Saturday, April 21, 2012
Hypertensive Nephropathy is caused by?
Hypertensive renal disease is how is it?
[A] benign hypertension with mild hypertension does not lead to renal dysfunction, moderate to severe hypertension can cause renal dysfunction, but is less severe renal dysfunction. Small renal arteries of these patients have disease, glomerular and tubular damage, kidney slightly smaller, cortical thinning, surface irregular granules, called benign glomerular Benign hypertensive renal disease manifestations:
[1] related to the level of proteinuria and hematuria, and hypertension.
[2] urinary sodium excretion, due to increased renal vascular pressure affect the renal tubular function.
[3] azotemia and uremia. Treatment: the need for long-term antihypertensive treatment to reduce proteinuria and renal function improved.
[Two] malignant hypertension renal afferent arterioles and capillary plexus extensive fibrinous necrosis of the basic features of malignant hypertension. Wall thickening of small blood vessels, thereby increasing renal ischemia, renal impairment. Of the disease are associated with kidney damage, such as no effective treatment will rapidly to renal failure. Malignant hypertensive renal disease manifestations:
[1] proteinuria and hematuria, proteinuria serious than benign hypertension, gross hematuria.
[2] renal dysfunction: diastolic blood pressure over 130 mm Hg, and accompanied by 3 - 4 fundus changes in glomerular filtration rate fell by an average 28.6 percent annually, renal blood flow decreased by 38.6% annually. Treatment: untreated year of death, accounting for four-fifths of the patients died of uremia, cerebral hemorrhage, pulmonary edema. Effective antihypertensive therapy in renal function damage and stable renal function, or even apparent recovery, and reduce mortality. In uremia occurred, required dialysis. In short, regardless of the kind of situation, attention should be paid to the prevention of hypertension, aggressive treatment of high blood pressure, especially early in the discovery of high blood pressure, attention to be given treatment can prevent the formation of the consequences of hypertensive nephrosclerosis.
Reasonable diet of chronic nephritis
People's diet and health, and longevity are closely related. Two thousand
years ago, our ancestors with many well-known medical scientist has proposed a
"balanced diet" diet, health care, health, longevity, accumulated rich
experience. "Yellow Emperor" put forward the principle of compatibility of the
grain for the support, the five fruits in order to assist, five animals for the
benefit, five dishes for the charge, the smell together serving to complement
the fine Qi "meal. Patients with kidney disease are often not strict diet and a
variety of complications or aggravate the condition. Therefore, to strengthen
the health education of the patient's diet is an important part of recovery from
disease.
Varying degrees of kidney dysfunction in each kidney patients, and the excretion of nitrogenous waste, electrolyte, and can endure the amount of protein and other ingredients, and thus their condition. Different periods of the same patient diet program diet program different in different individuals of the same disease.
For the Asymptomatic: the general symptoms are very slight, and so not be overly restricted in the diet.
Nephropathy type: a daily supplement of a lot of protein, 2-3 grams per day per kilogram of body weight to the total daily protein up to 100-150 g, and preferably more choices of food containing high quality protein, such as dairy, meat fish and shrimp, bean products.Patients associated with elevated cholesterol, egg yolks should be limited as appropriate, other cholesterol-containing foods, such as brains, roe, fat, and animal offal should be eating. Swelling extent based on the patient were given salt or no salt diet. And to limit foods that stimulate renal parenchymal cells, such as wine and alcoholic beverages, spicy seasonings and volatile oil, capsaicin, oxalic acid and a variety of vegetables (such as spinach, leeks, celery, garlic, onions and baby carrots, etc.). Such as anemia in patients with serious, but also to add some iron-rich foods, such as vitamin B12, folic acid, fungus, red dates, longan, red bean and green leafy vegetables such as rape, cabbage and so on. Conducive to the swelling subsided, the diuretic effect of food carp, crucian carp (boiled soup consumption), goat's milk, melon, watermelon, mung bean, red bean, corn, wild rice, eggplant, gourd, etc.. Watermelon rind boiled water water effect was more obvious, the method of Peel and fine fresh water. Summer to fresh Peel and cut into small slices line wearing, in the shade dried until watermelon season use.Patients if concentrated functional dysfunction, but normal urination, water can be unrestricted. Only when patients with renal insufficiency phenomena, such as decreased urine output, will have to strictly limit the moisture and protein. In accordance with uremia diet treatment.
Type of hypertension: Note the use of salt or no salt diet, protein and calories in general should not be too high. For the prevention of atherosclerosis, but also pay attention to limit cholesterol, heart failure, water and salt to strictly control the
Varying degrees of kidney dysfunction in each kidney patients, and the excretion of nitrogenous waste, electrolyte, and can endure the amount of protein and other ingredients, and thus their condition. Different periods of the same patient diet program diet program different in different individuals of the same disease.
For the Asymptomatic: the general symptoms are very slight, and so not be overly restricted in the diet.
Nephropathy type: a daily supplement of a lot of protein, 2-3 grams per day per kilogram of body weight to the total daily protein up to 100-150 g, and preferably more choices of food containing high quality protein, such as dairy, meat fish and shrimp, bean products.Patients associated with elevated cholesterol, egg yolks should be limited as appropriate, other cholesterol-containing foods, such as brains, roe, fat, and animal offal should be eating. Swelling extent based on the patient were given salt or no salt diet. And to limit foods that stimulate renal parenchymal cells, such as wine and alcoholic beverages, spicy seasonings and volatile oil, capsaicin, oxalic acid and a variety of vegetables (such as spinach, leeks, celery, garlic, onions and baby carrots, etc.). Such as anemia in patients with serious, but also to add some iron-rich foods, such as vitamin B12, folic acid, fungus, red dates, longan, red bean and green leafy vegetables such as rape, cabbage and so on. Conducive to the swelling subsided, the diuretic effect of food carp, crucian carp (boiled soup consumption), goat's milk, melon, watermelon, mung bean, red bean, corn, wild rice, eggplant, gourd, etc.. Watermelon rind boiled water water effect was more obvious, the method of Peel and fine fresh water. Summer to fresh Peel and cut into small slices line wearing, in the shade dried until watermelon season use.Patients if concentrated functional dysfunction, but normal urination, water can be unrestricted. Only when patients with renal insufficiency phenomena, such as decreased urine output, will have to strictly limit the moisture and protein. In accordance with uremia diet treatment.
Type of hypertension: Note the use of salt or no salt diet, protein and calories in general should not be too high. For the prevention of atherosclerosis, but also pay attention to limit cholesterol, heart failure, water and salt to strictly control the
Thursday, April 19, 2012
Chronic nephritis can be much longer? Can be cured?
Had chronic nephritis can be much longer this disease can be cured? Chronic nephritis, short for chronic glomerulonephritis, can be transformed from acute nephritis, the disease is quite stubborn, clinically complete cure is considerably more difficult. Some patients with chronic nephritis it very serious thought to be life threatening, there would be a "chronic nephritis can be much longer" questions, in fact, chronic nephritis that you did not think that serious, as long as the development of renal failure , uremia, is not life-threatening, so worry much longer is not necessary. In the case of patients with chronic nephritis, should ask is "chronic nephritis can be cured?" What methods can solve the problem of no recurrence!
What can cure chronic nephritis, even to the radical no recurrence of the purpose? The treatment of chronic nephritis is a gradual process, need to be persistent, and all those responsible for hospitals, doctors and patients should follow the objective law, not engage in the "Great Leap Forward" in the course of the treatment of chronic nephritis.
Lead to either chronic nephritis or other kidney disease, the reason is that of progression of kidney fibrosis injury, destruction of renal cell structure damage of the glomerular cell function. The cell structure was fibrosis of damage and failure is the root cause of various types of kidney disease, "this", due to functional damage caused by proteinuria, serum creatinine increased "standard".
Micro-based medicine to penetrate the treatment of chronic nephritis different from the other in order to reduce urinary protein excretion, lower creatinine of the "standard" the next big effort, but the micro-through from the start the factors leading to renal fibrosis - kidney disorders, ischemic , hypoxic began.
Treatment of chronic nephritis need treatment for impaired renal intrinsic cells from the fundamental blocking renal fibrosis process, fundamentally, the infiltration therapy of micro-based traditional Chinese medicine mainly play the following role to get treatment!Specific description is as follows:
1.Vasodilators: of micro-penetration therapy of Chinese medicine through effective Chinese medicines dilate blood vessels, effectively improve renal ischemia and hypoxia, and to provide more oxygen and blood for the kidneys, so as to better accelerate the repair of renal intrinsic cells.
2.micro therapy for the penetration of traditional Chinese medicine through the anti-inflammatory, anticoagulant to inactivate inflammatory factors, and virulence factors of renal fibrosis process, and to prevent blood clots, blood clotting occurs, further blocking renal fibrosis, and repair damaged of renal intrinsic cells.
3.Also note that for the treatment of chronic nephritis immunosorbent assay, clear the immune complexes of patients' bodies to provide a secure and stable environment within the patients with late repair.
Through the rational application of the above treatment, the mesangial cells of the glomerular capillary repair, will be natural recovery of its normal physiological function.Mesangial cells of the barrier function will receive a reply, after the recovery of these functions, protein and other clinical symptoms also vanish. Effective treatment of chronic nephritis, to achieve true "cure disease before treatment, the disease is cured cases from extinction, so as to effectively prevent relapse.
What can cure chronic nephritis, even to the radical no recurrence of the purpose? The treatment of chronic nephritis is a gradual process, need to be persistent, and all those responsible for hospitals, doctors and patients should follow the objective law, not engage in the "Great Leap Forward" in the course of the treatment of chronic nephritis.
Lead to either chronic nephritis or other kidney disease, the reason is that of progression of kidney fibrosis injury, destruction of renal cell structure damage of the glomerular cell function. The cell structure was fibrosis of damage and failure is the root cause of various types of kidney disease, "this", due to functional damage caused by proteinuria, serum creatinine increased "standard".
Micro-based medicine to penetrate the treatment of chronic nephritis different from the other in order to reduce urinary protein excretion, lower creatinine of the "standard" the next big effort, but the micro-through from the start the factors leading to renal fibrosis - kidney disorders, ischemic , hypoxic began.
Treatment of chronic nephritis need treatment for impaired renal intrinsic cells from the fundamental blocking renal fibrosis process, fundamentally, the infiltration therapy of micro-based traditional Chinese medicine mainly play the following role to get treatment!Specific description is as follows:
1.Vasodilators: of micro-penetration therapy of Chinese medicine through effective Chinese medicines dilate blood vessels, effectively improve renal ischemia and hypoxia, and to provide more oxygen and blood for the kidneys, so as to better accelerate the repair of renal intrinsic cells.
2.micro therapy for the penetration of traditional Chinese medicine through the anti-inflammatory, anticoagulant to inactivate inflammatory factors, and virulence factors of renal fibrosis process, and to prevent blood clots, blood clotting occurs, further blocking renal fibrosis, and repair damaged of renal intrinsic cells.
3.Also note that for the treatment of chronic nephritis immunosorbent assay, clear the immune complexes of patients' bodies to provide a secure and stable environment within the patients with late repair.
Through the rational application of the above treatment, the mesangial cells of the glomerular capillary repair, will be natural recovery of its normal physiological function.Mesangial cells of the barrier function will receive a reply, after the recovery of these functions, protein and other clinical symptoms also vanish. Effective treatment of chronic nephritis, to achieve true "cure disease before treatment, the disease is cured cases from extinction, so as to effectively prevent relapse.
Special project of the biochemical tests in kidney disease
Biochemical examination of the kidney disease diagnosis, differential diagnosis of some kidney disease, guide therapy and prognosis is important. The following is commonly used in several checks:
(1) selective monitoring of urine protein electrophoresis and urine protein.
White electrophoresis score an integral part of the urinary protein analysis to determine the source of urinary protein, which helps the cause of the diagnosis and prognosis. If there is a mixed proteinuria, indicating impaired renal function involving the glomerular and tubular.
