtration pressure and improve renal blood flow dynamics, inhibit the production and secretion of inflammatory factors and cytokines, suppression
System of mesangial cells, fibroblasts and macrophage activation and proliferation, to improve the permeability of the filtration membrane, reduce urinary
Protein excretion and so on to become the first choice for diabetic nephropathy. Therefore, in clinical practice, when patients with micro egg
White urine, with or without hypertension, should be given ACEI or ARB treatment. The recommended start small dose,
One dose every 1 to 2 weeks, patients able to tolerate the maximum dose is appropriate, that is not symptomatic low
Elevated blood pressure, drug-free serum creatinine, and hyperkalemia is appropriate. For trace, or a small amount of proteinuria the risk of
Usually the application of drugs, a dose of 1 to 2 times, the exclusion of other interfering factors,
A few months later the majority of patients with urinary protein standards. For patients with massive proteinuria, should first check 24
Urinary protein, and then gradually increase to a single drug dose can ACEI the ARB, based on each
Months urinary protein quantification check, and patients on drug tolerance of plus or minus dose (not yet
More and better evidence-based medicine evidence that combination therapy is better than single drug treatment). If the application of ACEI
Or ARB blood pressure can not be achieved and can be combined calcium antagonists. If accompanied by edema, can be combined diuretic
Agent.
beta blockers as first choice, but for the young, and rapid heart rate, history of ischemic heart disease
Patients can be applied. In addition, in the step-down at the same time, also need to limit sodium intake, increasing exercise, quitting smoking
Adjusting lifestyles treatment.
The relationship between hyperglycemia and diabetic nephropathy
High blood sugar can cause kidney a series of pathophysiological changes, including: non-enzymatic glycation end products increase, sorbitol increased production, enhanced oxidative stress, protein kinase C and transforming growth factor (TGF) beta activity increased, resulting in glomerular increased extracellular matrix, cell injury and proteinuria increased. Another long-term high blood sugar so that the glomerulus in a hyperfiltration state, resulting in glomerular hyperperfusion and ball pressure, so that the glomerular hypertrophy, basement membrane thickening, increased capillary permeability, proteinuria formation , eventually leading to glomerulosclerosis.
DCCT study conducted in 1441 patients with type 1 diabetes patients from 29 medical centers in the United States and Canada in 1993, with its strict design, large-scale observation for a long time been recognized as the most convincing studies that strict control high blood sugar can effectively delay the onset and development of diabetic nephropathy. Studies have shown that strict control of blood sugar can make of microalbuminuria in type 1 diabetes incidence decreased by 39%, the incidence of clinical proteinuria decreased by 54%. The United Kingdom Prospective Diabetes Study (UKPDS) is so far the longest Prospective Diabetes Study, intensive therapy group intervention on selected newly diagnosed patients with type 2 diabetes for more than 10 years, mean HbA1c was 7.0%, the conventional therapy group was 7.9%. Intensive treatment of the relative risk of any diabetes-related endpoint by 12%, mainly due to reduced risk of microvascular complications. Intensive glucose control can make the occurrence of microalbuminuria in patients with type 2 diabetes by 30 percent. Analysis found that intensive treatment HbA1c decreasing by 1%, 21% lower relative risk of any diabetes-related endpoint, the risk of microvascular complications can be reduced by 37%. For blood sugar control, with HbA1c as a blood glucose target value method. According to Chinese Medical Association in August 2010 Ninth National Endocrine Conference released the "China Adult 2
Diabetes, HbA1c control goal of the expert consensus, it is recommended that the HbA 1c monitoring the condition of patients every 3 to 6 months
OK time, blood glucose control targets must be individualized, individualized. For elderly patients with diabetes,
Existing cardiovascular disease or risk, the blood glucose target should be relaxed, to avoid the occurrence of hypoglycemia and
Increased risk of death.
The choice of antidiabetic drugs sulfonylureas mouth medication, insulin is the preferred biguanide drugs in renal function is
Often can be applied to the α-glucosidase inhibitors have fewer side effects, regardless of renal function can take. To
Insulin sensitizers current debate, the United States has been under the city, it is not recommended.
Expert tips
Diabetes is a disease of serious harm to human health. Closely related to the occurrence of diabetic nephropathy, development and high blood pressure, high blood sugar. Control of blood pressure and blood sugar levels were independent risk factors affecting the prognosis of diabetic nephropathy. Strict blood pressure, blood glucose control is of great significance to reduce proteinuria and protect renal function and prevention of cardiovascular and cerebrovascular complications, In addition, we should also pay attention to the regulation of lipid levels to statin cholesterol lowering agents, should be to control high uric acid hyperlipidemia, appropriate restrictions on the amount of protein intake, avoiding use of nephrotoxic drugs. Regular monitoring of urine, urinary protein excretion, renal function and blood sugar levels, in order to adjust the treatment plan, and strive to make the indicators achieved and delay the development of diabetic nephropathy, while reducing the occurrence of cardiovascular complications and fatal complications, improve quality of life of patients with diabetes.
Why diabetic patients are most afraid of kidney damage?
Diabetic nephropathy lesions in the glomeruli, early visible thickening of
the glomerular capillary ball basement membrane, followed by narrow blood
vessels, blocking blood flow through the kidneys is significantly reduced, or
even a "short circuit" in the blood waste can not be fully discharged and then
accumulate in the blood, up to a certain extent, is uremia.
Diabetic nephropathy have a long course of
Insulin-dependent diabetes, for example, initially to 10 years, almost no symptoms, often overlooked, "deceptive", so called occult period. In fact, if the urine microalbumin, and can often be found. Therefore, people with diabetes should regularly determination of urine protein, here needs to be emphasized is that the conventional urine protein examination is not found, the need to measure trace protein. The urine can be detected in the protein, this time more than the middle of the diabetic nephropathy, began intermittent fatigue and disease poorly controlled, and then gradually evolved into persistent proteinuria. Edema and hypertension is characteristic of diabetic nephropathy, diabetic nephropathy will eventually enter the renal failure of this period, the kidney is almost the loss of filtration and reabsorption, body waste is excreted by the kidneys, "sewage" Smirnov, uremic spread to various organizations. organs.
Non-insulin-dependent diabetes mellitus complicated by nephropathy course of short, this may be difficult to ascertain the onset time.
Diabetic nephropathy focuses on prevention, as necessary, restriction of dietary protein quality
Diabetic nephropathy, once formed, treatment is difficult, and therefore focuses on early prevention, early diagnosis and treatment. Trace protein determination of the project as a long-term routine examination, urine tested once every 1-3 months, even if the urine microalbumin negative should also be active prevention, to win a number of years of early diagnosis and treatment time.
When the development of diabetic nephropathy to renal damage is more significant under the guidance of a doctor to limit the quality of the protein in the diet. The total daily intake of 1.2 to 1.5 g per kg of standard body weight of the normal to the initial 1.0 to 1.2 grams, advanced 0.6 to 0.8 g. Many patients think that the protein is lost from the urine, would like to compensate by increasing the protein content of the diet, in fact, this method has not only failed to increase the protein content in the blood, but increased the burden on the kidneys, accelerated renal failure. This point, please bear in mind the diabetic patients. High-quality protein (animal protein) instead of the vegetable protein is a useful way, such a small but efficient initiatives can reduce the burden of renal function, and not too small so that the body protein, is a better expedient.
Hypertension to accelerate the process of renal failure
Hypertension is the most important factor to accelerate the process of renal failure, early, aggressive treatment. Have high blood pressure should strengthen management and monitoring, it is recommended that the measurement once a week. Low-salt contribute to blood pressure control, the daily intake of no more than 5 grams. Antihypertensive drugs should use the expansion of renal vascular, and help to improve renal function.
The patient end is not of renal failure, only dialysis or kidney transplantation. At this point, not only more costly, the patient will also be under tremendous suffering. Therefore, all the kidneys, the drug should avoid it, and actively prevent urinary tract infections, and properly protect your kidney function, so that the body's sewage treatment system in good working condition.
Diabetic nephropathy have a long course of
Insulin-dependent diabetes, for example, initially to 10 years, almost no symptoms, often overlooked, "deceptive", so called occult period. In fact, if the urine microalbumin, and can often be found. Therefore, people with diabetes should regularly determination of urine protein, here needs to be emphasized is that the conventional urine protein examination is not found, the need to measure trace protein. The urine can be detected in the protein, this time more than the middle of the diabetic nephropathy, began intermittent fatigue and disease poorly controlled, and then gradually evolved into persistent proteinuria. Edema and hypertension is characteristic of diabetic nephropathy, diabetic nephropathy will eventually enter the renal failure of this period, the kidney is almost the loss of filtration and reabsorption, body waste is excreted by the kidneys, "sewage" Smirnov, uremic spread to various organizations. organs.
Non-insulin-dependent diabetes mellitus complicated by nephropathy course of short, this may be difficult to ascertain the onset time.
Diabetic nephropathy focuses on prevention, as necessary, restriction of dietary protein quality
Diabetic nephropathy, once formed, treatment is difficult, and therefore focuses on early prevention, early diagnosis and treatment. Trace protein determination of the project as a long-term routine examination, urine tested once every 1-3 months, even if the urine microalbumin negative should also be active prevention, to win a number of years of early diagnosis and treatment time.
When the development of diabetic nephropathy to renal damage is more significant under the guidance of a doctor to limit the quality of the protein in the diet. The total daily intake of 1.2 to 1.5 g per kg of standard body weight of the normal to the initial 1.0 to 1.2 grams, advanced 0.6 to 0.8 g. Many patients think that the protein is lost from the urine, would like to compensate by increasing the protein content of the diet, in fact, this method has not only failed to increase the protein content in the blood, but increased the burden on the kidneys, accelerated renal failure. This point, please bear in mind the diabetic patients. High-quality protein (animal protein) instead of the vegetable protein is a useful way, such a small but efficient initiatives can reduce the burden of renal function, and not too small so that the body protein, is a better expedient.
Hypertension to accelerate the process of renal failure
Hypertension is the most important factor to accelerate the process of renal failure, early, aggressive treatment. Have high blood pressure should strengthen management and monitoring, it is recommended that the measurement once a week. Low-salt contribute to blood pressure control, the daily intake of no more than 5 grams. Antihypertensive drugs should use the expansion of renal vascular, and help to improve renal function.
The patient end is not of renal failure, only dialysis or kidney transplantation. At this point, not only more costly, the patient will also be under tremendous suffering. Therefore, all the kidneys, the drug should avoid it, and actively prevent urinary tract infections, and properly protect your kidney function, so that the body's sewage treatment system in good working condition.
Diabetic nephropathy diet What precautions?
