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.

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.

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.

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.

Histological types and clinical features of primary nephrotic syndrome

1, MCNS minimal change nephropathy (minimal change nephropathy) occurs in children (accounting for about 80% of children with nephrotic syndrome), the major clinical manifestations of sudden massive proteinuria and hypoproteinemia may be associated with high-fat acidosis and edema. Hematuria and hypertension are rare. , Hypertension and renal dysfunction is common in patients over the age of 60.
Light microscope, glomerular lesions, visible fatty degeneration of proximal tubular epithelial cells. Immunofluorescence was negative. Electron microscope, the characteristics of changes in glomerular visceral epithelial cell foot process fusion.
2, mesangial proliferative glomerulonephritis with mesangial proliferative glomerulonephritis (mesangial proliferative glomerulongphritis) is a common pathological type of primary nephrotic syndrome, accounting for about 30%, significantly higher than that of Europe and the United States (about 10%). The disease occurs in young people, male predominance. The majority of patients before the onset of prodromal symptoms of infection of upper respiratory tract infections, some patients with insidious onset. The main clinical manifestations were proteinuria and (or) hematuria, approximately 30% of nephrotic syndrome.
The pathological characteristics of the light microscope, the mesangial cells and extracellular matrix diffuse hyperplasia can be divided into mild, moderate to severe. According to the immunofluorescence results can be divided into IgA nephropathy (pure IgA or IgA deposition-based) and non-IgA mesangial proliferative glomerulonephritis (IgG or IgM, the deposition-based), often accompanied by C3 deposition in the kidney ball mesangial area or along the capillary wall granular deposition. Electron microscope, mesangial electron dense deposits.
3, focal segmental glomerular sclerosis focal segmental glomerulosclerosis (focal segmental glomerulosclerosis) is more common in young people, more men than women. Onset are more hidden, the major clinical manifestations of massive proteinuria or nephrotic syndrome. The majority of patients with hematuria, and some patients had gross hematuria; mild also can be expressed as asymptomatic proteinuria and (or) hematuria. Upper respiratory tract infection or other predisposing factors can make the clinical symptoms. The majority of patients to establish the diagnosis is often accompanied by hypertension and renal damage, and aggravated as the disease progresses. In some cases by the shift from minimal change nephropathy.
Pathological features of the light microscope, the glomerular lesions were focal, segmental distribution, increased mesangial matrix and plasma protein deposition and balloon adhesion as the main performance, may be associated with a small amount of mesangial cell proliferation, accompanied by the same nephron tubular atrophy and interstitial fibrosis in the kidney. The immunopathological visible lumps deposition of IgM and C3 in the glomerular lesions. Electron microscope, mesangial matrix increase, electron dense precipitation of the lesion, glomerular epithelial cells wide range of foot process fusion.
4, membranous nephropathy, membranous nephropathy (membranous nephropathy) occurs in the elderly, male predominance, the peak age of onset is 50 to 60 years old. Europe and the United States adult common pathological type of nephrotic syndrome, while China is not common. Membranous nephropathy onset more hiding, no history of prodromal infection. 70% to 80% of patients with nephrotic syndrome. Early in the disease without hypertension. Most patients with normal renal function or mild impairment. The higher the incidence of arterial and venous thrombosis, especially renal vein thrombosis is the most common (about 10% ~ 40%). The 10-year kidney survival rate is about 65%.
Membranous nephropathy under the light microscope the characteristic of the diffuse thickening of the glomerular basement membrane. The immunopathological characterized immunoglobulin and complement around the capillary wall diffuse granular deposition of IgG strength can also be the deposition of IgA and IgM. Electron microscope, the basement membrane subcutaneous or dispersed or rules for the distribution of electron dense precipitate within the basement membrane, epithelial cells wide range of foot process fusion. Part of the patients with membranous nephropathy have a tendency natural ease.
5, the mesangial capillary glomerulonephritis, also known as mesangial proliferative glomerulonephritis (membranoproliferative glomerulonephritis). The disease occurs in young people, men and women roughly equal proportion. Half of the patients have a precursor of the upper respiratory tract infection history. 50% of patients with nephrotic syndrome, 30% of the patients had asymptomatic proteinuria, often accompanied by recurrent episodes of microscopic hematuria or gross hematuria. 20% to 30% of the patients manifested as acute nephritic syndrome. Hypertension, anemia and renal dysfunction is common, often ongoing development. 75% of patients with persistent hypocomplementemia, is an important feature of this disease.
Of the disease pathology is characterized by light microscopy showed mesangial cells and mesangial matrix diffuse severe hyperplasia, widely inserted into the glomerular basement membrane and endothelial cells, glomerular basement membrane was thickened layering, capillary Ban was "double-track sign. Immune pathological examination showed IgG, C3 granular precipitation along the basement membrane and mesangial areas. Electron microscope, visible electron dense precipitate in the mesangial area and subendothelial.
How to Treat Proteinuria for Patients with FSGS Efficiently