The risk of glomerular disease, the filtration membrane permeability and filtration role change. Mild glomerular disease, the filtration membrane "loophole" in a smaller in molecular weight protein in urine-based, high molecular weight protein excretion rarely called selective proteinuria. Obvious glomerular lesions filtration membrane "loophole" in the urine is not only a large number of albumin, and there are a lot of high molecular weight protein (such as globulin), which is called non-selective proteinuria. Selective proteinuria determination results suggest that the pathological type, predict treatment response and prognosis. Children with nephrotic syndrome, proteinuria was highly selective, of which about 97% of patients with minimal change nephropathy; adults also the majority of small lesions or minor lesions, but can also be found in membranous glomerulonephritis, focal renal small glomerulonephritis, proliferative glomerulonephritis.Van Gogh selectivity can predict a good response to steroid and immunosuppressive therapy; high selectivity and a better prognosis, otherwise poor prognosis.
(2) blood, urine complement determination.
Increased serum total complement (CH50) found in a variety of inflammatory, acute phase reactants. Some malignant tumors increased complement activity. Reduce serum CH50 is common in acute and chronic glomerulonephritis, hemolytic anemia and systemic lupus erythematosus. Blood of acute glomerulonephritis C3 decline, especially in post-streptococcal acute glomerulonephritis decreased more significantly. Mesangial proliferative glomerulonephritis, lupus nephritis and renal transplant rejection, C3 can reduce blood. Determination of urinary C3 content may indirectly reflect the permeability of the glomerular basement membrane, mesangial proliferative glomerulonephritis, lupus nephritis urinary C3 almost all positive; positive rate of membranous nephropathy and focal segmental glomerulosclerosis high, minimal change is often negative. Urine C3-positive patients compared with negative patients with severe illness and poor prognosis, the higher the content of the disease the more severe.
(3) fibrin degradation products determination.
Urinary fibrin degradation product of positive means of coagulation and fibrinolysis in the kidney, suggesting that the inflammatory lesions. Non-inflammatory diseases are mostly negative. Primary glomerular nephropathy is usually negative, chronic nephritis and more positive. Urinary fibrin degradation products was increased to reflect the degree of renal impairment. In the course of treatment of chronic nephritis, the clinical symptoms, recovery of renal function, urinary fibrin degradation product decreased gradually or negative; positive that kidney disease inflammatory process is still ongoing disease activity, continuous positive prognosis after treatment poor.
(4) of glomerular urine protein examination.
If the glomerular filtration barrier injury, will appear in the urine albumin, transferrin, immunoglobulin G; in molecular weight protein of the immunoglobulin M and α2-macroglobulin. Urinary albumin to detect the early diagnosis contribute to the glomerular lesions. When the glomerular mild lesions, increased urinary albumin; when further damaged, urinary IgA and IgG increased urine IgM increased; of glomerular serious disease. Urinary albumin and IgG glomerular lesions prompted the transition to chronic urine IgM important in predicting renal failure.
(5) renal tubular urine protein examination.
Proximal tubule epithelial cell damage, obstacles to the normal filtration of protein reabsorption, urine low molecular weight proteins, mainly α1-microglobulin, β2-microglobulin, lysozyme, acid and vitamin A binding protein. This group proteinuria displacement increase is a sign of renal proximal tubule damage.
Sunday, April 15, 2012
Hypertensive nephropathy is how is it?
Hypertensive renal disease is how is it? We can see from the name,
hypertensive nephropathy is a complication caused by high blood pressure, Why,
then, hypertensive nephropathy? Due to hypertensive kidney disease for people
very dangerous, in order to be able to let everyone know something about this,
the following analysis.
[A] benign hypertension with mild hypertension does not lead to renal dysfunction, moderate to severe hypertension can cause renal dysfunction, but is less severe renal dysfunction. Small renal arteries of these patients have disease, glomerular and tubular damage, kidney slightly smaller, cortical thinning, surface irregular granules, called benign glomerular What are the manifestations of benign hypertensive renal disease?
[1] related to the level of proteinuria and hematuria, and hypertension.
[2] urinary sodium excretion, due to increased renal vascular pressure affect the renal tubular function.
[3] azotemia and uremia. Treatment: the need for long-term antihypertensive treatment to reduce proteinuria and renal function improved.
[Two] malignant hypertension renal afferent arterioles and capillary plexus extensive fibrinous necrosis of the basic features of malignant hypertension. Wall thickening of small blood vessels, thereby increasing renal ischemia, renal impairment. Of the disease are associated with kidney damage, such as no effective treatment will rapidly to renal failure. Malignant Hypertensive Nephropathy manifestations:
[1] proteinuria and hematuria, proteinuria serious than benign hypertension, gross hematuria.
[2] renal dysfunction: diastolic blood pressure over 130 mm Hg, and accompanied by 3 - 4 fundus changes in glomerular filtration rate fell by an average 28.6 percent annually, renal blood flow decreased by 38.6% annually. Treatment: untreated year of death, accounting for four-fifths of the patients died of uremia, cerebral hemorrhage, pulmonary edema. Effective antihypertensive therapy in renal function damage and stable renal function, or even apparent recovery, and reduce mortality. In uremia occurred, required dialysis. In short, regardless of the kind of situation, attention should be paid to the prevention of hypertension, aggressive treatment of high blood pressure, especially early in the discovery of high blood pressure, attention to be given treatment can prevent the formation of the consequences of hypertensive nephrosclerosis.
[A] benign hypertension with mild hypertension does not lead to renal dysfunction, moderate to severe hypertension can cause renal dysfunction, but is less severe renal dysfunction. Small renal arteries of these patients have disease, glomerular and tubular damage, kidney slightly smaller, cortical thinning, surface irregular granules, called benign glomerular What are the manifestations of benign hypertensive renal disease?
[1] related to the level of proteinuria and hematuria, and hypertension.
[2] urinary sodium excretion, due to increased renal vascular pressure affect the renal tubular function.
[3] azotemia and uremia. Treatment: the need for long-term antihypertensive treatment to reduce proteinuria and renal function improved.
[Two] malignant hypertension renal afferent arterioles and capillary plexus extensive fibrinous necrosis of the basic features of malignant hypertension. Wall thickening of small blood vessels, thereby increasing renal ischemia, renal impairment. Of the disease are associated with kidney damage, such as no effective treatment will rapidly to renal failure. Malignant Hypertensive Nephropathy manifestations:
[1] proteinuria and hematuria, proteinuria serious than benign hypertension, gross hematuria.
[2] renal dysfunction: diastolic blood pressure over 130 mm Hg, and accompanied by 3 - 4 fundus changes in glomerular filtration rate fell by an average 28.6 percent annually, renal blood flow decreased by 38.6% annually. Treatment: untreated year of death, accounting for four-fifths of the patients died of uremia, cerebral hemorrhage, pulmonary edema. Effective antihypertensive therapy in renal function damage and stable renal function, or even apparent recovery, and reduce mortality. In uremia occurred, required dialysis. In short, regardless of the kind of situation, attention should be paid to the prevention of hypertension, aggressive treatment of high blood pressure, especially early in the discovery of high blood pressure, attention to be given treatment can prevent the formation of the consequences of hypertensive nephrosclerosis.
Friday, April 13, 2012
How to control the hypertension of patients with chronic nephritis?
Chronic nephritis, the residual and (or) had lesions of the renal unit in
compensatory hemodynamic status, systemic hypertension will undoubtedly add to
this condition, leading to glomerular injury, and therefore patients with
chronic nephritis should be actively controlled high blood pressure, prevent
deterioration of renal function.
In recent years, through a series of studies confirmed that most scholars have angiotensin converting enzyme inhibitors as first-line antihypertensive drugs. Lately, a lot of clinical studies confirmed that calcium antagonists such as nifedipine, nicardipine equal treatment of hypertension and renal function deterioration is more positive effect.That calcium antagonists, despite the slight expansion of the role of afferent arterioles, but it has significantly reduced the role of systemic blood pressure, so make the uninvolved or only partially involved glomerular hemodynamics, the high metabolic statusbe improved; In addition, calcium channel blockers reduce oxygen consumption, inhibition of platelet aggregation through the membrane effect of reducing the excessive oxidation of the calcium in the interstitial deposition and reduce the cell membrane, so as to achieve to reduce kidney damage and stable renal function. Clinical reports, short-term (4 weeks) or long (1-2 years) with calcium antagonist treatment of nephritis in patients with chronic renal insufficiency has not revealed any glomerular injury, but clearly demonstrated that it is angiotensin converting enzyme inhibitors is very similar to the efficacy of renal function deterioration. And angiotensin converting enzyme inhibitors at lowering urinary protein role for it in general. It should be noted that some scholars believe that the calcium antagonists impact on renal function is still a need for more long-term observation.
β-blockers, such as the United States and more peace of mind, Atenolol, has a good effect on the renin-dependent hypertension. beta-blockers reduce renin, although the drug reduce cardiac output, but does not affect renal blood flow and GFR, it is also used for the treatment of renal hypertension. It should be noted that some beta-blockers such as atenolol and naphthalene hydroxyl peace of mind, low-fat-soluble, since renal excretion, so renal insufficiency should pay attention to adjust the dose and extending administration time.
In addition, vasodilators such as hydralazine antihypertensive effect, it can be combined with beta-blockers reduce vasodilators stimulate renin angiotensin system side effects (such as rapid heartbeat, water and sodium retention ), and may improve the therapeutic effect. Hydralazine general daily 200mg, but must be alert to the possibility of drug-induced lupus erythematosus-like syndrome.
Edema renal, can add to a thiazide diuretic; poor renal function (serum creatinine> 200μmol / L), thiophene triazine efficacy or invalid, it should use loop diuretics marrow .Chronic nephritis patients treated with diuretics should be noted that the electrolyte imbalance in the body, and to pay attention to the tendency to aggravate hyperlipidemia, hypercoagulable state.
In recent years, through a series of studies confirmed that most scholars have angiotensin converting enzyme inhibitors as first-line antihypertensive drugs. Lately, a lot of clinical studies confirmed that calcium antagonists such as nifedipine, nicardipine equal treatment of hypertension and renal function deterioration is more positive effect.That calcium antagonists, despite the slight expansion of the role of afferent arterioles, but it has significantly reduced the role of systemic blood pressure, so make the uninvolved or only partially involved glomerular hemodynamics, the high metabolic statusbe improved; In addition, calcium channel blockers reduce oxygen consumption, inhibition of platelet aggregation through the membrane effect of reducing the excessive oxidation of the calcium in the interstitial deposition and reduce the cell membrane, so as to achieve to reduce kidney damage and stable renal function. Clinical reports, short-term (4 weeks) or long (1-2 years) with calcium antagonist treatment of nephritis in patients with chronic renal insufficiency has not revealed any glomerular injury, but clearly demonstrated that it is angiotensin converting enzyme inhibitors is very similar to the efficacy of renal function deterioration. And angiotensin converting enzyme inhibitors at lowering urinary protein role for it in general. It should be noted that some scholars believe that the calcium antagonists impact on renal function is still a need for more long-term observation.
β-blockers, such as the United States and more peace of mind, Atenolol, has a good effect on the renin-dependent hypertension. beta-blockers reduce renin, although the drug reduce cardiac output, but does not affect renal blood flow and GFR, it is also used for the treatment of renal hypertension. It should be noted that some beta-blockers such as atenolol and naphthalene hydroxyl peace of mind, low-fat-soluble, since renal excretion, so renal insufficiency should pay attention to adjust the dose and extending administration time.
In addition, vasodilators such as hydralazine antihypertensive effect, it can be combined with beta-blockers reduce vasodilators stimulate renin angiotensin system side effects (such as rapid heartbeat, water and sodium retention ), and may improve the therapeutic effect. Hydralazine general daily 200mg, but must be alert to the possibility of drug-induced lupus erythematosus-like syndrome.
Edema renal, can add to a thiazide diuretic; poor renal function (serum creatinine> 200μmol / L), thiophene triazine efficacy or invalid, it should use loop diuretics marrow .Chronic nephritis patients treated with diuretics should be noted that the electrolyte imbalance in the body, and to pay attention to the tendency to aggravate hyperlipidemia, hypercoagulable state.
Angiotensin converting enzyme inhibitors for patients with chronic nephritis What is the significance?
In recent years by a large number of animal experiments and nephritis in
patients with controlled clinical observation has been confirmed, unless there
are certainly antihypertensive efficacy of the drug can reduce glomerular
pressure, there is certainly delay the deterioration of renal function, lower
urinary protein (20% to 40%) and reduce the role of glomerular sclerosis.