Diabetic nephropathy is less than for people with diabetes to avoid any complications, many patients know it's terrible, but still can not be avoided. Note that this Armed Police Beijing Corps hospital diabetes treatment experts to diabetic nephropathy in patients with kidney disease diet: the diet of diabetic nephropathy arrangements more difficult, it is necessary to ensure adequate calories and nutrients, but also limit the carbohydrates, fats and protein. So, if conditions should be under the guidance of the dietitians, according to the condition, adjust the three meals a day.
Protein intake
Long-term to take high-protein diet may increase kidney filtration state, while increasing the generation and retention of the body of toxic nitrogen metabolites, leading to further renal damage. Therefore, we propose to limit the right amount of protein in the diet to reduce kidney damage.
Myth: patients, mainly vegetarian or do not eat meat, dairy products, eggs, low-protein diet, but less vegetarian vegetable protein containing essential amino acids, can not meet the needs of the body's long-term consumption may cause the protein nutritional bad, is not conducive to the recovery of renal function.
How to limit the intake of protein
Limit the total amount of protein. General proposition, the protein in the daily diet, according to the 0.6-0.8 g / kg standard weight given to increase the proportion of high-quality protein, but also within the scope of the limited star. In patients with diabetic nephropathy 3,4 adhere to other principles of diabetes nutrition therapy at the same time, grasp the quality and quantity of the daily protein intake, and out of balance, it may be beneficial for the recovery of the kidneys. For example: height 170 cm, the standard weight of 65 kg, urine albumin 80 mg / min in early diabetic nephropathy. Total protein in the daily diet should be: 65 x 0.6-65 × 0.8 = 39 grams to 52 grams of high quality protein should be accounted for more than 25 grams.
When the development of diabetic nephropathy to end stage renal disease, protein restriction should be more stringent. The clinical part of the wheat starch diet as a major source of energy, instead of rice and flour. Staple foods such as rice and flour contains a higher amount of non-high-quality vegetable protein (50 g each containing about 4 grams), while little protein content of wheat starch in plants. However, wheat starch production is not easy, can also be used the marketing of corn flour instead. This can save a plant protein, to be supplemented with animal protein, and thus more conducive to meet the body's physiological needs.
The supply of amino acids: as much as possible the intake of essential amino acids, can also be oral alpha acid (renal Tablets) to replace part of the essential amino acids; or renal amino acid supplement.
Heat: in the low protein diet, heat supply must be adequate to maintain normal physiological needs. Daily intake of 30-35 kcal / kg body weight of the heat. You can select some high in calories and low protein content of staple foods such as potatoes, lotus root starch, vermicelli, taro, sweet potatoes, yams, pumpkin, water chestnut flour, water chestnut powder, dietary total calories of the standard range. Ensure the supply and demand balance.
Fat: end stage renal disease is often associated with lipid metabolism disorders, insist on a low fat intake. Olive oil, peanut oil contains a rich monounsaturated fatty acids, can be used as the source of energy.
Salt restriction: ESRD to a certain stage of development can often have high blood pressure, performance as a reduction of edema or urine output, limiting salt can effectively prevent the progress of complications. Accompanied by vomiting, diarrhea, should not unduly limit the sodium salt, or even need to add.
Water: master patient fluid intake and balance is also very important. End stage renal disease in uremia, oliguria or anuria, when the water intake Chang very important, too much intake of water will increase the burden on the kidneys, leading to disease progression, it is generally a day into the fluid volume for the previous day's urine output plus 500 ml; However, when patients with fever, vomiting, diarrhea and other symptoms, it should be more fluid. Therefore, patients need to understand the water content of the food, Expenditure and Revenues.
Potassium: the daily urine output greater than 1000 ml and normal serum potassium amount, not to restrict the intake of minutes, can generally be free to choose fresh vegetables and fruits. Kidney excretion of potassium decreased, if hyperkalemia, often on the body to cause harm or even life-threatening and should therefore be appropriate to limit high potassium foods, should be lower than the 1500-2000 mg daily. General, like fruits and vegetables (pumpkin, melon, gourd), apples, pears, pineapple, watermelon, grapes, and potassium content are relatively low, you can eat high potassium foods such as rape, spinach, leeks, tomatoes, seaweed, bananas, peaches, etc., should be limited as appropriate; but does not mean that absolutely can not eat, but should choose to eat in the total range, while avoiding the consumption of concentrated fruit juice, gravy, you should eat more; when hypokalemia high potassium food.
Calcium, phosphorus: kidney damage, the excretion of phosphorus will be reduced, resulting in hyperphosphatemia increased. Loss, affect the absorption of calcium and vitamin D3 synthesis. Reduce the concentration of calcium in the blood, prone to osteoporosis, so ideal for the treatment of dietary calcium content should be increased as much as possible to reduce the phosphorus content. Low-protein diet reduces the intake of phosphorus, in favor of treatment.
The majority of patients with diabetic nephropathy is not to eat do not worry, experts have warned that patients with diabetes, the diabetic condition was not effectively controlled can cause a variety of complications, diabetic nephropathy is only one of the above introduction. Therefore, how to treat
Tuesday, August 7, 2012
Summary of focal segmental glomerulosclerosis
Focal segmental glomerulosclerosis (focal segmental glomeralosclerosis) lesions as focal, segmental, involving only a small part of the glomerular Lesions of the glomerular capillary plexus showed segmental sclerosis is a common cause nephrotic syndrome, one of the reasons. More common in children and young people. This type of nephritis for patients on hormone treatment is not ideal. More than to continue to develop as diffuse sclerosing glomerulonephritis.
Pathological changes
Lesions as focal, often from the deep renal cortex near the medulla part of the small number of glomerular Only a small number of early glomerular involvement, other glomerular no obvious lesions or minor lesions. Lesions of the glomerular capillary plexus part of the capillary collapse, mesangial widening, sclerosis, hyalinization. Deposition of lipid droplets and the glass-like substance often mesorectal and capillaries. Sometimes seen engulfed lipid accumulation of foam cells. Electron microscope, the hardening part of the capillary basement membrane shrinkage, uneven thickness. The meantime visible electron-dense material and lipid droplets. Epithelial cell foot processes disappear. Immunofluorescence examination showed lesions of the glomeruli of immunoglobulin and complement deposition, mainly IgM and C3.
Glomerular capillary plexus, some sclerosis, hyalinization × 350
Lesions continue to develop the involvement of the glomerulus gradually increased. Some glomerular capillary plexus all fibrosis, sclerosis, hyalinization (global sclerosis). Corresponding tubular atrophy and fibrosis. Hyperplasia of the renal interstitial fibrosis, a small amount of lymphocytes and mononuclear cell infiltration, sometimes visible and the accumulation of foam cells. Late, a large number of glomerular sclerosis can lead to the development of diffuse sclerosing glomerulonephritis and renal insufficiency.
Clinical features and outcome
About 80% of patients with focal segmental glomerulosclerosis with nephrotic syndrome. Nephrotic syndrome in general, of which about 2/3, accompanied by hematuria, and often have high blood pressure. Massive proteinuria, and more non-selective. The patient bad effects of hormone therapy, only 20% to 30% efficiency. Lesions, often continue to develop, can lead to renal insufficiency. General outcomes for children than adults.
learn:Can FSGS be Cured
Hypertensive nephropathy creatinine 7.9 how treatment
Hypertensive kidney disease, kidney disease due to hypertension-induced secondary. Creatinine is a symptom of the performance of many kidney patients. Hypertensive nephropathy creatinine 7.9 how to treat it? Here I introduce you to help!
Hypertensive nephropathy refers to as primary hypertension-induced nephropathy, hypertensive nephropathy age of onset is usually in the 25-45 years of age, and hypertension-induced kidney damage clinical symptoms, age 40-60 years old. Hypertensive nephropathy for several years now to do dialysis, creatinine 7.9 how to do? Earliest symptoms of nocturia increased, reflecting the tubular ischemic lesions, urine concentration function began to subside. And proteinuria, indicating that the glomerular lesions.
Hemodialysis as renal replacement therapy used in renal failure, uremia patients. Hypertensive nephropathy for several years now to do dialysis, creatinine, or 7.9 how to do? When the deterioration of renal patients progress to renal failure stage, patients in clinical practice will produce a series of symptoms of a serious threat to the patient's quality of life issues and life and health status.
At this point, clinical renal failure patients in hemodialysis renal replacement therapy, in the short time stability of the patient's physical condition, to avoid an emergency, serious concurrent symptoms. However, the work characteristics of hemodialysis, hemodialysis only as renal replacement therapy for renal failure patients, temporary removal of the in vivo accumulation of harmful substances.
Renal lesions did not get a true sense of the treatment, the toxins will continue to siltation of the patient's body, you will need ongoing hemodialysis instead of their own kidneys work. Hypertensive nephropathy for several years now to do dialysis, creatinine 7.9 how to do? Accompanied by damage to kidney tissue increasing the scope of the accumulation of toxic substances will be more and more, hemodialysis time will be constantly reduced their own kidneys to gradually shrink, the cost. Once the development of this stage, no return of kidney patients will eventually embark on dialysis, accelerating the advent of the end of life.
Through the introduction of the above experts, hypertension nephropathy creatinine 7.9 how treatment whether or not to have a certain understanding? Must not panic, and actively cooperate with medical treatment kidney disease, then soon recover.
Hypertensive nephropathy refers to as primary hypertension-induced nephropathy, hypertensive nephropathy age of onset is usually in the 25-45 years of age, and hypertension-induced kidney damage clinical symptoms, age 40-60 years old. Hypertensive nephropathy for several years now to do dialysis, creatinine 7.9 how to do? Earliest symptoms of nocturia increased, reflecting the tubular ischemic lesions, urine concentration function began to subside. And proteinuria, indicating that the glomerular lesions.
Hemodialysis as renal replacement therapy used in renal failure, uremia patients. Hypertensive nephropathy for several years now to do dialysis, creatinine, or 7.9 how to do? When the deterioration of renal patients progress to renal failure stage, patients in clinical practice will produce a series of symptoms of a serious threat to the patient's quality of life issues and life and health status.
At this point, clinical renal failure patients in hemodialysis renal replacement therapy, in the short time stability of the patient's physical condition, to avoid an emergency, serious concurrent symptoms. However, the work characteristics of hemodialysis, hemodialysis only as renal replacement therapy for renal failure patients, temporary removal of the in vivo accumulation of harmful substances.
Renal lesions did not get a true sense of the treatment, the toxins will continue to siltation of the patient's body, you will need ongoing hemodialysis instead of their own kidneys work. Hypertensive nephropathy for several years now to do dialysis, creatinine 7.9 how to do? Accompanied by damage to kidney tissue increasing the scope of the accumulation of toxic substances will be more and more, hemodialysis time will be constantly reduced their own kidneys to gradually shrink, the cost. Once the development of this stage, no return of kidney patients will eventually embark on dialysis, accelerating the advent of the end of life.
Through the introduction of the above experts, hypertension nephropathy creatinine 7.9 how treatment whether or not to have a certain understanding? Must not panic, and actively cooperate with medical treatment kidney disease, then soon recover.
Hypertensive nephropathy meals must pay attention to diet
Want to stabilize the disease for patients with hypertensive nephropathy,
eating three meals a day in their daily lives is very important, are often
exacerbate the condition because of poor eating habits, there is a lot of people
do not care about their health in a busy work stable patients with hypertensive
nephropathy is also not the first time to detect, so often wasted the best
treatment, however you want better treatment, we first and kidney specialists
look at diet is very important.
Daily life for patients with hypertension often less for obesity should be the smaller meals, very often have to eat low heat to food, so that the total calories should be controlled every 8 or 36 megajoules, there are sure to pay attention to every days of the staple food of 150-250 grams, so that this will lead to animal protein and vegetable protein is 50%.Also note that the dinner should be small and light, for patients with excessive greasy food will induce a stroke. So the cooking oil to use with vitamin E and linoleic acid in vegetable oil, do not eat sweets.
The patient must pay attention to diet, low salt, usually per person per day salt amount should be strictly controlled at 2-5 g, most of that is about one teaspoon. There is a study found that, this time in elderly hypertensive patients with plasma ferritin lower than normal, so to say that I eat peas, fungus and other iron-rich foods, this is the case not only can lower blood pressure, which can prevent anemia in the elderly .
Above here is the latest hypertensive nephropathy meals must pay attention to diet information, want more than high blood pressure daily diet for patients with certain diseases early treatment in order to maintain a good attitude is also very important.
learn:Good fruits for Hypertension Nephropathy patients
Daily life for patients with hypertension often less for obesity should be the smaller meals, very often have to eat low heat to food, so that the total calories should be controlled every 8 or 36 megajoules, there are sure to pay attention to every days of the staple food of 150-250 grams, so that this will lead to animal protein and vegetable protein is 50%.Also note that the dinner should be small and light, for patients with excessive greasy food will induce a stroke. So the cooking oil to use with vitamin E and linoleic acid in vegetable oil, do not eat sweets.
The patient must pay attention to diet, low salt, usually per person per day salt amount should be strictly controlled at 2-5 g, most of that is about one teaspoon. There is a study found that, this time in elderly hypertensive patients with plasma ferritin lower than normal, so to say that I eat peas, fungus and other iron-rich foods, this is the case not only can lower blood pressure, which can prevent anemia in the elderly .
Above here is the latest hypertensive nephropathy meals must pay attention to diet information, want more than high blood pressure daily diet for patients with certain diseases early treatment in order to maintain a good attitude is also very important.
learn:Good fruits for Hypertension Nephropathy patients
Hypertensive nephropathy is how to better select the diet
Hypertensive nephropathy how to better select the diet! Long-term high blood pressure causes the renal function gradually decline, will the patient's life to bring the troubled, let us introduce change under hypertensive renal disease patients on diet?
Hypertensive renal disease patients on the table to develop the "four little over three" good habit, let us to understand correctly.
1, eat sweets
Sweets with high sugar content can be converted into fat in the body, easy to promote atherosclerosis.
2, salt diet
The diet should be light and appropriate, to eat less salty. For hypertensive patients, a simple limit of salt can make blood pressure returned to normal; the right, in patients with severe hypertension, salt restriction can not only improve the efficacy of antihypertensive drugs, but also the dose of antihypertensive drugs to reduce, thus greatly reducing the antihypertensive drugs side effects and drug costs.
(3) eat less animal fat
Animals including high cholesterol, can accelerate atherosclerosis. Such as liver, kidney, brain, heart, etc. should be eating.
(4) drink less
If high blood pressure in patients with smoking and alcohol, lead to heart, brain and kidney damage due to excessive alcohol and tobacco.
Hypertensive nephropathy how to better select the diet! Hypertensive renal disease patients usually develop good habits, kidney disease symptoms to select the regular kidney hospital for treatment, I wish you a happy life.
learn:Hypertensive nephropathy
Saturday, August 4, 2012
FSGS kidney disease, in addition to hormones, there are other ways?
Number of FSGS kidney patients may have such concerns: I would like to cure
my kidney, want to avoid the use of hormones, but also more effective than
hormone treatment? Now detailed knowledge of the FSGS kidney disease and
treatment programs.
What is the FSGS kidney disease? What are clinical manifestations of FSGS kidney disease?
Glomerular capillary nephrotic FSGS kidney disease called focal segmental glomerulosclerosis whole, refers to the glomerular capillary loops with focal segmental glomerular sclerosis or hyaline degeneration, no significant cell proliferation. FSGS kidney disease is the primary a common pathological type, 50% of primary patients with the pathological type of FSGS kidney disease, renal biopsy can be clear of the disease.
The disease mostly occurs in children and young people, more men than women, a small number of patients with FSGS kidney disease before the onset of upper respiratory tract infection or allergic reaction history. Of FSGS kidney disease can be familial tendency FSGS kidney disease is relatively common in the atopic population, the main clinical manifestations and characteristics:
(1) The first clinical symptoms, microscopic to common hematuria, and occasionally gross hematuria, and adults, about 2/3 of patients with mild persistent hypertension.
(2) urine routine examination, a small number of patients with FSGS kidney disease is asymptomatic. Proteinuria and the vast majority of non-selective, but early high or moderate selectivity.
(3) blood test serum C3 levels were normal, IgG levels decline.
(4) of FSGS kidney patients more the performance of proximal tubular dysfunction, progressive decline of glomerular filtration rate, upper respiratory tract infection or allergic allows a variety of symptoms get worse.
Do not want to reuse hormone, how to treat?
For the treatment of FSGS kidney disease, current clinical is still a lack of effective measures. Western medicine clinical application of hormone combination therapies for treatment. Corticosteroid therapy, a small number of patients with FSGS kidney disease (30% - 40%) of the condition can be eased. However, the attendant. Indeed, a large number of side effects of hormone produced by kidney patients on the treatment of their disease has concerns about the mental. Especially after the application of hormones or immunosuppressive agents in kidney patients discontinued the course of medication in the face of the predisposing factors (such as colds, fever, fatigue, allergies, etc.), kidney disease condition is very easy to relapse and increase.
Typically, FSGS kidney patients face hormone inevitably there are concerns about the psychological. Therefore, in search of better treatment methods, to avoid the side effects of hormones, become the common aspiration of the FSGS kidney patients. In fact, the micro therapy for the penetration of traditional Chinese medicine to break this traditional treatment model. Why do you say? Infiltration therapy of micro-based traditional Chinese medicine can effectively block the fibrosis of the kidney lesions, activation of cell lesions of the kidney metabolic function, and rebuilt repair and reconstruction of damaged kidneys to mention the essential nutrients. Kidney area skin penetration into the body of the micro-penetration therapy of Chinese medicine to improve the repair environment can damage the kidneys, the gradual recovery of kidney disease, glomerular effective filtration, enhanced compensatory ability of the kidneys of healthy cells. In this way, the root causes of nephropathy proceed slowly to restore renal function, fundamentally eliminate the patient's urine protein.
However, for Miss Jiang is now applied hormone therapy, hormone medication principle limit, not the temerity to disable the hormone drugs. Because the hormone withdrawal there is a pattern, sudden withdrawal can cause hormone arrest reaction, exacerbate kidney disease. Therefore, you want to really get rid of the hormone, wants to fundamentally cure kidney disease, should be gradual infiltration therapy in the application of micro-based traditional Chinese medicine treatment of kidney disease during hormone dosage reduction, and ultimately achieve the purpose of treating kidney disease and completely get rid of the hormone.
Learn more:Recurrent FSGS Treatment Options- Immunotherapy
What is the FSGS kidney disease? What are clinical manifestations of FSGS kidney disease?
Glomerular capillary nephrotic FSGS kidney disease called focal segmental glomerulosclerosis whole, refers to the glomerular capillary loops with focal segmental glomerular sclerosis or hyaline degeneration, no significant cell proliferation. FSGS kidney disease is the primary a common pathological type, 50% of primary patients with the pathological type of FSGS kidney disease, renal biopsy can be clear of the disease.
The disease mostly occurs in children and young people, more men than women, a small number of patients with FSGS kidney disease before the onset of upper respiratory tract infection or allergic reaction history. Of FSGS kidney disease can be familial tendency FSGS kidney disease is relatively common in the atopic population, the main clinical manifestations and characteristics:
(1) The first clinical symptoms, microscopic to common hematuria, and occasionally gross hematuria, and adults, about 2/3 of patients with mild persistent hypertension.
(2) urine routine examination, a small number of patients with FSGS kidney disease is asymptomatic. Proteinuria and the vast majority of non-selective, but early high or moderate selectivity.
(3) blood test serum C3 levels were normal, IgG levels decline.
(4) of FSGS kidney patients more the performance of proximal tubular dysfunction, progressive decline of glomerular filtration rate, upper respiratory tract infection or allergic allows a variety of symptoms get worse.
Do not want to reuse hormone, how to treat?
For the treatment of FSGS kidney disease, current clinical is still a lack of effective measures. Western medicine clinical application of hormone combination therapies for treatment. Corticosteroid therapy, a small number of patients with FSGS kidney disease (30% - 40%) of the condition can be eased. However, the attendant. Indeed, a large number of side effects of hormone produced by kidney patients on the treatment of their disease has concerns about the mental. Especially after the application of hormones or immunosuppressive agents in kidney patients discontinued the course of medication in the face of the predisposing factors (such as colds, fever, fatigue, allergies, etc.), kidney disease condition is very easy to relapse and increase.
Typically, FSGS kidney patients face hormone inevitably there are concerns about the psychological. Therefore, in search of better treatment methods, to avoid the side effects of hormones, become the common aspiration of the FSGS kidney patients. In fact, the micro therapy for the penetration of traditional Chinese medicine to break this traditional treatment model. Why do you say? Infiltration therapy of micro-based traditional Chinese medicine can effectively block the fibrosis of the kidney lesions, activation of cell lesions of the kidney metabolic function, and rebuilt repair and reconstruction of damaged kidneys to mention the essential nutrients. Kidney area skin penetration into the body of the micro-penetration therapy of Chinese medicine to improve the repair environment can damage the kidneys, the gradual recovery of kidney disease, glomerular effective filtration, enhanced compensatory ability of the kidneys of healthy cells. In this way, the root causes of nephropathy proceed slowly to restore renal function, fundamentally eliminate the patient's urine protein.
However, for Miss Jiang is now applied hormone therapy, hormone medication principle limit, not the temerity to disable the hormone drugs. Because the hormone withdrawal there is a pattern, sudden withdrawal can cause hormone arrest reaction, exacerbate kidney disease. Therefore, you want to really get rid of the hormone, wants to fundamentally cure kidney disease, should be gradual infiltration therapy in the application of micro-based traditional Chinese medicine treatment of kidney disease during hormone dosage reduction, and ultimately achieve the purpose of treating kidney disease and completely get rid of the hormone.