Commonly used preparations the mercapto tensiomin proline acid, typical doses of
25 to 50 mg / 3 times a day, clinical; without thiol according to Na Puli, the
long duration of action, the commonly used dose of 5 to 10 mg / day 1.The drugs
to reduce the main mechanism of ball pressure, protect and stabilize the renal
function as follows:
① The expansion of glomerular artery, small arteries of the ball is more significant than the afferent artery dilation, and therefore reduce the pressure inside the ball, reducing renal ball high blood dynamics;
② The angiotensin II-stimulated proximal tubular ammonium, class preparation can reduce the angiotensin II level and (or) l hyperkalemia and reduce the production of ammonium, will help reduce the renal hypertrophy and avoid excessive ammonium generated by the alternative pathway activation of complement induced tubulointerstitial lesions.
The application of such agents should pay attention to can cause hyperkalemia (especially renal dysfunction), other side effects include rash, itching, fever, flu-like symptoms, diminished sense of taste and rare granulocytes reduce. Some people think that class preparation may cause acute drug-induced interstitial nephritis.
① The expansion of glomerular artery, small arteries of the ball is more significant than the afferent artery dilation, and therefore reduce the pressure inside the ball, reducing renal ball high blood dynamics;
② The angiotensin II-stimulated proximal tubular ammonium, class preparation can reduce the angiotensin II level and (or) l hyperkalemia and reduce the production of ammonium, will help reduce the renal hypertrophy and avoid excessive ammonium generated by the alternative pathway activation of complement induced tubulointerstitial lesions.
The application of such agents should pay attention to can cause hyperkalemia (especially renal dysfunction), other side effects include rash, itching, fever, flu-like symptoms, diminished sense of taste and rare granulocytes reduce. Some people think that class preparation may cause acute drug-induced interstitial nephritis.
How is the prognosis of chronic nephritis?
The natural history of patients with chronic nephritis vary widely, as part
of the patient's condition is relatively stable after 5-6 years, or even 20 to
30 years before developingrenal insufficiency of a very small number of patients
and relieve itself. Another part of thepatient's condition continued to develop
or repeated acute attacks, the development ofrenal failure in 2 to 3 years. Is
generally believed that the poor prognosis of sustained hypertension of chronic
nephritis and persistent renal dysfunction.
In summary, chronic nephritis is a glomerular disease with sexual orientation, and the prognosis is relatively poor. Pathological types of renal biopsy in the prognosis is more reliable and is generally believed that good with minimal change nephropathy and puremesangial proliferative glomerulonephritis and prognosis of membranous nephropathyprogress is slow, the prognosis is better than that of nephritis, most cases in a few years,renal insufficiency, focal segmental glomerular sclerosis prognosis is poor.
Recent studies show that, in addition to glomerular lesions, tubular, renal vascular and renal interstitial lesion significantly affect the prognosis. Tubular atrophy, renal vascular sclerosis, a large number of renal interstitial lymphocytic infiltration and interstitial fibrosis, poor prognosis.
In summary, chronic nephritis is a glomerular disease with sexual orientation, and the prognosis is relatively poor. Pathological types of renal biopsy in the prognosis is more reliable and is generally believed that good with minimal change nephropathy and puremesangial proliferative glomerulonephritis and prognosis of membranous nephropathyprogress is slow, the prognosis is better than that of nephritis, most cases in a few years,renal insufficiency, focal segmental glomerular sclerosis prognosis is poor.
Recent studies show that, in addition to glomerular lesions, tubular, renal vascular and renal interstitial lesion significantly affect the prognosis. Tubular atrophy, renal vascular sclerosis, a large number of renal interstitial lymphocytic infiltration and interstitial fibrosis, poor prognosis.
Tuesday, April 10, 2012
IgA nephropathy Note
1.In the past the medical profession that the IGA nephropathy development
is slow, causing a paralysis of thought in recent years, the serious
consequences of the IGAnephropathy development, once the creatinine began to
increase, and soon will bedevelopment of uremia. So, regardless of severity
should seize the time for effective treatment, should lose no time.
2.The treatment of hematuria can not use hemostatic necessary to clear the the IGAsediment to heal. TCM and more use to stop bleeding prescription, the sight of blood to stop bleeding, headache medicine head rule France, although at that time to eliminatethe symptoms, but delay the best time for treatment.
3.If inappropriate medication, only a temporary solution, and will acceleratedeterioration, delay the timing of treatment, and ultimately become uremia, so the choice is very important.
2.The treatment of hematuria can not use hemostatic necessary to clear the the IGAsediment to heal. TCM and more use to stop bleeding prescription, the sight of blood to stop bleeding, headache medicine head rule France, although at that time to eliminatethe symptoms, but delay the best time for treatment.
3.If inappropriate medication, only a temporary solution, and will acceleratedeterioration, delay the timing of treatment, and ultimately become uremia, so the choice is very important.
IgA nephropathy etiology and pathogenesis
The etiology and pathogenesis of IgA nephropathy has not yet been fully
understood, is generally believed that IgA nephropathy is a glomerular disease
caused by immune complexes. TCM etiology and pathogenesis of IgA nephropathy
understanding can be summarized as:
, Pathogenic foreign attacks
Wind clip hot evil foreign attacks, the homes in the lung, downstream bladderwaterways negative, hot forged focus, can cause edema and hematuria.
Second, liver and kidney
Ferrite deficiency, or over-the troubles that liver and kidney yin deficiency, the raw heat,thermal injury Shenluotong hematuria.
Third, spleen and kidney Qi
Ferrite deficiency of qi, or overwork, injuries to the spleen and kidney, resulting inspleen and kidney Qi, Shengqing spleen, kidney failure to seal Tibet, proteinuria, the gas is not taken blood, hematuria.
In short, of IgA nephropathy total yin or qi deficiency-based wind cold, damp heat,blood stasis as the standard, Yin Chang, chief damp heat, qi deficiency with blood stasis.
, Pathogenic foreign attacks
Wind clip hot evil foreign attacks, the homes in the lung, downstream bladderwaterways negative, hot forged focus, can cause edema and hematuria.
Second, liver and kidney
Ferrite deficiency, or over-the troubles that liver and kidney yin deficiency, the raw heat,thermal injury Shenluotong hematuria.
Third, spleen and kidney Qi
Ferrite deficiency of qi, or overwork, injuries to the spleen and kidney, resulting inspleen and kidney Qi, Shengqing spleen, kidney failure to seal Tibet, proteinuria, the gas is not taken blood, hematuria.
In short, of IgA nephropathy total yin or qi deficiency-based wind cold, damp heat,blood stasis as the standard, Yin Chang, chief damp heat, qi deficiency with blood stasis.
Children with IgA nephropathy renal damage which several types?
IgA nephropathy (1gAGN) is a group associated with system disease, renal
biopsy immune pathology in glomerular mesangial granular deposition of IgA-based
disease.IgAGN for the pathological diagnosis of an immune name, clinical
glomerulonephritis with hematuria as the main manifestation, but also led to one
of the main end-stage renal failure. That the Department of an independent
clinical a pathological syndrome. Renal damage following types:
First, episodes of gross hematuria
Often in a variety of respiratory tract infections in 1-3d after gross hematuria, it is also known as pharyngitis synchronization hematuria, this common sense of acute chain glomerulonephritis. Deformability of urinary red cell morphology, suggestive of glomerular hematuria. I have seen homes in addition to gross hematuria, and in some cases accompanied by the waist and (or) severe abdominal pain, often misdiagnosed as urinary calculi, acute abdomen (appendicitis). Such abdominal pain mechanism may be associated with inflammatory lesions of small arteries in the ureter or gastrointestinal mucosa manifestations of systemic small vessel vasculitis lesions. In addition, the electron microscope shows submucosal small artery injury was fibrinoid necrosis, IgA, and C3, and fibrin deposition to support IgAGN gastrointestinal tract has also been compromised. Low back pain associated with urinary retention or temporary oliguria may be of small blood clots occur in the urinary tract caused by a temporary obstruction.
Second, the nephrotic syndrome
Individually or in some cases associated with hypertension, hematuria. If the histopathological glomerular sclerosis and renal vascular sclerosis poor prognosis.Shanghai Children's Hospital have reported 20 cases IgAGN, which manifested as nephrotic-type, 9 cases (47%), showing that this type of a certain proportion of children IgAGN.
Third, the nephritic syndrome
This type of performance with / without mild edema of asymptomatic microscopic hematuria, often misdiagnosed as the chain sense glomerulonephritis more common in urine screening examination and confirmed by biopsy.
Fourth, the simple proteinuria
Proteinuria as the first symptom in the pediatric majority showed mild or moderate proteinuria without edema and other symptoms of kidney damage.
Fifth, rapidly progressive glomerulonephritis
Rare. Continuous gross hematuria, proteinuria associated with heart, brain involvement, the abrupt deterioration of short-term renal function, renal biopsy widely (50% -100%) glomerular crescent form. Severe hematuria hemoglobin on renal tubular toxicity and tubular obstruction with acute tubular necrosis.
First, episodes of gross hematuria
Often in a variety of respiratory tract infections in 1-3d after gross hematuria, it is also known as pharyngitis synchronization hematuria, this common sense of acute chain glomerulonephritis. Deformability of urinary red cell morphology, suggestive of glomerular hematuria. I have seen homes in addition to gross hematuria, and in some cases accompanied by the waist and (or) severe abdominal pain, often misdiagnosed as urinary calculi, acute abdomen (appendicitis). Such abdominal pain mechanism may be associated with inflammatory lesions of small arteries in the ureter or gastrointestinal mucosa manifestations of systemic small vessel vasculitis lesions. In addition, the electron microscope shows submucosal small artery injury was fibrinoid necrosis, IgA, and C3, and fibrin deposition to support IgAGN gastrointestinal tract has also been compromised. Low back pain associated with urinary retention or temporary oliguria may be of small blood clots occur in the urinary tract caused by a temporary obstruction.
Second, the nephrotic syndrome
Individually or in some cases associated with hypertension, hematuria. If the histopathological glomerular sclerosis and renal vascular sclerosis poor prognosis.Shanghai Children's Hospital have reported 20 cases IgAGN, which manifested as nephrotic-type, 9 cases (47%), showing that this type of a certain proportion of children IgAGN.
Third, the nephritic syndrome
This type of performance with / without mild edema of asymptomatic microscopic hematuria, often misdiagnosed as the chain sense glomerulonephritis more common in urine screening examination and confirmed by biopsy.
Fourth, the simple proteinuria
Proteinuria as the first symptom in the pediatric majority showed mild or moderate proteinuria without edema and other symptoms of kidney damage.
Fifth, rapidly progressive glomerulonephritis
Rare. Continuous gross hematuria, proteinuria associated with heart, brain involvement, the abrupt deterioration of short-term renal function, renal biopsy widely (50% -100%) glomerular crescent form. Severe hematuria hemoglobin on renal tubular toxicity and tubular obstruction with acute tubular necrosis.
Monday, April 9, 2012
Best time of summer, chronic kidney disease treatment
Many kidney specialists pointed out that sick patients with chronic kidney
disease need to raise slowly, but in the period of recuperation, the need to
receive standard treatment, as early as day treatment for kidney protection
significance is not the same, in the summer of kidney patients to ignore is the
treatment chronic nephropathy season.
Why summer is the best season for the treatment of chronic kidney disease? Chinese medicine believes that, especially the dog days of summer, as temperatures rise, the human body yang rising, meridian accessible, with plenty of blood, the resistance is relatively high; the same time, the human body in various tissues and organs function, ability to repair itself in a year the best level. At this point, patients with chronic kidney disease often feel "good", the external symptoms of a variety of kidney disease also are relatively mild. Therefore, some patients are often in the summer of their condition "underestimate the enemy," the idea, they do not rush to be treated in the summer, even mistakenly believe that their own stable condition, and began to recover, the more relaxed the idea of continued treatment. Do you not know that, according to Chinese medicine the dialectical, a lot of chronic kidney disease, chronic nephritis, nephrotic syndrome, all belong to the actual situation mixed, the vacuity of the card. Patients can take advantage of the summer of this favorable opportunity, use of standard means of treatment of certain cold nephropathy, the virtual nephropathy will be able to drive the wind dispelling tonic fitness, to adjust the body's yin and yang balance, a multipliertreatment. This is in fact very simple, as we boil water, under normal circumstances, summer boil a pot of water, certainly better than the winter fast.
Chronic kidney disease, impaired renal intrinsic cells ability to repair itself the highest kidney fibrosis progression is relatively slow. If the patient is able to seize the summer of this favorable opportunity for the treatment of chronic kidney disease, standard treatment of chronic kidney disease, you will be able to receive those who spend less effective, and in stable condition after treatment recurrence.
Therefore, the treatment of chronic kidney disease should seize the favorable opportunity, and early treatment and early rehabilitation. Do not wait until the advent of autumn and winter, the weather cools, human yang latent, relatively low resistance, and again the treatment of chronic kidney disease, when the difficulty of treatment is bound to be greatly enhanced! The reason because of the weather, the patient vulnerable to cold, to the treatment of chronic kidney disease and stable recovery a great deal of variables.
Why summer is the best season for the treatment of chronic kidney disease? Chinese medicine believes that, especially the dog days of summer, as temperatures rise, the human body yang rising, meridian accessible, with plenty of blood, the resistance is relatively high; the same time, the human body in various tissues and organs function, ability to repair itself in a year the best level. At this point, patients with chronic kidney disease often feel "good", the external symptoms of a variety of kidney disease also are relatively mild. Therefore, some patients are often in the summer of their condition "underestimate the enemy," the idea, they do not rush to be treated in the summer, even mistakenly believe that their own stable condition, and began to recover, the more relaxed the idea of continued treatment. Do you not know that, according to Chinese medicine the dialectical, a lot of chronic kidney disease, chronic nephritis, nephrotic syndrome, all belong to the actual situation mixed, the vacuity of the card. Patients can take advantage of the summer of this favorable opportunity, use of standard means of treatment of certain cold nephropathy, the virtual nephropathy will be able to drive the wind dispelling tonic fitness, to adjust the body's yin and yang balance, a multipliertreatment. This is in fact very simple, as we boil water, under normal circumstances, summer boil a pot of water, certainly better than the winter fast.
Chronic kidney disease, impaired renal intrinsic cells ability to repair itself the highest kidney fibrosis progression is relatively slow. If the patient is able to seize the summer of this favorable opportunity for the treatment of chronic kidney disease, standard treatment of chronic kidney disease, you will be able to receive those who spend less effective, and in stable condition after treatment recurrence.
Therefore, the treatment of chronic kidney disease should seize the favorable opportunity, and early treatment and early rehabilitation. Do not wait until the advent of autumn and winter, the weather cools, human yang latent, relatively low resistance, and again the treatment of chronic kidney disease, when the difficulty of treatment is bound to be greatly enhanced! The reason because of the weather, the patient vulnerable to cold, to the treatment of chronic kidney disease and stable recovery a great deal of variables.
Chronic kidney disease: out of the understanding of misunderstanding
The nephropathy non-kidney protein low Mo in bed real do not have chronic
kidney disease in the modern medical diagnosis of definite chronic nephritis,
nephrotic syndrome, chronic renal failure, uremia, chronic kidney disease.
Difficult treatment of these diseases, longer duration, is recognized worldwide
as difficult to cure. The majority of kidney patients look to the medical
treatment, but due to the treatment of chronic diseases and nursed back to
health there is misunderstanding, making it difficult to receive satisfactory
results.
Misunderstanding one: chronic kidney disease as kidney, kidney and method of treatment. Here there are two reasons doctors and patients. Longer duration of chronic kidney disease, there are many obvious weak symptoms, patients often think "kidney", and the seeking of herbs treatment. Some doctors kidney disease as kidney, by the ancient "kidney virtual" said. Kidney disease can not be equated in the kidney, chronic kidney disease is autoimmune disease, its onset is often associated with a cold or infection. Chinese medicine point of view, its pathogenesis are evils, in-depth Blood stasis collaterals. True its nature is hot, the treatment Yiqing should diarrhea, cooling blood, and to be based on the patient's specific condition, diagnosis and treatment, in order to receive the desired therapeutic effect.
Misunderstanding two: patients with chronic kidney disease need to eat more protein-rich foods. The clinical features of chronic kidney disease is one of persistent proteinuria, especially nephrotic syndrome have a lot of protein loss from the urine, often can lead to hypoproteinemia, and to induce edema. In this case, modern medicine advocates kidney patients should be eating high protein food to supplement the loss of protein, which is lost protein, complement proteins, point of view. Under the influence of this view, patients with kidney disease tend to believe that the more the better to eat protein-rich foods, excessive exposure, increasing the burden on the kidneys, but not conducive to the recovery of nephropathy. Therefore, should be appropriate to limit the intake of high protein food, a reasonable allocation of the diet, so that a balanced diet and not excessive, so as to reduce the burden on the kidneys, which will help the rehabilitation of the kidney.
Misunderstanding three: that patients with chronic kidney disease should stay in bed to avoid exercise. Under normal circumstances, when patients with chronic kidney disease to see a doctor, often this advice: "Try to avoid exercise, the best of bed rest." So, the patient returned home, bed rest, clothing to hand out food to mouth, but alsoeuphemistically called "I would like the doctor's advice, An Xinjing support". In fact, bed rest and non-good way, this may hinder the circulation of qi and blood, increase the microcirculation, and prolonged bed rest can weaken the immune function, making the body increasingly frail, but the overall rehabilitation. The correct way should adhere to a moderate form of exercise according to their specific situation, combination of outdoor walking speed, at least 1-2 hours a day, the line of the day, sustained, will be able to enhance physical fitness, promote kidney disease. rehabilitation.
Misunderstanding one: chronic kidney disease as kidney, kidney and method of treatment. Here there are two reasons doctors and patients. Longer duration of chronic kidney disease, there are many obvious weak symptoms, patients often think "kidney", and the seeking of herbs treatment. Some doctors kidney disease as kidney, by the ancient "kidney virtual" said. Kidney disease can not be equated in the kidney, chronic kidney disease is autoimmune disease, its onset is often associated with a cold or infection. Chinese medicine point of view, its pathogenesis are evils, in-depth Blood stasis collaterals. True its nature is hot, the treatment Yiqing should diarrhea, cooling blood, and to be based on the patient's specific condition, diagnosis and treatment, in order to receive the desired therapeutic effect.
Misunderstanding two: patients with chronic kidney disease need to eat more protein-rich foods. The clinical features of chronic kidney disease is one of persistent proteinuria, especially nephrotic syndrome have a lot of protein loss from the urine, often can lead to hypoproteinemia, and to induce edema. In this case, modern medicine advocates kidney patients should be eating high protein food to supplement the loss of protein, which is lost protein, complement proteins, point of view. Under the influence of this view, patients with kidney disease tend to believe that the more the better to eat protein-rich foods, excessive exposure, increasing the burden on the kidneys, but not conducive to the recovery of nephropathy. Therefore, should be appropriate to limit the intake of high protein food, a reasonable allocation of the diet, so that a balanced diet and not excessive, so as to reduce the burden on the kidneys, which will help the rehabilitation of the kidney.
Misunderstanding three: that patients with chronic kidney disease should stay in bed to avoid exercise. Under normal circumstances, when patients with chronic kidney disease to see a doctor, often this advice: "Try to avoid exercise, the best of bed rest." So, the patient returned home, bed rest, clothing to hand out food to mouth, but alsoeuphemistically called "I would like the doctor's advice, An Xinjing support". In fact, bed rest and non-good way, this may hinder the circulation of qi and blood, increase the microcirculation, and prolonged bed rest can weaken the immune function, making the body increasingly frail, but the overall rehabilitation. The correct way should adhere to a moderate form of exercise according to their specific situation, combination of outdoor walking speed, at least 1-2 hours a day, the line of the day, sustained, will be able to enhance physical fitness, promote kidney disease. rehabilitation.
Patients with chronic kidney disease care "Eight Principles"
To prevent fatigue
Proper rest and avoid fatigue, nephrotic syndrome and chronic kidney disease can be improved first. When the patients in the acute phase, mainly to absolute bed rest; until a stable condition only after an appropriate increase in activity, to prevent limb thrombosis still need to be taken to avoid fatigue.
Prevention of infection
Seasonal change, seasonal cold air frequently patronized, to go with a jacket, wear a scarf when the wind blows, pay attention to respiratory warm, reducing the exposure to external adverse stimuli. Incidence at first, often associated with colds and other diseases have been implicated in kidney disease-related bacteria, such as hemolytic streptococcus is invasion of the human body. Indoor environment clean, fresh air, and to maintain a certain temperature and humidity.
Frequent mouth
Resistance to kidney disease patients is poor, and accompanied by indigestion, Dwelling "accident" bacteria in the mouth easy to breed, thus kidney disease patients with ulcerative stomatitis in more, so gargle with warm salt water after meals is quite necessary .
Regular exercise
Suffering from chronic kidney disease, patients often do not exercise, afraid to increase the burden on the kidney, and aggravate the condition. In fact, when a stable condition, the consent of the physician, should be appropriate to participate in certain physical exercise such as walking, cycling and feel happy, work and rest, to reduce complications and can reduce blood lipids, enhance physical fitness, improve disease resistance.
Reduce sexual intercourse
Unmarried patients with chronic kidney disease should be thinking about marriage in a stable condition after 2-3 years after marriage, but also a number of restrictive life.Married kidney disease patients should pay attention to the unstable condition, not sex.Stable condition after 3-6 months, does not exist edema, normal urine output, urine protein, red blood cells or cell tube, sex needs to moderation.
Careful medication
Kidney disease, kidney damage to the excretory function are also affected, kidney disease resistance diminished capacity, it is not casual drug use, such as certain antibiotics (kanamycin, gentamicin), some antipyretic analgesics. will produce harmful effects on the kidneys. Similarly, there is no guidance of the physician and do not abuse the nourishing substances. Prescription issued by physicians, time and quantity taking arbitrary reduction withdrawal would be dangerous and harmful, especially hormonal drugs, there will be repeated illness, should be very careful when increasing or decreasing. Taking blood pressure, lipid-lowering or anticoagulant drugs, and prevent complications.
To diet
Although the patients with nephrotic syndrome from urinary loss of protein, high-protein diet will increase the glomerular filtration, increased proteinuria, and promote the malignant progression of kidney disease. The correct way is the quality of the total protein of the daily intake of 30-35 grams, and calculation of vegetables, fruits, rice contains protein. The high-quality protein diet rich in animal protein, essential amino acids, such as lean beef, pork, lamb and fresh fish.
To prevent deterioration
The data indicate that primary glomerular nephropathy and respiratory infections and allergies, it is necessary to actively combat these factors, as early investigation, examinations of urine, and strive to the early detection of the presence of nephropathy.As part of the acute nephritis can be transformed into a chronic nephritis, acute nephritis should be attached great importance to conduct a thorough treatment, and strictly follow the doctor's advice. Should actively seek medical treatment for a diagnosed chronic glomerulonephritis, efficient and kidneys, handling, and regular follow-up changes in renal function to prevent chronic kidney disease to chronic renal insufficiency into.
Proper rest and avoid fatigue, nephrotic syndrome and chronic kidney disease can be improved first. When the patients in the acute phase, mainly to absolute bed rest; until a stable condition only after an appropriate increase in activity, to prevent limb thrombosis still need to be taken to avoid fatigue.
Prevention of infection
Seasonal change, seasonal cold air frequently patronized, to go with a jacket, wear a scarf when the wind blows, pay attention to respiratory warm, reducing the exposure to external adverse stimuli. Incidence at first, often associated with colds and other diseases have been implicated in kidney disease-related bacteria, such as hemolytic streptococcus is invasion of the human body. Indoor environment clean, fresh air, and to maintain a certain temperature and humidity.
Frequent mouth
Resistance to kidney disease patients is poor, and accompanied by indigestion, Dwelling "accident" bacteria in the mouth easy to breed, thus kidney disease patients with ulcerative stomatitis in more, so gargle with warm salt water after meals is quite necessary .
Regular exercise
Suffering from chronic kidney disease, patients often do not exercise, afraid to increase the burden on the kidney, and aggravate the condition. In fact, when a stable condition, the consent of the physician, should be appropriate to participate in certain physical exercise such as walking, cycling and feel happy, work and rest, to reduce complications and can reduce blood lipids, enhance physical fitness, improve disease resistance.