Learn more:Recurrent FSGS Treatment Options- Immunotherapy
FSGS nephritis can be cured?
The nephritis Note points? Chronic glomerulonephritis, urinary protein, eyes swollen, very yellow urine drug treatment a year, the effect is very bad. The nephritis how conservative treatment? How kind of effect? Nephritis there is no effective treatment method?
Chronic glomerulonephritis, referred to as chronic nephritis, refers to proteinuria, hematuria, hypertension, edema of the basic clinical manifestations, onset in different ways, persistent disease, the lesions slowly progress can be varying degrees of renal dysfunction will eventually the development of a group of chronic renal failure, glomerular disease. Acute kidney disease or illness is serious, bed rest, such as systemic edema, and even pleural effusion, ascites; impaired heart and lung function, cough, wheezing, dyspnea, hemoptysis; severe high blood pressure, dizziness, headache significantly ; severe hematuria; renal damage severe oliguria and vomiting, should rest in bed. I have read the information you submit in patients with renal biopsy result is that the focal stage of glomerulosclerosis, this situation is due to all causes of kidney ischemia and hypoxia, leading to glomerular sclerosis, so that it can not function normally, a result of urine abnormalities, so the most critical now is to improve renal ischemia and hypoxia, blocking renal fibrosis, repair damaged cells now, vasodilators, anti-inflammatory, anticoagulant standard treatment, degradation of the integrated system can be achieved clinical cure, and you do not worry, the diet should also pay attention to low salt, low protein diet, soy products, seafood, beef and mutton, spicy foods forbidden to eat. Do not know the patients what age, have no history of primary, such as hypertension, coronary heart disease, diabetes and other patients with urine test results, how? This history is long? Now taking any medication? Would like to submit a detailed medical records so that I can do a detailed analysis and guidance, what can contact me.
Learn more:The Chronic FSGS Diet
FSGS kidney disease is it? Is there any way? Difficult to treat you?
FSGS kidney disease is it? Is there any way? Difficult to treat you? Simply:
a nephrotic syndrome, renal biopsy results. Mainly three high and one low: a
large number of urine protein, a high degree of edema, hypoalbuminemia, and
hyperlipidemia.
The FSGS write down the full focal segmental glomerulosclerosis focal segmental glomerulosclerosis. Focal segmental glomerulosclerosis (FSGS) leading to massive proteinuria, a common cause, which in some patients quickly develop end-stage renal failure.
FSGS is the onset of nephrotic syndrome in children and adolescents, also contributed to the important cause of adult kidney failure.
The disease is also known as focal glomerulosclerosis (of focal the glomerular sclerosis), or focal nodular glomerulosclerosis (of focal nodular glomerulosclerosis).
The disease accounts for about one sixth of the cases of nephrotic syndrome, minimal change disease (Minimal Change Disease, referred to MCD) is the most important reason to result in children with nephrotic syndrome. MCD and FSGS may have similar reasons for the disease.
FSGS Clinical divided into 5 subtypes:
1 .. classic: hardened parts are mainly located in blood vessels around the capillary loops.
(2) the top type: hardened parts are mainly located in the urinary pole.
Collapse type: microfold capillary loops shrink, collapse was the segment or the ball distribution.
4-cell: the focal mesangial cells and endothelial cells also increased podocyte.
Non-special type: not accrue to the subtype. Hardening can occur in any part of the
For the treatment of FSGS nephrotic hormones, hormone treatment fundamentally, the proposal is still in Integrative Medicine, our hospital is the main Western medicine monoclonal antibody plasma exchange Maikang Composition treatment of traditional Chinese medicine of Chinese micro-penetration therapy.
Learn more:Treatment for Proteinuria of FSGS
The FSGS write down the full focal segmental glomerulosclerosis focal segmental glomerulosclerosis. Focal segmental glomerulosclerosis (FSGS) leading to massive proteinuria, a common cause, which in some patients quickly develop end-stage renal failure.
FSGS is the onset of nephrotic syndrome in children and adolescents, also contributed to the important cause of adult kidney failure.
The disease is also known as focal glomerulosclerosis (of focal the glomerular sclerosis), or focal nodular glomerulosclerosis (of focal nodular glomerulosclerosis).
The disease accounts for about one sixth of the cases of nephrotic syndrome, minimal change disease (Minimal Change Disease, referred to MCD) is the most important reason to result in children with nephrotic syndrome. MCD and FSGS may have similar reasons for the disease.
FSGS Clinical divided into 5 subtypes:
1 .. classic: hardened parts are mainly located in blood vessels around the capillary loops.
(2) the top type: hardened parts are mainly located in the urinary pole.
Collapse type: microfold capillary loops shrink, collapse was the segment or the ball distribution.
4-cell: the focal mesangial cells and endothelial cells also increased podocyte.
Non-special type: not accrue to the subtype. Hardening can occur in any part of the
For the treatment of FSGS nephrotic hormones, hormone treatment fundamentally, the proposal is still in Integrative Medicine, our hospital is the main Western medicine monoclonal antibody plasma exchange Maikang Composition treatment of traditional Chinese medicine of Chinese micro-penetration therapy.
Learn more:Treatment for Proteinuria of FSGS
In children with renal comprehensive common complication
1) infection is the most common complications of this disease, infection not
only make the condition repeatedly affect the treatment effect, and might lead
directly to death. This disease is prone to the cause of infection:
① humoral immune function is low (IgG in urine, blood loss, decreased synthesis of catabolism increase);
② often cellular immune dysfunction;
③ transferrin and zinc-binding protein is lost in the urine, influence immune regulation and lymphocyte function changes;
④ protein metabolism in malnutrition, and abnormalities of the complement system;
⑤ edema caused by local circulatory disorders;
⑥ glucocorticoids and immunosuppressants long period of time.
Infection can occur in the respiratory tract, urinary tract, skin and soft tissue; bacterial peritonitis is also not uncommon. More pneumococcal infections, mainly tuberculosis infection in recent years has also increased. Generally do not advocate routine prophylactic use of antibacterial drugs, but should be strengthened to protect, should be timely and thorough treatment of bacterial infections. Viral infection compared with the previous increase, particularly when receiving corticosteroids, immunosuppressive therapy, varicella, herpes zoster virus infection, the disease than the average children's weight, should strengthen the anti-viral treatment. Contacts should be ascertained hormones, immunosuppressants temporary reduction, and given a gamma globulin injection. Long-term application of corticosteroids, immunosuppressants patients should also be noted that the activities or spread of tuberculosis in the body, and secondary fungal infection.
2) low blood volume and electrolyte imbalance NS part of the children with low blood volume, even if the blood is dissolved is not low effective circulating volume due to hypoalbuminemia, plasma colloid osmotic pressure leaving a fragile state some incentive effect prone to cause low blood volume, or even shock. The common causes are:
① vomiting, diarrhea, diuretic, ascites, bleeding break fluid loss;
② long-term corticosteroids, causing their own adrenal suppressed under stress the body to retain sodium and water capacity;
③ sick child for a long time to ban salt or low-salt diet induced hyponatremia.
Common electrolyte disorder in patients with kidney disease have hyponatremia, hypokalemia, hypocalcemia. Some parents of children with NS inappropriate long-term ban salt or eat sodium free salt substitutes; or edema excessive use of diuretics; and infection, vomiting, diarrhea and other factors can cause hyponatremia. In the above-mentioned incentives, such as children with the sudden appearance of anorexia, fatigue, drowsiness, blood pressure, or even shock, convulsions and other performance should be considered hyponatremia may be. A large number of diuretic use high-dose diuretic or corticosteroids, should be alert to the emergence of hypokalemia. Nephrotic syndrome with massive proteinuria, 25 - hydroxy calciferol binding protein loss induced calcium metabolism disorders, intestinal calcium malabsorption, reduced the sensitivity of the bone to parathyroid hormone, can cause hypocalcemia, even a low calcium convulsion.
3) a hypercoagulable state and thrombus formation of NS patients blood Yi showing hypercoagulable state, the main Increased
① liver synthesis of clotting factors, such as II, Ⅴ, VII, VIII factor increase and hyperfibrinogenemia;
② plasma anti-clotting substances, decreased urinary loss of antithrombin Ⅲ too much;
③ high ester hyperlipidemia slow blood flow, increased blood viscosity, such as extensive use of diuretics to hypovolemia, hemoconcentration;
④ platelet count increased, the increase in adhesion and aggregation;
⑤ infection or other factors caused vascular wall damage and easy to activate the intrinsic coagulation system;
⑥ large doses of corticosteroid application may promote a hypercoagulable state. These procoagulant factors lead to the patient moving, venous thrombosis, of which the most common renal vein thrombosis, the incidence of each report is different to adult kidney disease from 5% to as high as 14%. Membrane proliferative glomerulonephritis, followed by membranous nephropathy complicated by. Children with nephrotic thrombosis can occur in different parts of the renal vein, deep venous, femoral artery, pulmonary artery, superior mesenteric artery, cerebral artery, but also the renal vein thrombosis more common, acute typical cases showed a sudden onset of gross hematuria. low back pain, spinal rib angle tenderness, kidney area, mass, in the case of bilateral renal rapid decrease in proteinuria aggravate; chronic often edema, proteinuria continued remission, and their symptoms are not obvious. X-ray examination the ipsilateral renal enlargement, ureter notch. B super addition to the kidney increases, showing that renal vein thrombosis. Renal venography can be confirmed.
In addition to renal vein thrombosis, such as sick children:
① both sides of the lower limb edema asymmetry does not change with body position changes;
② skin burst purpura, and rapidly expanding with pain;
③ scrotal edema was purple;
④ refractory ascites does not go away;
⑤ leg pain accompanied by the dorsalis pedis artery pulse disappeared, and so on, should be considered thrombosis.
4), acute renal insufficiency in children with NS occurrence of acute renal failure is rare, but if the following conditions, namely, acute renal failure may occur.
① hypovolemia or hypovolemic shock, renal blood hypoperfusion can be caused by prerenal azotemia, such as its persistence can lead to tubular necrosis
② glomerular lesions, especially proliferative glomerulonephritis lesions can be caused by glomerular filtration rate decreased, the occurrence of acute renal dysfunction;
③ small lesions, but can be decreased effectively due to renal interstitial edema or renal tubular protein casts obstruction, caused by the proximal tubule and the renal capsule hydrostatic pressure increased, resulting in glomerular filtration;
④ Because the application of non-steroidal anti-inflammatory drugs, diuretics, antibiotics induced acute interstitial nephritis;
⑤ the glomerular lesions deteriorated, especially when complicated by crescentic glomerulonephritis;
⑥ acute renal vein thrombosis.