Reduce sexual intercourse
Unmarried patients with chronic kidney disease should be thinking about marriage in a stable condition after 2-3 years after marriage, but also a number of restrictive life.Married kidney disease patients should pay attention to the unstable condition, not sex.Stable condition after 3-6 months, does not exist edema, normal urine output, urine protein, red blood cells or cell tube, sex needs to moderation.
Careful medication
Kidney disease, kidney damage to the excretory function are also affected, kidney disease resistance diminished capacity, it is not casual drug use, such as certain antibiotics (kanamycin, gentamicin), some antipyretic analgesics. will produce harmful effects on the kidneys. Similarly, there is no guidance of the physician and do not abuse the nourishing substances. Prescription issued by physicians, time and quantity taking arbitrary reduction withdrawal would be dangerous and harmful, especially hormonal drugs, there will be repeated illness, should be very careful when increasing or decreasing. Taking blood pressure, lipid-lowering or anticoagulant drugs, and prevent complications.
To diet
Although the patients with nephrotic syndrome from urinary loss of protein, high-protein diet will increase the glomerular filtration, increased proteinuria, and promote the malignant progression of kidney disease. The correct way is the quality of the total protein of the daily intake of 30-35 grams, and calculation of vegetables, fruits, rice contains protein. The high-quality protein diet rich in animal protein, essential amino acids, such as lean beef, pork, lamb and fresh fish.
To prevent deterioration
The data indicate that primary glomerular nephropathy and respiratory infections and allergies, it is necessary to actively combat these factors, as early investigation, examinations of urine, and strive to the early detection of the presence of nephropathy.As part of the acute nephritis can be transformed into a chronic nephritis, acute nephritis should be attached great importance to conduct a thorough treatment, and strictly follow the doctor's advice. Should actively seek medical treatment for a diagnosed chronic glomerulonephritis, efficient and kidneys, handling, and regular follow-up changes in renal function to prevent chronic kidney disease to chronic renal insufficiency into.
Sunday, April 8, 2012
IgA nephritis should be treated?
IgA nephritis should be treated?
The traditional method of treatment of IgA there is no satisfactory treatment options. Of the disease associated with renal insufficiency adrenal corticosteroids with or without immunosuppressants results are not consistent. Recent data suggest that the proteinuria of more than 1g / d, and subjected to every other day medication adrenal cortex hormone beneficial to the improvement of proteinuria. IgA deposition of minimal change nephropathy may alleviate proteinuria. Used in combination with cyclophosphamide, dipyridamole and warfarin to reduce proteinuria and glomerular filtration rate; combined use of cyclosporin A may also reduce proteinuria, and then also reduced creatinine clearance. Efficacy of phenytoin, anti-platelet drugs, the anthocyanin acid disodium diphenyl Sealand due to such drugs is uncertain. Notwithstanding the reports of urokinase may have a role to protect the glomerular filtration rate, but far from conclusive.Recurrent tonsillitis, tonsillectomy may be useful; antibiotics to prevent and treat infections that may be helpful to some acute nephritic syndrome and acute renal failure for the performers. A small series of observations found that the use of fish oil preparations reducing the role of proteinuria and increased glomerular filtration rate.Severe IgA nephropathy (glomerular filtration rate monthly decline 2 ~ 4ml/min) the use of large doses of immune globulin intravenous infusion period, to stop the glomerular filtration rate, improvement of hematuria and proteinuria, but after stopping often relapse.Cases of hypertension and severe proteinuria, glomerular filtration rate of converting enzyme inhibitors may slow down the rate of descent and reduce proteinuria and severe IgA nephropathy, converting enzyme inhibitors are the preferred antihypertensive drugs.Conversion of normal blood pressure, whether effective inhibitors is unclear.
End-stage IgA nephropathy in a kidney transplant, the transplanted kidney happen soon mesangial IgA deposition; subclinical IgA nephropathy if the donor kidney for renal mesangial IgA deposits after implantation of non-IgA nephropathy uremia often rapidly disappearing. Renal transplantation with recurrence does not necessarily progressive renal failure in IgA nephropathy, however Shi after renal transplantation immunosuppressive therapy including cyclosporine A also did not prevent its development. Cadaveric renal transplantation, 1 year and 3-year graft survival up to 87% and 77%, however, individual IgA antibody IgA anti-HLA antigens of renal transplant recipients, 2-year graft survival of up to 100%. reason to believe that these antibodies against HLA antigens played a useful role in increasing graft survival.
Purpura nephritis of Chinese medicine
Allergic purpura nephritis according to clinical manifestations, the purpuric
stage with medicine "spotted" the "spot", associated with kidney damage, and
Traditional Chinese Medicine "Blood" and "edema". The formation of this disease
more than Qiyin weakness, you can not beat evil, resulting in six evils evil
disturbance network, blood sub-volt heat, the spillover skin see purpura, within
infiltration kidney see blood in the urine than
TCM Differential Treatment on the treatment of this disease the main performance of the heat syndrome, advised using the method of detoxification, cooling hemostasis.Performance deficiency, qi and blood, spleen Ning heart, nourish liver and kidney, France. Based on the cause and pathogenesis of this disease, focusing on Qufeng method and the method of blood circulation use of drugs such as search and expel pathogenic wind, black snake, earthworm, white silkworm, the can Qufeng evil, anti-allergy . Blood circulation drugs such as Salvia, Chuanxiong, leeches, etc., can change the blood hypercoagulable state, improve microcirculation, regulate immune function, alleviate immune injury. Blood circulation drugs can also play a role similar to western medicine anticoagulants and compared to the more secure and reliable, no side effects.Several of proprietary Chinese medicine treatment of allergic purpura nephritis as follows: (for reference only, the best medication under the guidance of experts)
Of proprietary Chinese medicine treatment of allergic purpura nephritis:
1, Huang Wan Xijiaodihuang: clearing and detoxifying, cooling blood hemostatic efficacy.For the early stage of the disease is excessive heat to force the blood. Aged 3 to 6 per serving, 1/2 pills, 6 to 9 years per 1 pill, 9 to 12-year-old 1 to 2 pills per serving, served on the 2nd.
Lotus leaf pill: Qingreliangxue stasis hemostatic effect. For the disease early hematuria obvious. 3 to 6 years old per serving, 1/3 pills, aged 6 to 9 1/2 pill per serving, 9 to 12 years of age per serving 2/3 pill, day 2 to 3 times.
3, 100 Po Dan: blood circulation, meridians bleeding effect. For this disease hematuria clearly the blood stasis, meridian Jian astringent. Per serving, 3 to 6-year-old O, 1g, each serving 6 to 9-year-old 0,2 g, 0,3 g, per serving of 12-year-old, 4 hours for 1.
4 Dabuyin pill; the effectiveness of the training of the Qingyuan, nourishing yin. For this disease is a wang. 3 to 6 years old per serving, 1/3 pills, aged 6-9 years per serving, 1/2 pill, 9 to 12 years old each take 1 pill for 3 times.
5, Jishengshenqiwan pill: Warming yang, the effectiveness of the gas lines of the water.For this disease is a kidney decline, to be filled with the cloud overcast. Aged 3 to 6 per serving, 2g, 6 to 9-year-old per serving, 4g, 9 to 12-year-old 6g, each serving 2 to 3 times.
Proprietary Chinese medicines more convenient, but the treatment there are significant limitations. Chinese and Western medicine to their talents, complementary short, Western medicine can play a symptomatic effect of Chinese medicine and micro-penetration therapy of Chinese medicine to cure the root of the same time greatly reduce the side effects of steroids, and thus improve the efficacy, shorten treatment time. Micro therapy for the penetration of traditional Chinese medicine with conventional Western treatment at the same time, the selection of traditional Chinese medicine promoting blood circulation through the network, blood stasis and disinfection, cooling blood detoxification, breeze heat detoxification method of dialectical therapy, achieving a multiplier effect.
Recurring allergic purpura nephritis can aggravate kidney damage, kidney damage is the process of renal fibrosis, allergic purpura nephritis, renal failure or in patients with uremia, renal already appeared in a lot of fibrosis. Micro-based medicine contains an active substance can induce muscle fibroblast apoptosis, to prevent the synthesis of difficult to degrade collagen. Its mechanism of action: TCM active substances in the human body and myofibroblasts molecules closely integrated (combined) molecules bond, fusion, degradation of myofibroblasts, prompting muscle fibroblast cell lysis, broken. Muscle after the cracker broken into fibroblasts by macrophage phagocytosis or pieces removed from the body, which is reached renal fibrosis in the clearance of immune complexes. Muscle fibroblasts were swallowed or discharged, damaged kidney tissue in the role of micro-Chinese medicine slowly to restore kidney function in order to achieve the fundamental purpose of the treatment of renal failure or uremia.
Henoch-Schonlein purpura nephritis, purpura nephritis, renal failure, or purpura nephritis, uremia, whether one should be early treatment and timely treatment. Ill keep in mind must be in a specialized hospital treatment or drug treatment under the guidance of experts.
TCM Differential Treatment on the treatment of this disease the main performance of the heat syndrome, advised using the method of detoxification, cooling hemostasis.Performance deficiency, qi and blood, spleen Ning heart, nourish liver and kidney, France. Based on the cause and pathogenesis of this disease, focusing on Qufeng method and the method of blood circulation use of drugs such as search and expel pathogenic wind, black snake, earthworm, white silkworm, the can Qufeng evil, anti-allergy . Blood circulation drugs such as Salvia, Chuanxiong, leeches, etc., can change the blood hypercoagulable state, improve microcirculation, regulate immune function, alleviate immune injury. Blood circulation drugs can also play a role similar to western medicine anticoagulants and compared to the more secure and reliable, no side effects.Several of proprietary Chinese medicine treatment of allergic purpura nephritis as follows: (for reference only, the best medication under the guidance of experts)
Of proprietary Chinese medicine treatment of allergic purpura nephritis:
1, Huang Wan Xijiaodihuang: clearing and detoxifying, cooling blood hemostatic efficacy.For the early stage of the disease is excessive heat to force the blood. Aged 3 to 6 per serving, 1/2 pills, 6 to 9 years per 1 pill, 9 to 12-year-old 1 to 2 pills per serving, served on the 2nd.
Lotus leaf pill: Qingreliangxue stasis hemostatic effect. For the disease early hematuria obvious. 3 to 6 years old per serving, 1/3 pills, aged 6 to 9 1/2 pill per serving, 9 to 12 years of age per serving 2/3 pill, day 2 to 3 times.
3, 100 Po Dan: blood circulation, meridians bleeding effect. For this disease hematuria clearly the blood stasis, meridian Jian astringent. Per serving, 3 to 6-year-old O, 1g, each serving 6 to 9-year-old 0,2 g, 0,3 g, per serving of 12-year-old, 4 hours for 1.
4 Dabuyin pill; the effectiveness of the training of the Qingyuan, nourishing yin. For this disease is a wang. 3 to 6 years old per serving, 1/3 pills, aged 6-9 years per serving, 1/2 pill, 9 to 12 years old each take 1 pill for 3 times.
5, Jishengshenqiwan pill: Warming yang, the effectiveness of the gas lines of the water.For this disease is a kidney decline, to be filled with the cloud overcast. Aged 3 to 6 per serving, 2g, 6 to 9-year-old per serving, 4g, 9 to 12-year-old 6g, each serving 2 to 3 times.
Proprietary Chinese medicines more convenient, but the treatment there are significant limitations. Chinese and Western medicine to their talents, complementary short, Western medicine can play a symptomatic effect of Chinese medicine and micro-penetration therapy of Chinese medicine to cure the root of the same time greatly reduce the side effects of steroids, and thus improve the efficacy, shorten treatment time. Micro therapy for the penetration of traditional Chinese medicine with conventional Western treatment at the same time, the selection of traditional Chinese medicine promoting blood circulation through the network, blood stasis and disinfection, cooling blood detoxification, breeze heat detoxification method of dialectical therapy, achieving a multiplier effect.