5) vitamin D and calcium metabolism disorders of children with NS massive proteinuria, can cause blood vitamin D binding protein (molecular weight 59 000) since the urinary loss of vitamin D deficiency affect intestinal calcium absorption, and therefore such a sick child more hypocalcemia associated with renal tubular change may also affect the 1-25 - (OH) 2D3 formation; long-term application of corticosteroids; further exacerbated by vitamin D and calcium metabolism disorders. Hypocalcemia, regular feedback to cause hyperparathyroidism, bone calcification exception is therefore often show clinical hypocalcemia, serum 25 - hydroxy calciferol is decreased, the blood parathyroid hormone increased, osteoporosis, osteomalacia, especially in the rapid growth in children during these changes more pronounced.
Endocrine changes in 6).
① reduce the thyroid hormone function: sick children when the NS basal metabolic rate, blood protein binding iodine value decreased. Most scholars believe that the Department of thyroid binding globulin caused by urine loss may also increase in thyroid hormone synthesis decline in its distribution of the extravascular space; there is blood when the kidney disease inhibitory factor preventing thyroxine and globulin combination.
② thymic hormone decreased significantly: with blood zinc low related, since the urine is lost outside the NS in addition to the zinc-binding protein, and also the decrease due to the lack of transferrin induced intestinal absorption of zinc. Thus affecting the synthesis of thymosin;
(3) growth hormone - abnormal peptide growth factors: NS in children with growth delay gradually cause for concern, especially long-term high-dose corticosteroid treatment of the sick child, the exact mechanism is not entirely clear, it was considered that corticosteroids may impede collagen metabolism affect bone growth, the recent report of children NS activity of serum insulin-like growth factor I and II (IGF1, 2) concentration decreased, but the relationship with growth delay is unclear. Researchers believe the NS sick child growth delay, not only with protein malnutrition, with the impact of corticosteroids on the IGF / GH axis, and impaired GH (growth hormone) and IGF gene expression is growth retardation of the latest reasons.
(4) adrenal cortical hormone and adrenal crisis: foreign reports NS blood cortisol levels decreased, and the gland to ACTH response has been reduced. Clinically more important is the feedback inhibition of corticosteroids on hypothalamic - pituitary - adrenal system, survey data show that: the application of high-dose corticosteroids to NS, its own plasma cortisol significantly inhibited by the gradual reduction children with NS to every other day 0.68mg/kg, Dayton clothing, plasma cortisol concentrations returned to normal, common, long-term therapy withdrawal in February of ACTH test 96% normal, so the application of large doses of corticosteroid therapy, such as suddenly disabled the speed of the hormone or hormone reduction during the treatment too fast, or the body to stressful situations (such as severe infection or trauma, surgery, etc.), subject to the inhibitory state of the adrenal cortex are not able to produce enough sugar, salt, corticosteroids, and failed to replenish sufficient quantities of the original sex hormone, in children with adrenal crisis, acute adrenal insufficiency: manifested as sudden onset of nausea, vomiting, abdominal pain, heart rate increased, decreased blood pressure, difficulty breathing, skin bruising hair cool, and soon to shock or even coma, if not get immediate treatment, prone to cause death.
7), renal tubular dysfunction in children with NS does not alleviate the continuing massive proteinuria, or accompanied by tubulointerstitial lesions or renal vein thrombosis who were seen varying degrees of renal tubular change, especially the proximal tubular function obstacles. Such as diabetes, urinary amino acids, phosphorus and urine, urinary potassium loss, tubular proteinuria, urinary low molecular weight proteins: lysozyme, β2-microglobulin, retinol binding protein. This is mostly temporary reversible changes, such as the persistence prompted occult renal dysfunction and poor prognosis.
① humoral immune function is low (IgG in urine, blood loss, decreased synthesis of catabolism increase);
② often cellular immune dysfunction;
③ transferrin and zinc-binding protein is lost in the urine, influence immune regulation and lymphocyte function changes;
④ protein metabolism in malnutrition, and abnormalities of the complement system;
⑤ edema caused by local circulatory disorders;
⑥ glucocorticoids and immunosuppressants long period of time.
Infection can occur in the respiratory tract, urinary tract, skin and soft tissue; bacterial peritonitis is also not uncommon. More pneumococcal infections, mainly tuberculosis infection in recent years has also increased. Generally do not advocate routine prophylactic use of antibacterial drugs, but should be strengthened to protect, should be timely and thorough treatment of bacterial infections. Viral infection compared with the previous increase, particularly when receiving corticosteroids, immunosuppressive therapy, varicella, herpes zoster virus infection, the disease than the average children's weight, should strengthen the anti-viral treatment. Contacts should be ascertained hormones, immunosuppressants temporary reduction, and given a gamma globulin injection. Long-term application of corticosteroids, immunosuppressants patients should also be noted that the activities or spread of tuberculosis in the body, and secondary fungal infection.
2) low blood volume and electrolyte imbalance NS part of the children with low blood volume, even if the blood is dissolved is not low effective circulating volume due to hypoalbuminemia, plasma colloid osmotic pressure leaving a fragile state some incentive effect prone to cause low blood volume, or even shock. The common causes are:
① vomiting, diarrhea, diuretic, ascites, bleeding break fluid loss;
② long-term corticosteroids, causing their own adrenal suppressed under stress the body to retain sodium and water capacity;
③ sick child for a long time to ban salt or low-salt diet induced hyponatremia.
Common electrolyte disorder in patients with kidney disease have hyponatremia, hypokalemia, hypocalcemia. Some parents of children with NS inappropriate long-term ban salt or eat sodium free salt substitutes; or edema excessive use of diuretics; and infection, vomiting, diarrhea and other factors can cause hyponatremia. In the above-mentioned incentives, such as children with the sudden appearance of anorexia, fatigue, drowsiness, blood pressure, or even shock, convulsions and other performance should be considered hyponatremia may be. A large number of diuretic use high-dose diuretic or corticosteroids, should be alert to the emergence of hypokalemia. Nephrotic syndrome with massive proteinuria, 25 - hydroxy calciferol binding protein loss induced calcium metabolism disorders, intestinal calcium malabsorption, reduced the sensitivity of the bone to parathyroid hormone, can cause hypocalcemia, even a low calcium convulsion.
3) a hypercoagulable state and thrombus formation of NS patients blood Yi showing hypercoagulable state, the main Increased
① liver synthesis of clotting factors, such as II, Ⅴ, VII, VIII factor increase and hyperfibrinogenemia;
② plasma anti-clotting substances, decreased urinary loss of antithrombin Ⅲ too much;
③ high ester hyperlipidemia slow blood flow, increased blood viscosity, such as extensive use of diuretics to hypovolemia, hemoconcentration;
④ platelet count increased, the increase in adhesion and aggregation;
⑤ infection or other factors caused vascular wall damage and easy to activate the intrinsic coagulation system;
⑥ large doses of corticosteroid application may promote a hypercoagulable state. These procoagulant factors lead to the patient moving, venous thrombosis, of which the most common renal vein thrombosis, the incidence of each report is different to adult kidney disease from 5% to as high as 14%. Membrane proliferative glomerulonephritis, followed by membranous nephropathy complicated by. Children with nephrotic thrombosis can occur in different parts of the renal vein, deep venous, femoral artery, pulmonary artery, superior mesenteric artery, cerebral artery, but also the renal vein thrombosis more common, acute typical cases showed a sudden onset of gross hematuria. low back pain, spinal rib angle tenderness, kidney area, mass, in the case of bilateral renal rapid decrease in proteinuria aggravate; chronic often edema, proteinuria continued remission, and their symptoms are not obvious. X-ray examination the ipsilateral renal enlargement, ureter notch. B super addition to the kidney increases, showing that renal vein thrombosis. Renal venography can be confirmed.
In addition to renal vein thrombosis, such as sick children:
① both sides of the lower limb edema asymmetry does not change with body position changes;
② skin burst purpura, and rapidly expanding with pain;
③ scrotal edema was purple;
④ refractory ascites does not go away;
⑤ leg pain accompanied by the dorsalis pedis artery pulse disappeared, and so on, should be considered thrombosis.
4), acute renal insufficiency in children with NS occurrence of acute renal failure is rare, but if the following conditions, namely, acute renal failure may occur.
① hypovolemia or hypovolemic shock, renal blood hypoperfusion can be caused by prerenal azotemia, such as its persistence can lead to tubular necrosis
② glomerular lesions, especially proliferative glomerulonephritis lesions can be caused by glomerular filtration rate decreased, the occurrence of acute renal dysfunction;
③ small lesions, but can be decreased effectively due to renal interstitial edema or renal tubular protein casts obstruction, caused by the proximal tubule and the renal capsule hydrostatic pressure increased, resulting in glomerular filtration;
④ Because the application of non-steroidal anti-inflammatory drugs, diuretics, antibiotics induced acute interstitial nephritis;
⑤ the glomerular lesions deteriorated, especially when complicated by crescentic glomerulonephritis;
⑥ acute renal vein thrombosis.
5) vitamin D and calcium metabolism disorders of children with NS massive proteinuria, can cause blood vitamin D binding protein (molecular weight 59 000) since the urinary loss of vitamin D deficiency affect intestinal calcium absorption, and therefore such a sick child more hypocalcemia associated with renal tubular change may also affect the 1-25 - (OH) 2D3 formation; long-term application of corticosteroids; further exacerbated by vitamin D and calcium metabolism disorders. Hypocalcemia, regular feedback to cause hyperparathyroidism, bone calcification exception is therefore often show clinical hypocalcemia, serum 25 - hydroxy calciferol is decreased, the blood parathyroid hormone increased, osteoporosis, osteomalacia, especially in the rapid growth in children during these changes more pronounced.
Endocrine changes in 6).
① reduce the thyroid hormone function: sick children when the NS basal metabolic rate, blood protein binding iodine value decreased. Most scholars believe that the Department of thyroid binding globulin caused by urine loss may also increase in thyroid hormone synthesis decline in its distribution of the extravascular space; there is blood when the kidney disease inhibitory factor preventing thyroxine and globulin combination.
② thymic hormone decreased significantly: with blood zinc low related, since the urine is lost outside the NS in addition to the zinc-binding protein, and also the decrease due to the lack of transferrin induced intestinal absorption of zinc. Thus affecting the synthesis of thymosin;
(3) growth hormone - abnormal peptide growth factors: NS in children with growth delay gradually cause for concern, especially long-term high-dose corticosteroid treatment of the sick child, the exact mechanism is not entirely clear, it was considered that corticosteroids may impede collagen metabolism affect bone growth, the recent report of children NS activity of serum insulin-like growth factor I and II (IGF1, 2) concentration decreased, but the relationship with growth delay is unclear. Researchers believe the NS sick child growth delay, not only with protein malnutrition, with the impact of corticosteroids on the IGF / GH axis, and impaired GH (growth hormone) and IGF gene expression is growth retardation of the latest reasons.