Recurring allergic purpura nephritis can aggravate kidney damage, kidney damage is the process of renal fibrosis, allergic purpura nephritis, renal failure or in patients with uremia, renal already appeared in a lot of fibrosis. Micro-based medicine contains an active substance can induce muscle fibroblast apoptosis, to prevent the synthesis of difficult to degrade collagen. Its mechanism of action: TCM active substances in the human body and myofibroblasts molecules closely integrated (combined) molecules bond, fusion, degradation of myofibroblasts, prompting muscle fibroblast cell lysis, broken. Muscle after the cracker broken into fibroblasts by macrophage phagocytosis or pieces removed from the body, which is reached renal fibrosis in the clearance of immune complexes. Muscle fibroblasts were swallowed or discharged, damaged kidney tissue in the role of micro-Chinese medicine slowly to restore kidney function in order to achieve the fundamental purpose of the treatment of renal failure or uremia.
Henoch-Schonlein purpura nephritis, purpura nephritis, renal failure, or purpura nephritis, uremia, whether one should be early treatment and timely treatment. Ill keep in mind must be in a specialized hospital treatment or drug treatment under the guidance of experts.
Children's HSPN
With the change in recent years, pediatric spectrum of disease, kidney
disease was arelative increase in trend. Nephritis, is quietly attacks on
children.
Child disease is allergic to certain factors, causing systemic vascular inflammatorylesions, skin manifestations point as a red rash, which is called purpura, kidney damage to the called purpura nephritis. Purpura nephritis may be associated with infection andallergy. In some cases before the onset of infection, the most common upper respiratory tract infection (non-specific or streptococcal infection), such as chlamydia, chicken poxand parasites, and so on. Many cases of disease, drugs (antibiotics, iodine and amines, salicylates, barbiturates, and iodide) or food (dairy, fish, shrimp, crabs and clams, etc.)allergies.
Purpura nephritis, purpura and rash, a part of the main leg front, knee, near the ankle andhip, and of varying sizes, different shapes, often symmetry. Purpura slightly higher than the leather, the pressure does not fade, with a slight itching. Began to bright red, laterbecome dark red, brown. The small number of patients also can be expressed asurticaria, angioedema, erythema multiforme, and even ulcers, necrosis. Purpura can also be integrated into the film, often in batches repeatedly, and some may be associated with localized or diffuse edema of the head, face, eyelids.
Children suffering from purpura nephritis and extrarenal symptoms include skin purpura, abdominal pain, blood in the stool. Some sick child very severe pain, severeintussusception, intestinal perforation, intestinal bleeding. General there are knee, ankle, wrist or elbow pain. Renal symptoms of view, generally two weeks to two months after theskin purpura, there will be hematuria, oliguria, edema, high blood pressure.
To remind parents that this happens, do not blindly give a child medication according todoctor's diagnosis and the child's symptomatic treatment.
Child disease is allergic to certain factors, causing systemic vascular inflammatorylesions, skin manifestations point as a red rash, which is called purpura, kidney damage to the called purpura nephritis. Purpura nephritis may be associated with infection andallergy. In some cases before the onset of infection, the most common upper respiratory tract infection (non-specific or streptococcal infection), such as chlamydia, chicken poxand parasites, and so on. Many cases of disease, drugs (antibiotics, iodine and amines, salicylates, barbiturates, and iodide) or food (dairy, fish, shrimp, crabs and clams, etc.)allergies.
Purpura nephritis, purpura and rash, a part of the main leg front, knee, near the ankle andhip, and of varying sizes, different shapes, often symmetry. Purpura slightly higher than the leather, the pressure does not fade, with a slight itching. Began to bright red, laterbecome dark red, brown. The small number of patients also can be expressed asurticaria, angioedema, erythema multiforme, and even ulcers, necrosis. Purpura can also be integrated into the film, often in batches repeatedly, and some may be associated with localized or diffuse edema of the head, face, eyelids.
Children suffering from purpura nephritis and extrarenal symptoms include skin purpura, abdominal pain, blood in the stool. Some sick child very severe pain, severeintussusception, intestinal perforation, intestinal bleeding. General there are knee, ankle, wrist or elbow pain. Renal symptoms of view, generally two weeks to two months after theskin purpura, there will be hematuria, oliguria, edema, high blood pressure.
To remind parents that this happens, do not blindly give a child medication according todoctor's diagnosis and the child's symptomatic treatment.
Saturday, April 7, 2012
The performance of lupus nephritis
1, systemic manifestations
Systemic manifestations of lupus nephritis with fever, arthritis and skin and mucous membrane damage is the most common. The system is accompanied by involvement of the liver, heart, central nervous system and blood-forming organs, more than 1/3 of patients with polyserositis (pleural and pericardial). Pulmonary hemorrhage may also be the main one of the manifestations of the disease, with Goodpasture's disease and small vessel vasculitis differentiated, Renault sign found in 40% of patients.
2, the renal manifestations
The ① subclinical or "silent" type: kidney involvement, performance, urine negative, but the pathology is often varying degrees of disease.
② Light: 30% to 50% without clinical symptoms, the only light to moderate proteinuria (
③ nephrotic syndrome: about 40% to 60%, showed massive proteinuria, hypoalbuminemia and edema, occasional elevated blood cholesterol, diseases, late hypertension, renal dysfunction, the majority of patients to renal failure.
④ chronic nephritis: about 35% to 50%, hypertension and varying degrees of proteinuria, urinary sediment, a large number of red blood cells and casts, and more with impaired renal function.
The ⑤ acute nephritis: the performance of the clinical manifestations of acute nephritis.
⑥ rapidly progressive nephritis oliguric acute renal failure, or light or by the nephrotic syndrome; in a short period of time
Transformed from Pathology showed crescentic glomerulonephritis
⑦ tubule interstitial damage; clinical manifestations of renal tubular acidosis, nocturia, increased blood pressure, increased urine β2-microglobulin, half of the patients with renal dysfunction.
⑧ of antiphospholipid antibodies: antiphospholipid antibody positive, major clinical manifestations of large and small arterial and venous thrombosis and embolism, platelet reduction and tendency to abortion.
To ⑨ acute renal failure type; oliguric acute renal failure and pathologic findings for acute tubular necrosis in a short period of time
⑩ chronic renal failure, type: varying degrees of proteinuria, hematuria, and edema, impaired renal function.
In summary, the above is about the performance of lupus nephritis? Allows people to timely diagnosis of lupus nephritis, lupus nephritis patients but also timely symptomatic treatment, eat more fruits and vegetables.
Systemic manifestations of lupus nephritis with fever, arthritis and skin and mucous membrane damage is the most common. The system is accompanied by involvement of the liver, heart, central nervous system and blood-forming organs, more than 1/3 of patients with polyserositis (pleural and pericardial). Pulmonary hemorrhage may also be the main one of the manifestations of the disease, with Goodpasture's disease and small vessel vasculitis differentiated, Renault sign found in 40% of patients.
2, the renal manifestations
The ① subclinical or "silent" type: kidney involvement, performance, urine negative, but the pathology is often varying degrees of disease.
② Light: 30% to 50% without clinical symptoms, the only light to moderate proteinuria (
③ nephrotic syndrome: about 40% to 60%, showed massive proteinuria, hypoalbuminemia and edema, occasional elevated blood cholesterol, diseases, late hypertension, renal dysfunction, the majority of patients to renal failure.
④ chronic nephritis: about 35% to 50%, hypertension and varying degrees of proteinuria, urinary sediment, a large number of red blood cells and casts, and more with impaired renal function.
The ⑤ acute nephritis: the performance of the clinical manifestations of acute nephritis.
⑥ rapidly progressive nephritis oliguric acute renal failure, or light or by the nephrotic syndrome; in a short period of time
Transformed from Pathology showed crescentic glomerulonephritis
⑦ tubule interstitial damage; clinical manifestations of renal tubular acidosis, nocturia, increased blood pressure, increased urine β2-microglobulin, half of the patients with renal dysfunction.
⑧ of antiphospholipid antibodies: antiphospholipid antibody positive, major clinical manifestations of large and small arterial and venous thrombosis and embolism, platelet reduction and tendency to abortion.
To ⑨ acute renal failure type; oliguric acute renal failure and pathologic findings for acute tubular necrosis in a short period of time
⑩ chronic renal failure, type: varying degrees of proteinuria, hematuria, and edema, impaired renal function.
In summary, the above is about the performance of lupus nephritis? Allows people to timely diagnosis of lupus nephritis, lupus nephritis patients but also timely symptomatic treatment, eat more fruits and vegetables.
Immunology of the lupus nephritis nine check
1, the general inspection: the majority of patients (80%) moderate anemia (positive cells are hypochromic anemia), even showed hemolytic anemia, thrombocytopenia, 1/4 patients with pancytopenia 90% ESR. Patients globulin significantly increased.
2, the immunological tests
(1) antinuclear antibodies: anti-nuclear antibody test sensitivity of 90% or more, but the specificity is lower in mixed connective tissue disease, rheumatoid arthritis, Sjogren's syndrome, etc. can be positive results. Therefore this experiment can not be used as a diagnosis only indicator may be used as the reference indicator of disease activity, but its titer and kidney involvement or not, and severity.
(2) anti-double stranded DNA antibodies: one of the marker antibodies for diagnosis of SLE, sensitivity 72%, its titer is closely related to lupus activity. Only, even in Sjogren's syndrome, rheumatoid arthritis and activity of hepatitis was positive.
(3) anti-Sm antibodies and anti-RNP antibodies: anti-Sm antibodies found in 25% -40% of patients with this disease, anti-RNP antibodies found in the 26% -45% of the patients.Anti-Sm antibodies in the diagnosis of systemic lupus erythematosus-specific high.
(4) anti-histone antibodies: found in 25% -60% of patients. Specificity is also good, even seen in rheumatoid arthritis and Sjogren's syndrome.
(5) anti-SSA and anti-SSB antibodies: the former is seen in 30% -40%
Patients, only 0-15% of the latter. Both antibodies were mainly seen in Sjogren's syndrome.
(6) other antibodies: SLE, there are a variety of other autoantibodies such as anti-erythrocyte antibodies in hemolytic anemia, and necrotizing vasculitis neutrophil cytoplasmic antibody (ANCA). In recent years, especially great importance of antiphospholipid antibodies, seen in 34% of the patients.
⑺ complement: the C3, C4, and of CH50 can be reduced, especially C3 decline in the judgment of lupus activity, a sensitive and reliable indicators.
(8) skin lupus band: the epidermis and dermis link at the non-lesional skin by direct immunofluorescence can check an IgG and (or) C3 were granular calm yellow-green fluorescence band. Found in more than 70% of patients with this disease.
(9): rheumatoid factor (RF), cryoglobulin test in disease activity were positive.
In summary, the above described method of examination of lupus nephritis allows people to better diagnosis of lupus nephritis, lupus nephritis patients but also to eat more fruits and vegetables, do not eat spicy spicy food appropriate exercise and strengthen its own resistance.
2, the immunological tests
(1) antinuclear antibodies: anti-nuclear antibody test sensitivity of 90% or more, but the specificity is lower in mixed connective tissue disease, rheumatoid arthritis, Sjogren's syndrome, etc. can be positive results. Therefore this experiment can not be used as a diagnosis only indicator may be used as the reference indicator of disease activity, but its titer and kidney involvement or not, and severity.
(2) anti-double stranded DNA antibodies: one of the marker antibodies for diagnosis of SLE, sensitivity 72%, its titer is closely related to lupus activity. Only, even in Sjogren's syndrome, rheumatoid arthritis and activity of hepatitis was positive.
(3) anti-Sm antibodies and anti-RNP antibodies: anti-Sm antibodies found in 25% -40% of patients with this disease, anti-RNP antibodies found in the 26% -45% of the patients.Anti-Sm antibodies in the diagnosis of systemic lupus erythematosus-specific high.
(4) anti-histone antibodies: found in 25% -60% of patients. Specificity is also good, even seen in rheumatoid arthritis and Sjogren's syndrome.
(5) anti-SSA and anti-SSB antibodies: the former is seen in 30% -40%
Patients, only 0-15% of the latter. Both antibodies were mainly seen in Sjogren's syndrome.
(6) other antibodies: SLE, there are a variety of other autoantibodies such as anti-erythrocyte antibodies in hemolytic anemia, and necrotizing vasculitis neutrophil cytoplasmic antibody (ANCA). In recent years, especially great importance of antiphospholipid antibodies, seen in 34% of the patients.