(4) adrenal cortical hormone and adrenal crisis: foreign reports NS blood cortisol levels decreased, and the gland to ACTH response has been reduced. Clinically more important is the feedback inhibition of corticosteroids on hypothalamic - pituitary - adrenal system, survey data show that: the application of high-dose corticosteroids to NS, its own plasma cortisol significantly inhibited by the gradual reduction children with NS to every other day 0.68mg/kg, Dayton clothing, plasma cortisol concentrations returned to normal, common, long-term therapy withdrawal in February of ACTH test 96% normal, so the application of large doses of corticosteroid therapy, such as suddenly disabled the speed of the hormone or hormone reduction during the treatment too fast, or the body to stressful situations (such as severe infection or trauma, surgery, etc.), subject to the inhibitory state of the adrenal cortex are not able to produce enough sugar, salt, corticosteroids, and failed to replenish sufficient quantities of the original sex hormone, in children with adrenal crisis, acute adrenal insufficiency: manifested as sudden onset of nausea, vomiting, abdominal pain, heart rate increased, decreased blood pressure, difficulty breathing, skin bruising hair cool, and soon to shock or even coma, if not get immediate treatment, prone to cause death.
7), renal tubular dysfunction in children with NS does not alleviate the continuing massive proteinuria, or accompanied by tubulointerstitial lesions or renal vein thrombosis who were seen varying degrees of renal tubular change, especially the proximal tubular function obstacles. Such as diabetes, urinary amino acids, phosphorus and urine, urinary potassium loss, tubular proteinuria, urinary low molecular weight proteins: lysozyme, β2-microglobulin, retinol binding protein. This is mostly temporary reversible changes, such as the persistence prompted occult renal dysfunction and poor prognosis.
Causes of symptoms and symptoms of nephrotic syndrome
Of this disease is a series of clinical performance originated in massive
proteinuria, plasma proteins in a large number of urine loss, leading to
hypoproteinemia, thereby causing edema, hyperlipidemia, and other organ system
complications.
Proteinuria (Proteinuria) normal glomerular capillary wall filtration barrier - that is, filtration membrane (including endothelial cells, basement membrane, epithelial cells and the hole film) limit through most of the protein, and thus the glomerular cysts The original urine protein concentration of only 0.01-0.1g / L. When the glomerular filtration membrane injury by immune or other pathogenic factors, the charge barrier and (or) aperture barrier weakened, plasma protein filtration increase, a significant increase in induced urinary protein. Small lesions, the charge barrier weakened physiological PH negatively charged low molecular weight (MW = 70000-150000) protein (mainly albumin) loss of urine; aperture barrier in non-minimal change involvement, high molecular weight (MW => 150000) proteins such as of IgM, α2-macroglobulin, fibrinogen, high-density lipoprotein is also leaking from the non-selective proteinuria.
Discovered in recent years NS when in addition to loss of plasma albumin, loss of other protein components, resulting in organ system dysfunction or complications. Carrier protein, such as trace elements are missing: like transferrin loss can cause iron deficiency anemia; zinc binding protein loss induced taste disorders in children, poor appetite, but also affect the thymosin synthesis and lymphocyte proliferation induced by cellular immune abnormalities. A variety of hormone binding protein loss: loss of 25 - hydroxy calciferol binding protein, caused by calcium metabolic disorders, reduction in intestinal calcium absorption, serum calcium decreased; thyroxine-binding protein is lost, causing the blood of the T3, T4, decreased thyroid dysfunction ; cortisol-binding protein decreased the elevated free cortisol in the blood, caused by abnormal cortisol metabolism. The loss of immunoglobulin, prone to cause a reduced ability of anti-infective. Prostaglandin-binding protein is lost, allow prostaglandin metabolic changes, and even affect the blood clots form. Antithrombin III is lost, easy to trigger a hypercoagulable state. Loss of lipoprotein lipase, it will affect the very low density lipoprotein and low density lipoprotein metabolism, and promote a form of hyperlipidemia.
Low albumin (hypoalbuminemia) is a direct consequence of massive proteinuria is low serum albumin, the disease is also the pathophysiology of the syndrome to change the main influencing factors. Environmental stability of its body and the metabolism of a variety of substances have a significant impact, when the serum albumin decreased to less than 25g / L, the plasma colloid osmotic pressure decreased significantly change the body of liquid distribution, a large number of intravascular fluid to the inter-organizational transfer caused by interstitial edema; at the same time caused the effective circulating blood volume decreased, resulting in the body a series of physiological and pathological changes. Such as nerve - endocrine system disorders; sodium and water retention; abnormal lipoprotein metabolism caused by hyperlipidemia; the formation of a hypercoagulable state.
Lost due to hypoalbuminemia mainly plasma protein in urine, but its lower degree of urinary protein is sometimes not completely consistent, so many scholars believe that may be associated with this disease, albumin insufficient synthesis and catabolism (renal tubular Office) to increase or extrarenal pathways (such as the loss of the gastrointestinal tract). Scholars note with urinary protein loss in this disease increase in liver protein synthesis, hepatic protein synthesis in normal daily 130-200mg/Kg 500mg/Kg compensatory increased synthesis rate and liver function related to, but also protein intake and calorie intake, when the amount of intake (daily protein 1.2-2.0g/Kg daily calorie 35Kcal/Kg) synthesis better. In NS often failed to show this compensatory effect may be related to the lack of children intake. About 5-12% of normal blood circulation to albumin catabolism in the kidney, intestine, liver and surrounding tissue, etc., about 10% of the total decomposition of renal local, animal experiments show that nephropathy in rats albumin catabolism was significantly increased. local kidney percentage of increase. Notwithstanding the report of gastrointestinal albumin loss in this syndrome, but failed to get the consensus of most scholars.
Hyperlipidemia (hyperlipidemia) Primary NS, more associated with hyperlipidemia, the higher the degree is often associated with the degree of proteinuria and serum albumin level, in addition to patients' age, diet, renal function status, corticosteroids The application of a variety of factors. Hyperlipidemia often reflected hyperlipoproteinemia, NS in children with blood cholesterol increased significantly, triglycerides different individuals or stage of disease vary, but persistent massive proteinuria and severe low serum albumin more than an increase in , early in the disease very low density lipoprotein (VLDL, the main carrier of triglycerides) and low-density lipoprotein (LDL, the main carrier of cholesterol) is increased. High-density lipoprotein (HDL) can be normal, reduced or increased. Also rely on at the drop of the plasma albumin level (Table 2-1-5) and the nature of the primary disease, the decline of of HDL2 than HDL3, and apolipoprotein in the urine is also increased.
NS when hyperlipidemia reason is more complex, may be associated with lipoprotein metabolism disorder, the first increased liver synthesis of lipoproteins, which is the Liver hypoalbuminemia and plasma osmolality caused by blood viscosity changes the reaction is not directly linked with liver albumin synthesis. Followed by decreased lipoprotein clearance rate decreased due to the activity of the enzyme, such as lipoprotein lipase (can be cleared in VLDL triglyceride) activity decreased by 30-60%, lecithin turn acyl enzyme (catalytic cholesterol esterification) activity due to hypoproteinemia and reduced, and the enzyme is lost in the urine.
Adverse effects of hyperlipidemia on the body: ① glomerular filter out the toxic effects of lipoprotein in mesangial cells, may lead to glomerular sclerosis; ② increased platelet aggregation, may trigger a hypercoagulable and thromboembolism complications; ③ long hyperlipidemia, especially LDL rise and HDL decreased, can produce atherosclerosis. However, minimal change disease urinary loss of HDL, less than other non-minimal change nephrotic HDL so the blood is relatively high, and thus atherosclerotic cardiovascular complications are rare.
Edema (edema) are common symptoms of NS sick child, and its mechanism, the traditional view that the large number of urinary protein loss, decreased serum albumin concentration, resulting in lower plasma colloid osmotic pressure and intravascular fluid leakage into the interstitial space, plasma volume decreased enable the body to retain water capacity and pressure receptors, sodium-related neurohumoral factors are activated: If prompted sympathetic nerve release of catecholamines, renin - angiotensin - aldosterone system activity, secondary to inappropriate antidiuretic hormone secretion increased natriuretic factor is inhibited, resulting in a body of water, sodium retention and edema. This theory emphasizes that the volume fell to this mechanism, it is known as filling the lack of doctrine (underfilling theory). But in recent years some scholars have observed to NS when not accompanied by decreased blood volume, plasma renin - angiotensin levels may not necessarily be increased, it is proposed that the intrinsic primary water and sodium retention, rather than blood The decrease in the capacity to stay due to the primary water and sodium retention can lead to blood volume expansion, in contrast to the above theory, it is also known as the doctrine of over-filling (overfilled theory). In fact the mechanism of NS in edema magazine may be a combination of factors, and different patients with different diseases of the mechanism may vary.
Proteinuria (Proteinuria) normal glomerular capillary wall filtration barrier - that is, filtration membrane (including endothelial cells, basement membrane, epithelial cells and the hole film) limit through most of the protein, and thus the glomerular cysts The original urine protein concentration of only 0.01-0.1g / L. When the glomerular filtration membrane injury by immune or other pathogenic factors, the charge barrier and (or) aperture barrier weakened, plasma protein filtration increase, a significant increase in induced urinary protein. Small lesions, the charge barrier weakened physiological PH negatively charged low molecular weight (MW = 70000-150000) protein (mainly albumin) loss of urine; aperture barrier in non-minimal change involvement, high molecular weight (MW => 150000) proteins such as of IgM, α2-macroglobulin, fibrinogen, high-density lipoprotein is also leaking from the non-selective proteinuria.
Discovered in recent years NS when in addition to loss of plasma albumin, loss of other protein components, resulting in organ system dysfunction or complications. Carrier protein, such as trace elements are missing: like transferrin loss can cause iron deficiency anemia; zinc binding protein loss induced taste disorders in children, poor appetite, but also affect the thymosin synthesis and lymphocyte proliferation induced by cellular immune abnormalities. A variety of hormone binding protein loss: loss of 25 - hydroxy calciferol binding protein, caused by calcium metabolic disorders, reduction in intestinal calcium absorption, serum calcium decreased; thyroxine-binding protein is lost, causing the blood of the T3, T4, decreased thyroid dysfunction ; cortisol-binding protein decreased the elevated free cortisol in the blood, caused by abnormal cortisol metabolism. The loss of immunoglobulin, prone to cause a reduced ability of anti-infective. Prostaglandin-binding protein is lost, allow prostaglandin metabolic changes, and even affect the blood clots form. Antithrombin III is lost, easy to trigger a hypercoagulable state. Loss of lipoprotein lipase, it will affect the very low density lipoprotein and low density lipoprotein metabolism, and promote a form of hyperlipidemia.