⑺ complement: the C3, C4, and of CH50 can be reduced, especially C3 decline in the judgment of lupus activity, a sensitive and reliable indicators.
(8) skin lupus band: the epidermis and dermis link at the non-lesional skin by direct immunofluorescence can check an IgG and (or) C3 were granular calm yellow-green fluorescence band. Found in more than 70% of patients with this disease.
(9): rheumatoid factor (RF), cryoglobulin test in disease activity were positive.
In summary, the above described method of examination of lupus nephritis allows people to better diagnosis of lupus nephritis, lupus nephritis patients but also to eat more fruits and vegetables, do not eat spicy spicy food appropriate exercise and strengthen its own resistance.
Mesangialproliferative glomerulonephritis treatment
The disease caused by nephrotic syndrome is often more difficult. Small doses the next day prednisone therapy may help to improve renal function. West et al use the next day oral steroids long-term treatment, biopsy before and after treatment, the results prove this method is conducive to the survival of the kidney. At present, most nephrologists only symptomatic treatment.
Treatment of type Ⅰ, in addition to glucocorticoids, but also with other drugs such as immune suppression drugs and anticoagulants.
MPGN patients of all ages, with normal renal function showed only mild asymptomatic proteinuria without receiving steroids, immunosuppressive drug therapy. Only every 3 to 4 months follow-up, close observation of renal function, proteinuria and blood pressure control. Adults and children with primary MPGN patients, urinary protein> 3g / d, renal damage and biopsy of renal interstitial disease may be given hormones, immunosuppressive drug therapy.
May be effective in the treatment of 6 to 12 months for proteinuria (> 3g / d) or impaired renal function in children with primary MPGN patients, large doses of glucocorticoids next day 40mg/m2. If that does not stop taking glucocorticoids, we recommend close follow-up, focusing on conservative treatment (ie, control of blood pressure, applied to reduce urinary protein drugs and correction of metabolic disorders).
Proteinuria (> 3g / d) or adults with impaired renal function in patients with primary MPGN, should be given aspirin (325mg / d), dipyridamole (dipyridamole) treatment (75 to 100mg, 2 times / d), or both combined 12 months if the treatment plan is invalid is disabled. Great importance to be able to slow the decline in kidney function factors and close follow-up should be part of the treatment plan.
Several treatment studies have reported the next day, or daily oral corticosteroids, intravenous high-dose glucocorticoids, and the combined application of the results: a more rigorous research confirmed: children MPGN, hormone therapy in slowing renal ball filtration rate (GFR) decline in the effective and stable renal function. Most of the 80 cases were type Ⅰ MPGN, prednisone (prednisone) 40mg/m2 every other day oral average treatment time of 13 months, 61% of treatment group children at the research stage renal stable, while The placebo group only 12%. Proved children MPGN patients with glucocorticoid is effective. Studies have shown that children's of MPGN early application of high-dose prednisone (prednisone) can effectively shorten the course of the disease. But remains controversial, still with a rigorous randomized controlled trials to verify.
Danadio and other study dipyridamole (dipyridamole), aspirin and warfarin in MPGN treatment on renal outcome (including the impact of urinary protein excretion rate) and platelet half-life (bleeding tendency). Lower urinary protein excretion rate, but no significant changes in GFR. Cattran and other 59 cases of MPGN patients taking cyclophosphamide, warfarin and dipyridamole (dipyridamole) the efficacy of the treatment time of 18 months. The detailed description of how the research only I MPGN patients will have a clearer treatment of type Ⅱ disease is not strong enough evidence to conclude.
Type Ⅱ there is no effective treatment. Reasonable solution to the treatment of this disease is still controversial, treatment options should carefully weigh the efficacy of the treatment of adverse reactions. Leaves any higher recommended using the following program: dipyridamole (dipyridamole) 50 ~ 300mg / d, divided into three doses. If nephrotic syndrome, the available symptomatic of the way and try the standard regimen of hormones, to be tapered to maintenance dose (the next day morning serving Dayton prednisone 0.4mg/kg), and then to maintain the application a longer period, such ashave high blood pressure, it is recommended to use the new staircase method antihypertensive therapy. In the implementation of treatment programs should be closely observed side effects, to exceed and achieve therapeutic effect.
Other treatment, including lipid-lowering, ACE inhibitors, the ARB, low molecular weight heparin, in recent years, scholars have reported that mycophenolate mofetil (MMF) treatment of the disease, showing initial results, but the number of cases was small, and the lack of control and long-term observational study.
In addition, the application of cytotoxic drugs, plasmapheresis methods, traditional Chinese medicine treatment in some studies the treatment of some efficacy.
In deciding what type of patients when the treatment, the clinician must consider the pros and cons of the expected course and outcome of the disease, and treatment, renal insufficiency development and drug treatment due to poor compliance.
The Membranoproliferative glomerulonephritis pathogenesis
MPGN pathogenesis is not clear that related to the immunological mechanisms.
50% to 60% of MPGN serum complement C3, C1q and C4 lower, suggesting that the
alternative pathway and classical pathway are activated and lead to complement
lower blood.Accompanied by a mild increase in immune complexes and
cryoglobulinemia, and immunoglobulin and complement deposition in glomeruli.
However, the relationship between complement abnormalities and disease, the role
of immune complexes remains to be further explored.
According to the extent of a variety of immune complex deposition in the form of glomerular basement membrane and mesangial area and deposition of different MPGN divided into three types.
Main complex deposition within the subcutaneous type Ⅰ mesangial area. Type Ⅰ and viral, bacterial and parasitic infections and some immune complex diseases (such as the lack of genetic complement, SLE, mixed cryoglobulinemia, SBE in shunt nephritis, lymphoma, schistosomiasis), but often as idiopathic. Hypocomplementemia I MPGN patients, 33 percent to 50 percent, 25 percent to 30 percent in patients with Clq, C4 and C5 lower, 15% to 20% of patients with B-factor decreased.
Type II is known as autoimmune diseases, can be observed in the electron microscope was uniform ribbon deposition along the basement membrane laminin layer, this type is also known as dense deposit disease (DDD), also often accompanied by subepithelial hump-like sediment deposition. PAS staining is sometimes visible banded deep dye on the capillary loop. Type Ⅱ with streptococcal infection, Streptococcus kidney antigen cross-reactive antibody-mediated can cause kidney damage. Type Ⅱ often complicated by low plasma C3 level, as part of the blood in patients with complement activator, an autoantibody, also known as induced nephritis factor C3 nephritis factor, the direct anti-C3bBb, change the C3 bypass conversion by converting enzyme combination to prevent some of the normal inhibitory factor, such as the role of factor H, an increase of complement activation and consumption. C3 nephritis factor is more common in type I and type II MPGN, especially in the more common type Ⅱ. Part Lipodystrophy. MPGN II-type basement membrane damage and, if the dense sediment deposition in the basement membrane, these sediments can activate complement, complement some special substances, such as ribozyme activation is usually activate the alternative pathway, so that C3 nephritis factor secondary continues to increase, which led to the decline of the blood complement C3. Type Ⅱ MPGN in. 70% of patients C3 and factor B reduced.
III-type endothelial, mesangial and subepithelial have sediment deposition. Type III and type Ⅰ difference is that the subepithelial deposition.
Accompanied by the migration of time, the MPGN The pathological changes of more than from hyperplasia to a significant hardening. Subtypes, the focal type MPGN lesions may shift behavior filled with classic MPGN. Some children or young people, began to diffuse MPGN subtype of multi-leaf type, shift behavior focally or complete remission.
According to the extent of a variety of immune complex deposition in the form of glomerular basement membrane and mesangial area and deposition of different MPGN divided into three types.
Main complex deposition within the subcutaneous type Ⅰ mesangial area. Type Ⅰ and viral, bacterial and parasitic infections and some immune complex diseases (such as the lack of genetic complement, SLE, mixed cryoglobulinemia, SBE in shunt nephritis, lymphoma, schistosomiasis), but often as idiopathic. Hypocomplementemia I MPGN patients, 33 percent to 50 percent, 25 percent to 30 percent in patients with Clq, C4 and C5 lower, 15% to 20% of patients with B-factor decreased.
Type II is known as autoimmune diseases, can be observed in the electron microscope was uniform ribbon deposition along the basement membrane laminin layer, this type is also known as dense deposit disease (DDD), also often accompanied by subepithelial hump-like sediment deposition. PAS staining is sometimes visible banded deep dye on the capillary loop. Type Ⅱ with streptococcal infection, Streptococcus kidney antigen cross-reactive antibody-mediated can cause kidney damage. Type Ⅱ often complicated by low plasma C3 level, as part of the blood in patients with complement activator, an autoantibody, also known as induced nephritis factor C3 nephritis factor, the direct anti-C3bBb, change the C3 bypass conversion by converting enzyme combination to prevent some of the normal inhibitory factor, such as the role of factor H, an increase of complement activation and consumption. C3 nephritis factor is more common in type I and type II MPGN, especially in the more common type Ⅱ. Part Lipodystrophy. MPGN II-type basement membrane damage and, if the dense sediment deposition in the basement membrane, these sediments can activate complement, complement some special substances, such as ribozyme activation is usually activate the alternative pathway, so that C3 nephritis factor secondary continues to increase, which led to the decline of the blood complement C3. Type Ⅱ MPGN in. 70% of patients C3 and factor B reduced.
III-type endothelial, mesangial and subepithelial have sediment deposition. Type III and type Ⅰ difference is that the subepithelial deposition.
Accompanied by the migration of time, the MPGN The pathological changes of more than from hyperplasia to a significant hardening. Subtypes, the focal type MPGN lesions may shift behavior filled with classic MPGN. Some children or young people, began to diffuse MPGN subtype of multi-leaf type, shift behavior focally or complete remission.
Mesangial proliferative glomerulonephritis is caused by what
(A) causes
Membranoproliferative glomerulonephritis according to their clinical and laboratorycharacteristics are divided into primary and secondary glomerular disease.
Primary membranoproliferative glomerulonephritis of unknown etiology, is generally believed that type Ⅰ immune complex disease; type II immune complexes andautoantibodies in disease, may be related to heredity.
Secondary mixed cryoglobulinemia, membranoproliferative glomerulonephritis, there arethree kinds of subtypes. Type Ⅰ cryoglobulinemia monoclonal peaks globulin, usually amyeloma protein. Type Ⅱ usually a combination of IgG monoclonal peak of IgM globulin, also known as anti-IgG rheumatoid factor, and type Ⅲ is a multi-strain peakimmunoglobulin. Type Ⅱ and Ⅲ cryoglobulinemia prone to kidney damage. Itspathological features proliferated mesangial cells, white blood cells especiallymononuclear cell infiltration, glomerular basement membrane thickening of the double-track phenomenon. About 1/3 cases of small and medium-sized arteritis, capillarymicrothrombosis. The etiology and pathogenesis of MPGN is not very clear. Type ⅠMPGN immune complex disease, repeatedly sustained by the relatively large insolubleimmune complex deposition. Patients with type II MPGN serum immune complexes,cryoglobulin, complement abnormalities, sustained reductions in serum C3. Promptimmune complexes in the type of MPGN II. Can be detected in patients with type II MPGNserum C3 nephritis factor (C3NeF), C3NeF, C3bBb converting enzyme autoantibodies,C3bBb role to strengthen, leading to sustained activation of the complement bypass, resulting in the degeneration of sustained hypocomplementemia and basement membrane. Complement metabolic disorder as the central link.
In addition, the type II MPGN kidney transplantation often relapse may be due to materialdeposition can cause abnormal glycoproteins in the basement membrane nephritis inserum.
The disease may be related to inheritance, type II MPGN often in patients with HLA-B7.Most of type Ⅰ MPGN patients with a special B-cell alloantigen.
Membranoproliferative glomerulonephritis according to their clinical and laboratorycharacteristics are divided into primary and secondary glomerular disease.
Primary membranoproliferative glomerulonephritis of unknown etiology, is generally believed that type Ⅰ immune complex disease; type II immune complexes andautoantibodies in disease, may be related to heredity.