Low albumin (hypoalbuminemia) is a direct consequence of massive proteinuria is low serum albumin, the disease is also the pathophysiology of the syndrome to change the main influencing factors. Environmental stability of its body and the metabolism of a variety of substances have a significant impact, when the serum albumin decreased to less than 25g / L, the plasma colloid osmotic pressure decreased significantly change the body of liquid distribution, a large number of intravascular fluid to the inter-organizational transfer caused by interstitial edema; at the same time caused the effective circulating blood volume decreased, resulting in the body a series of physiological and pathological changes. Such as nerve - endocrine system disorders; sodium and water retention; abnormal lipoprotein metabolism caused by hyperlipidemia; the formation of a hypercoagulable state.
Lost due to hypoalbuminemia mainly plasma protein in urine, but its lower degree of urinary protein is sometimes not completely consistent, so many scholars believe that may be associated with this disease, albumin insufficient synthesis and catabolism (renal tubular Office) to increase or extrarenal pathways (such as the loss of the gastrointestinal tract). Scholars note with urinary protein loss in this disease increase in liver protein synthesis, hepatic protein synthesis in normal daily 130-200mg/Kg 500mg/Kg compensatory increased synthesis rate and liver function related to, but also protein intake and calorie intake, when the amount of intake (daily protein 1.2-2.0g/Kg daily calorie 35Kcal/Kg) synthesis better. In NS often failed to show this compensatory effect may be related to the lack of children intake. About 5-12% of normal blood circulation to albumin catabolism in the kidney, intestine, liver and surrounding tissue, etc., about 10% of the total decomposition of renal local, animal experiments show that nephropathy in rats albumin catabolism was significantly increased. local kidney percentage of increase. Notwithstanding the report of gastrointestinal albumin loss in this syndrome, but failed to get the consensus of most scholars.
Hyperlipidemia (hyperlipidemia) Primary NS, more associated with hyperlipidemia, the higher the degree is often associated with the degree of proteinuria and serum albumin level, in addition to patients' age, diet, renal function status, corticosteroids The application of a variety of factors. Hyperlipidemia often reflected hyperlipoproteinemia, NS in children with blood cholesterol increased significantly, triglycerides different individuals or stage of disease vary, but persistent massive proteinuria and severe low serum albumin more than an increase in , early in the disease very low density lipoprotein (VLDL, the main carrier of triglycerides) and low-density lipoprotein (LDL, the main carrier of cholesterol) is increased. High-density lipoprotein (HDL) can be normal, reduced or increased. Also rely on at the drop of the plasma albumin level (Table 2-1-5) and the nature of the primary disease, the decline of of HDL2 than HDL3, and apolipoprotein in the urine is also increased.
NS when hyperlipidemia reason is more complex, may be associated with lipoprotein metabolism disorder, the first increased liver synthesis of lipoproteins, which is the Liver hypoalbuminemia and plasma osmolality caused by blood viscosity changes the reaction is not directly linked with liver albumin synthesis. Followed by decreased lipoprotein clearance rate decreased due to the activity of the enzyme, such as lipoprotein lipase (can be cleared in VLDL triglyceride) activity decreased by 30-60%, lecithin turn acyl enzyme (catalytic cholesterol esterification) activity due to hypoproteinemia and reduced, and the enzyme is lost in the urine.
Adverse effects of hyperlipidemia on the body: ① glomerular filter out the toxic effects of lipoprotein in mesangial cells, may lead to glomerular sclerosis; ② increased platelet aggregation, may trigger a hypercoagulable and thromboembolism complications; ③ long hyperlipidemia, especially LDL rise and HDL decreased, can produce atherosclerosis. However, minimal change disease urinary loss of HDL, less than other non-minimal change nephrotic HDL so the blood is relatively high, and thus atherosclerotic cardiovascular complications are rare.
Edema (edema) are common symptoms of NS sick child, and its mechanism, the traditional view that the large number of urinary protein loss, decreased serum albumin concentration, resulting in lower plasma colloid osmotic pressure and intravascular fluid leakage into the interstitial space, plasma volume decreased enable the body to retain water capacity and pressure receptors, sodium-related neurohumoral factors are activated: If prompted sympathetic nerve release of catecholamines, renin - angiotensin - aldosterone system activity, secondary to inappropriate antidiuretic hormone secretion increased natriuretic factor is inhibited, resulting in a body of water, sodium retention and edema. This theory emphasizes that the volume fell to this mechanism, it is known as filling the lack of doctrine (underfilling theory). But in recent years some scholars have observed to NS when not accompanied by decreased blood volume, plasma renin - angiotensin levels may not necessarily be increased, it is proposed that the intrinsic primary water and sodium retention, rather than blood The decrease in the capacity to stay due to the primary water and sodium retention can lead to blood volume expansion, in contrast to the above theory, it is also known as the doctrine of over-filling (overfilled theory). In fact the mechanism of NS in edema magazine may be a combination of factors, and different patients with different diseases of the mechanism may vary.
Clinical classification of nephrotic syndrome
Children with nephrotic syndrome with clinical manifestations of these four, but different causes pathological changes in the different variety of glomerular diseases, and therefore researchers from different angles to give a classification or type, in order to guide clinical work and to explore disease is the essence.
Clinical classification of pediatric clinical traditional view, this syndrome is divided into three categories namely primary, secondary and congenital three kinds.
1) The primary nephrotic syndrome refers to the etiology is not clear, the primary lesion in glomerular diseases. In the process of primary glomerular diseases, such as acute glomerulonephritis, rapidly progressive glomerulonephritis, chronic glomerulonephritis, the NS can be found in the disease process. Domestic clinical classification can be divided into simple-type (Ⅰ) and nephritis (Ⅱ). The former only have these massive proteinuria, hypoalbuminemia, hyperlipidemia, and edema of the four characteristics; the latter in addition to have these four clinical manifestations, but also have one or more performers in the following four:
① urine red blood cells> 10 / high power field (three times within two weeks centrifuged urine tests);
The ② repeated or sustained hypertension: school-age children> 17.3/12.0kPa (130/90mmHg), pre-school children> 16.0/10.7kPa (120/80mmHg), and the exclusion caused by the use of corticosteroids;
③ azotemia: plasma urea nitrogen> 10.7mmol / L (30mg/dl), to exclude hypovolemia due;
④ serum total complement the lower body activity or complement C3 repeatedly. Clinical common type Ⅰ: Ⅰ type is 68.4%, according to our data analysis of 1462 cases of hospitalized cases 31.6% of type II.
2) secondary nephrotic syndrome refers to the secondary to systemic disease (such as systemic lupus erythematosus), or with a clear cause (eg, infection). Its etiology is broad and complex, the following list only the more common of the children during the
(1) the generalized systemic disease: systemic lupus erythematosus, purpura, nodules nodosa, mixed connective tissue disease, dermatomyositis, etc..
(2) infections: bacterial infections: post-streptococcal glomerulonephritis, bacterial endocarditis, cardiac shunt infection nephritis; viruses and other infections: hepatitis B, hepatitis C, cytomegalovirus, varicella and Epstein-Barr virus; malaria, congenital or secondary syphilis.
(3) Drug Allergy: penicillamine, probenecid, mercury, three pairs of ketones, captopril, nonsteroidal anti-inflammatory drugs, interferon, serum and vaccination and so on.
(4) family of genetic diseases: Alport syndrome, a patella syndrome and sickle-cell anemia.
(5), metabolic diseases: diabetes mellitus, myxedema.
(6) tumor: Wilms' tumor, leukemia, Hodgkin's lymphoma and multiple myeloma and other.
(7): the response of chronic renal allograft Exhaust malignant glomerulosclerosis and renal artery stenosis
.
3), congenital nephrotic syndrome is often caused by genetic factors of the Finnish type and non-Finnish type congenital nephrotic.
1990 Steffensen three months will be born with congenital kidney disease is divided into five categories:
① Finnish type of congenital kidney disease: an autosomal recessive genetic disease;
② diffuse mesangial sclerosis: more common in full-term children, there is a tendency of familial disease, the rapid development of the disease, more than before the 3-year-old died of renal failure. Glomerular involvement, by a majority of the small ball of capillary lumen occlusion with fibrosis.
③ children with congenital nephrotic: the country is more common, the incidence in the 3 months to 3-year-old children, more common in 1-3 year-old infant. Diversify its pathological type, such as minimal change disease, focal glomerulosclerosis, proliferative nephritis (including diffuse, exudative, Department of membranous, crescent form of focal, membrane proliferative, etc.) as well as renal ball sclerosis. With primary nephrotic organizations to learn different points of this disease is mesangial proliferative glomerulonephritis without immune deposits visible.
④ secondary to congenital kidney disease: the majority of secondary syphilis infection and its pathological types of mesangial proliferative glomerulonephritis and membranous nephritis, basement membrane thickening is a major exception. Optical microscopy and electron microscopy showed subepithelial deposits (IgG, fibrin). Secondary to toxoplasmosis, renal pathology, diffuse mesangial small hardening. Secondary to cytomegalovirus inclusion virus infection, renal pathology showed the expansion of proximal tubule the ball moderate mesangial cell proliferation and interstitial inflammation.
⑤ congenital nephrotic combined with other genetic diseases such as nail - patella dysplasia (autosomal dominant disease), genital abnormalities, and eye - diaphragm - with renal syndrome (sex-linked recessive inheritance).
Nephrotic syndrome blood test
1) The serum protein of all patients had varying degrees of hypoalbuminemia,
serum total protein and albumin were decreased, especially serum albumin
decreased more significantly, when the serum concentration of 25g / L (or
lower), ie thesis can hypoalbuminemia in NS. Serum globulin is relatively
higher, was white / ball (A / G), inverted. The increase in liver synthesis of
serum of α2 and β globulin concentration increased or decrease of α1 globulin,
gamma globulin levels depending on the primary disease, the IgG levels can be
decreased significantly, IgA, IgM, IgE normal or increased.
2) blood lipid and lipoprotein every sick child should be for blood cholesterol, triglyceride, inspection, conditions can be made of phospholipids and fatty acids to check general, all the patients cholesterol were increased, then the three non-All patients were increased. Serum lipoprotein LDL and VLDL were significantly higher, HDL is usually normal.
3), serum BUN and Cr brief mild serum BUN and Cr increased, often prompted hypovolemia due to minimal change NS, if persistent, severe renal insufficiency is more suggestive of nephritis type NS or chronic nephritis NS .
4) serum electrolytes severe hypoalbuminemia and a high degree of edema disease in children are associated with body water and electrolyte disorders and acid-alkaline imbalance, common hyponatremia, hypokalemia, hypocalcemia, and varying degrees of metabolic acidosis, such as excessive The use of diuretics, the patient is also easy to merge hemoconcentration, hypovolemia.
5) serum complement, immune complex matter, and cytokine detection NS part of the patient serum complement C3 and total complement activity decreased (especially MPGN and lupus nephritis) C4, C2, of C1q may be normal. Part of the immune complex-mediated nephritis due to kidney patients, blood circulation can be detected in immune complexes in recent years, some scholars also found in MCNS blood vascular permeability factor (VPF), soluble immune suppressor (SIRS), interleukin 4 (IL-4) and leukocyte interleukin-8 (IL-8) and other cytokines were significantly increased.
6) a hypercoagulable state and thrombus formation on check the majority of primary NS sick children there are different levels of the hypercoagulable state: thrombocytosis, increased platelet aggregation rate, plasma fibrinogen increase the liver synthesis of clotting factors II and Ⅴ , Ⅶ, Ⅷ also increased urinary fibrin cleavage products (FDP) increased, according to laboratory conditions for the relevant examination. Suspected thrombosis, Doppler B-mode ultrasound examination, or digital subtraction angiography.
7). Serological detection of systemic disease secondary to systemic lupus erythematosus patients with NS should be for the serological detection of anti-nuclear antibody (ANA), anti-dsDNA antibody, Smith antibody; secondary to hepatitis B hepatitis C, congenital or secondary syphilitic NS should make relevant serum antigen and antibody detection to confirm the diagnosis.
8). Renal biopsy in children with NS the following circumstances, should be optional for percutaneous renal puncture biopsy: ① sufficient quantities of corticosteroids 6 weeks of treatment, urinary protein 2; ② has clearly part of the Effect of corticosteroids; ③ dependent on corticosteroids; ④ frequent recurrence of persons; to ⑤ suspected secondary nephropathy, clinical hard diagnosed; ⑥ The combined acute and chronic renal insufficiency.
2) blood lipid and lipoprotein every sick child should be for blood cholesterol, triglyceride, inspection, conditions can be made of phospholipids and fatty acids to check general, all the patients cholesterol were increased, then the three non-All patients were increased. Serum lipoprotein LDL and VLDL were significantly higher, HDL is usually normal.
3), serum BUN and Cr brief mild serum BUN and Cr increased, often prompted hypovolemia due to minimal change NS, if persistent, severe renal insufficiency is more suggestive of nephritis type NS or chronic nephritis NS .
4) serum electrolytes severe hypoalbuminemia and a high degree of edema disease in children are associated with body water and electrolyte disorders and acid-alkaline imbalance, common hyponatremia, hypokalemia, hypocalcemia, and varying degrees of metabolic acidosis, such as excessive The use of diuretics, the patient is also easy to merge hemoconcentration, hypovolemia.
5) serum complement, immune complex matter, and cytokine detection NS part of the patient serum complement C3 and total complement activity decreased (especially MPGN and lupus nephritis) C4, C2, of C1q may be normal. Part of the immune complex-mediated nephritis due to kidney patients, blood circulation can be detected in immune complexes in recent years, some scholars also found in MCNS blood vascular permeability factor (VPF), soluble immune suppressor (SIRS), interleukin 4 (IL-4) and leukocyte interleukin-8 (IL-8) and other cytokines were significantly increased.
6) a hypercoagulable state and thrombus formation on check the majority of primary NS sick children there are different levels of the hypercoagulable state: thrombocytosis, increased platelet aggregation rate, plasma fibrinogen increase the liver synthesis of clotting factors II and Ⅴ , Ⅶ, Ⅷ also increased urinary fibrin cleavage products (FDP) increased, according to laboratory conditions for the relevant examination. Suspected thrombosis, Doppler B-mode ultrasound examination, or digital subtraction angiography.
7). Serological detection of systemic disease secondary to systemic lupus erythematosus patients with NS should be for the serological detection of anti-nuclear antibody (ANA), anti-dsDNA antibody, Smith antibody; secondary to hepatitis B hepatitis C, congenital or secondary syphilitic NS should make relevant serum antigen and antibody detection to confirm the diagnosis.
8). Renal biopsy in children with NS the following circumstances, should be optional for percutaneous renal puncture biopsy: ① sufficient quantities of corticosteroids 6 weeks of treatment, urinary protein 2; ② has clearly part of the Effect of corticosteroids; ③ dependent on corticosteroids; ④ frequent recurrence of persons; to ⑤ suspected secondary nephropathy, clinical hard diagnosed; ⑥ The combined acute and chronic renal insufficiency.
Wednesday, August 1, 2012
Dietary treatment rule of diabetic nephropathy
After suffering from diabetic nephropathy, the most to worry about eating problems, diabetes, not to eat pasta and fat, kidney disease and not to eat more protein, not put people starved to death. Diet therapy is the treatment of diabetes "five horse cars, and is an essential part of the treatment of diabetic nephropathy. Adjustment of the diet of patients with diabetic nephropathy can enable patients to "eat" slow down the development of the disease. The diet of diabetic nephropathy should be in phases in different periods of management.
1.The correct amount of calories intake
The daily intake of moderate heat to maintain the body's nutrition and health is very important. For the body to provide the heat necessary for life; weight to help maintain human health; help the body to the rational use of proteins, proteins play an important role to rebuild muscle and organizational structure. If caloric intake is inadequate, it will consume the body fat and even muscle tissue, leading to malnutrition. Excessive intake will lead to human obesity, elevated blood lipids.
Suffering from diabetic nephropathy, the patient will be asked to reduce the dietary protein. While the heat is reduced, patients need to eat extra calories and less protein foods instead. To supplement the lack of heat in part of carbohydrate-rich foods such as lotus root starch, almond cream, wheat starch, etc., (starch flour, mung bean, sweet potato out of its protein product of the food exchange about 20 grams of starch and 25 g of raw flour effect on blood glucose.) food almost free of the plant protein, but high in calories containing almost the same as the heat and the same amount of flour. Rich in monounsaturated fatty acids of vegetable oils: olive oil, tea seed oil can also be appropriate to increase, for people with diabetes will not cause blood sugar, lowering blood lipids.
Some diabetic nephropathy who mistakenly believe that control of blood sugar should eat carbohydrates as possible; some people mistakenly believe that the starch will make blood sugar rise even higher. In fact carbohydrates provide the body with about 50% ~ 60% of the dietary energy (equivalent to about 4 to 6 two raw food), food intake, the body will use protein and fat to heat production in order to sustain life required, the results will make diabetic nephropathy in patients with ketoacidosis, endotoxin levels increased malnutrition.
2.Intake of the correct amount of protein
The human body needs the right amounts of protein the correct amounts of protein intake is very important for the health and comfort. The long-term low-protein diet will lead to malnutrition, prone to various complications. In order to maintain metabolic needs and disease resistance in human muscle tissue repair, and a variety of enzymes, blood cells, everyone must ensure that adequate dietary protein intake.
Currently advocated in the early stage of diabetic nephropathy, which should limit the intake of protein, soy intake caused by too much body waste creatinine excessive resulting in the decomposition of burden on the kidneys, it is one of the reasons for the formation of diabetic nephropathy. Three more than in patients with diabetic nephropathy, it should be in the keto acid formulations at the same time, the implementation of the method of low-protein diet, that is, eating 0.6 grams of quality protein per kilogram of body weight per day is appropriate.
But for those long-term dialysis patients, due to nutritional deficiency is more serious, and therefore this time should be appropriate to increase the protein intake, even when necessary in order to improve the nutritional status even more protein intake than healthy people, and soy products plant protein is no longer absolutely prohibited food. The existing studies suggest that the amount of vegetable protein is also beneficial to the prevention and control of lipid metabolism and atherosclerosis, but need to pay attention to the risk of accumulation of potassium and phosphorus.
3.Increase or decrease in food intake based on the weight change
Due to individual differences, each person on the digestion of dietary absorption capacity of different, each person's activity levels are also different, so the set can not be mechanically rigid fixed pattern of food intake and manner, but should learn according to weight changes in their diet volume.
Get up early in the morning fasting, emptying the toilet, wearing very little clothes weigh 2 to 3 weeks, body weight did not change, indicating that dietary energy consumption is basically the same.
Maintain appropriate body weight is very important. Body normal and lean patients with diabetic nephropathy in reducing dietary protein foods should be appropriate to increase the intake of starch and vegetable oil in order to maintain the calorie intake of the past, this same good blood glucose control. Obese diabetic nephropathy patients often need to lose weight if you need less weight should be invited to a nutritionist to help you maintain the health and slow weight loss. If your rapid weight gain, please tell your doctor.
The Causes and Symptoms of Diabetic Nephropathy
Nephrotic syndrome diagnosis and differential diagnosis
The diagnosis includes three aspects:
① confirmed NS;
② confirmation of etiology: First of all, except the secondary cause of genetic disease can be diagnosed as primary the NS; best renal biopsy to make a pathological diagnosis;
(3) determine whether the complication.
Ns of the need for differential diagnosis of secondary causes include the following diseases:
1, anaphylactoid purpura nephritis occurs in adolescence, the typical skin purpura may be associated with joint pain, abdominal pain and melena, hematuria and proteinuria, (or) a typical rash appears in more than l ~ 4 weeks after the rash appears will help on differential diagnosis.
, Systemic lupus erythematosus occurs in young and middle-aged women, the clinical manifestations and immunological tests based on multi-system damage can be detected in a variety of autoantibodies, generally is not difficult to confirm the diagnosis.
Hepatitis B virus (HBV) associated glomerulonephritis is more common in children and adolescents, proteinuria or NS as the main clinical manifestations of common pathological type of membranous nephropathy, followed by mesangial capillary glomerulonephritis. The following three points of the domestic basis for diagnosis: (1) serum HBV antigen-positive; (2) suffering from glomerular nephritis, and may, except lupus nephritis secondary glomerulonephritis; ③ renal biopsy slices to find the HBV antigens. Of viral hepatitis B high incidence of viral hepatitis B patients, children and young people proteinuria or NS patients, especially for film. Nephropathy, should be carefully to exclude.
4, diabetic nephropathy occurs in middle-aged, NS is common in patients with diabetes duration of more than lO years. Early can be found in the urinary albumin excretion increased, then gradually developed into a massive proteinuria NSo history of diabetes and the characteristic fundus changes helpful in differential diagnosis.
5, renal amyloidosis occurs in middle-aged, renal amyloidosis is part of multiple organ involvement. Primary amyloid degeneration mainly involving the heart, kidneys, digestive tract (including tongue), skin and nerves; secondary amyloidosis often secondary to chronic suppurative infections, tuberculosis, cancer and other diseases, mainly involving the kidney, liver and the spleen and other organs. Kidney involvement, increase in size, often has the NS. Renal amyloidosis often need renal biopsy diagnosis.
6, myeloma kidney disease occurs in middle-aged, male predominance, the patients may have clinical features of multiple myeloma, such as bone pain, increased serum monoclonal immunoglobulin, protein electrophoresis of M protein and urine Bence The protein is positive, bone marrow plasma cell dysplasia (more than the possession of nuclear cells in 159/5), accompanied by a qualitative change. Multiple myeloma involving the glomerular NS. The characteristic performance of the above myeloma differential diagnosis.
Subscribe to:
Posts (Atom)