Secondary mixed cryoglobulinemia, membranoproliferative glomerulonephritis, there arethree kinds of subtypes. Type Ⅰ cryoglobulinemia monoclonal peaks globulin, usually amyeloma protein. Type Ⅱ usually a combination of IgG monoclonal peak of IgM globulin, also known as anti-IgG rheumatoid factor, and type Ⅲ is a multi-strain peakimmunoglobulin. Type Ⅱ and Ⅲ cryoglobulinemia prone to kidney damage. Itspathological features proliferated mesangial cells, white blood cells especiallymononuclear cell infiltration, glomerular basement membrane thickening of the double-track phenomenon. About 1/3 cases of small and medium-sized arteritis, capillarymicrothrombosis. The etiology and pathogenesis of MPGN is not very clear. Type ⅠMPGN immune complex disease, repeatedly sustained by the relatively large insolubleimmune complex deposition. Patients with type II MPGN serum immune complexes,cryoglobulin, complement abnormalities, sustained reductions in serum C3. Promptimmune complexes in the type of MPGN II. Can be detected in patients with type II MPGNserum C3 nephritis factor (C3NeF), C3NeF, C3bBb converting enzyme autoantibodies,C3bBb role to strengthen, leading to sustained activation of the complement bypass, resulting in the degeneration of sustained hypocomplementemia and basement membrane. Complement metabolic disorder as the central link.
In addition, the type II MPGN kidney transplantation often relapse may be due to materialdeposition can cause abnormal glycoproteins in the basement membrane nephritis inserum.
The disease may be related to inheritance, type II MPGN often in patients with HLA-B7.Most of type Ⅰ MPGN patients with a special B-cell alloantigen.
Friday, April 6, 2012
What is a membranous nephropathy
What is membranous nephropathy, a? Believe that a lot of friends do not quite
understand, membranous nephropathy is kidney disease a membranous nephropathy
isdivided into several phases, each phase has its own features, here we come
tounderstand.
What is membranous nephropathy, a? Believe that a lot of friends do not quite understand, membranous nephropathy is kidney disease a membranous nephropathy isdivided into several phases, each phase has its own features, here we come tounderstand. In the understanding of the what is a membranous nephropathy,membranous nephropathy, membranous nephropathy, we briefly introduced the generalwas nephrotic syndrome (proteinuria, hypoalbuminemia, hyperlipidemia, high degree ofedema) or asymptomatic proteinuria. Membranous nephropathy, pathological changesare generally glomerular capillary loops, immune complexes in the epithelial cell calmcharacterized, followed by basement membrane thickening and deformation, the generalnon-proliferation of mesangial, endothelial or epithelial cells or cells infiltration.Immunofluorescence IgG and C3 showed diffuse and uniform granules along thebasement membrane distribution, rare IgM and IgA calm. Membranous nephropathy inseveral specific pathological changes as follows: ① accompanied by more pronouncedmesangial proliferation and mesangial matrix expansion; ② accompanied by interstitiallesions; ③ of the disease associated with glomerular progressive, segmentalhyalinization sclerosis, accompanied by interstitial fibrosis; ④ of the disease can be transformed into a crescent body nephritis type Ⅰ; ⑤ The occasional disease withmesangial IgA dominant immune pathological changes, namely, overlappingmembranous nephropathy and IgA nephropathy performance. A membranous nephropathy, membranous nephropathy, a number of pathological variant is lighter, onlymesangial proliferation, mesangial matrix increase, and the absence of interstitial,glomerular stage of hyalinization as well as the crescent, you renal biopsy puncture reportfully proved consistent with a membranous nephropathy.
What is membranous nephropathy, a? Believe that a lot of friends do not quite understand, membranous nephropathy is kidney disease a membranous nephropathy isdivided into several phases, each phase has its own features, here we come tounderstand. In the understanding of the what is a membranous nephropathy,membranous nephropathy, membranous nephropathy, we briefly introduced the generalwas nephrotic syndrome (proteinuria, hypoalbuminemia, hyperlipidemia, high degree ofedema) or asymptomatic proteinuria. Membranous nephropathy, pathological changesare generally glomerular capillary loops, immune complexes in the epithelial cell calmcharacterized, followed by basement membrane thickening and deformation, the generalnon-proliferation of mesangial, endothelial or epithelial cells or cells infiltration.Immunofluorescence IgG and C3 showed diffuse and uniform granules along thebasement membrane distribution, rare IgM and IgA calm. Membranous nephropathy inseveral specific pathological changes as follows: ① accompanied by more pronouncedmesangial proliferation and mesangial matrix expansion; ② accompanied by interstitiallesions; ③ of the disease associated with glomerular progressive, segmentalhyalinization sclerosis, accompanied by interstitial fibrosis; ④ of the disease can be transformed into a crescent body nephritis type Ⅰ; ⑤ The occasional disease withmesangial IgA dominant immune pathological changes, namely, overlappingmembranous nephropathy and IgA nephropathy performance. A membranous nephropathy, membranous nephropathy, a number of pathological variant is lighter, onlymesangial proliferation, mesangial matrix increase, and the absence of interstitial,glomerular stage of hyalinization as well as the crescent, you renal biopsy puncture reportfully proved consistent with a membranous nephropathy.
Membranous nephropathy etiology
The exact cause of this disease is not yet clear, Clinical according to their causes can be divided into primary MN and secondary MN two categories. The former is of unknown etiology, the latter because it often accompanied by autoimmune diseases such as systemic lupus erythematosus, the incidence of hepatitis B and C, is now generally believed that the disease exist autoimmune abnormalities. Secondary causes of membranous nephropathy caused by:
An autoimmune disease systemic lupus erythematosus, rheumatoid arthritis, diabetes, Hashimoto's thyroiditis, Graves disease, mixed connective tissue disease, Sjogren syndrome, primary biliary cirrhosis, ankylosing spondylitis and acute infectious polyneuritis.
(2) infected with hepatitis B, hepatitis C, syphilis, leprosy, filariasis, schistosomiasis and malaria.
Drugs and toxic organic gold, mercury, D-penicillamine, captopril and probenecid.
Tumors of lung cancer, colon cancer, breast cancer and lymphoma.
Sarcoidosis, graft recurrence of sickle cell disease and angiolymphoid hyperplasia (Kimura disease). 75% of membranous nephropathy can not find the above reasons, that is, belonging to idiopathic membranous nephropathy.
An autoimmune disease systemic lupus erythematosus, rheumatoid arthritis, diabetes, Hashimoto's thyroiditis, Graves disease, mixed connective tissue disease, Sjogren syndrome, primary biliary cirrhosis, ankylosing spondylitis and acute infectious polyneuritis.
(2) infected with hepatitis B, hepatitis C, syphilis, leprosy, filariasis, schistosomiasis and malaria.
Drugs and toxic organic gold, mercury, D-penicillamine, captopril and probenecid.
Tumors of lung cancer, colon cancer, breast cancer and lymphoma.
Sarcoidosis, graft recurrence of sickle cell disease and angiolymphoid hyperplasia (Kimura disease). 75% of membranous nephropathy can not find the above reasons, that is, belonging to idiopathic membranous nephropathy.
Asymptomatic glomerulonephritis, also known as asymptomatic hematuria or proteinuria ((and)asymptomatic hematuria and / or proteinuria), patients with no edema, hypertension and renal damage, only showed glomerular hematuriaor proteinuria (and) a group ofglomerular disease. Acute infection after glomerular nephritis, referred to as acute nephritis, is a clinical syndrome characterized by acute onset, hematuria, proteinuria, hypertension, edema, oliguria, renal damage, also known as acute nephritis syndrome.Its onset is often infection, streptococcal infection is immune complex type nephritis.
Asymptomatic glomerulonephritis also known as asymptomatic hematuria or proteinuria (and),but only a group of glomerular proteinuria and (or) hematuria of glomerular kidneydisease. The patients had no edema, hypertension, renal damage. This group of diseases caused by a variety of pathological types of primary glomerular disease, thepathological changes of more than a lighter. Hematuria performance IgA nephropathy.
Thursday, April 5, 2012
Clinical manifestations of membranous glomerulonephritis
Idiopathic membranous nephropathy can occur at any age, more common in adults, average age 35 years old, male to female ratio of about 1.5 to 2:1. Insidious onset, a small number of precursor infection after the onset. The first symptom of 15% to 20% of asymptomatic proteinuria, 80% with nephrotic syndrome, non-selective proteinuria.Microscopic hematuria in adults about 60% of children with gross hematuria, but rarely see the red tube. Early blood pressure more than normal, with about 50 percent of the progression of high blood pressure, relax and disappear with kidney disease. In the early days, the renal function is normal. 80% have varying degrees of edema, severe chest, ascites, and other body cavity effusions, the mechanism is multifactorial. There are two serious complications of idiopathic membranous nephropathy: ① high coagulation disorder and renal vein thrombosis: increased levels of blood coagulation factor due to nephrotic syndrome, enhanced platelet adhesion and cohesion, antithrombin Ⅲ Kangxian plasmin activity increased, resulting from high-blood clotting disorder.Dexamethasone can promote coagulation. This disease is about 50% of the incidence of renal vein thrombosis, no obvious symptoms, but the nephrotic syndrome increase the more common chronic form. Acute type can show the sudden appearance of low back pain, often more severe, accompanied by the kidney area, hit pain, hematuria, often gross hematuria, white blood cells in urine, a sudden increase in proteinuria, hypertension and acute renal dysfunction, bilateral renal vein thrombosis even oliguria and acute renal failure, the kidneys were increased. Chronic type of renal tubular dysfunction in performance such as: renal glucosuria, amino acids, urine, and renal tubular acidosis. In addition, it may be complicated by pulmonary embolism. Can also occur such as: brain, heart, legs, and extra-renal thrombosis. Clear diagnosis of the need for renal vein or renal artery angiography, radioactive renography and CT are also helpful in the diagnosis. ② combined anti-GBM crescentic glomerulonephritis: the basement membrane damage, membrane antigen exposure or release can lead to the formation of anti-basement membrane antibodies. May be detected in the serum anti-basement membrane antibodies, anti-neutrophil antibodies (ANCA). Therefore, if medically stable patients with rapid renal dysfunction and rapidly progressive glomerulonephritis-like performance, should be highly alert to the possibility of complications.
Symptoms of chronic glomerulonephritis
Chronic nephritis is diverse etiology, pathological and clinical manifestations similar to a group of glomerular diseases, they are common manifestations of edema, hypertensionand urinary abnormalities.
Edema: (1) in the whole course of the disease, most patients with varying degrees ofedema. Edema can be can be light weight, light in only the morning from the chronic nephritis edema found in the performance of the bed, around the eyes, facial swelling, or in the afternoon of both lower extremities ankle edema. Patients with severe, generalized edema. However, there are a very small number of patients throughout the course of the disease do not always appear edema, is often easily overlooked.
(2) high blood pressure: some patients are hypertension symptoms to hospital for treatment, doctors want them to laboratory urine, chronic nephritis caused by high blood pressure. For patients with chronic nephritis, the incidence of hypertension is one sooner or later, their blood pressure can be continuous, intermittent, and diastolic blood pressure (higher than 12.7kPa) is characterized by high blood pressure there are greatindividual differences in the degree of light only 18.7-21.3/12.7-13.3kPa, severe casescan even be more than 26.7/14.7kPa.
(3) urinary abnormalities: abnormal urine is almost a must in patients with chronic nephritis, including urine output changes and microscopic abnormalities. Edema in patients with decreased urine output, and the more severe edema, decreased urine output, the more obvious, and no edema in patients with normal urine majority. Whenpatients with kidney serious damage, urine concentration - dilution of functional disorder, but also increased nocturia and urine specific gravity decreased. The urine of patients with chronic nephritis put under the microscope, you can find almost all of the patients had proteinuria, urinary protein content ranging from (±) to (). Urine can see the levelranging from red blood cells, white blood cells, granular casts, transparent tube. Whenthe acute attack, may have significant hematuria, or even gross hematuria. In addition,patients with chronic nephritis also dizziness, insomnia, anorexia Shenpi fatigue,impatience, and varying degrees of anemia and other clinical symptoms.
Edema: (1) in the whole course of the disease, most patients with varying degrees ofedema. Edema can be can be light weight, light in only the morning from the chronic nephritis edema found in the performance of the bed, around the eyes, facial swelling, or in the afternoon of both lower extremities ankle edema. Patients with severe, generalized edema. However, there are a very small number of patients throughout the course of the disease do not always appear edema, is often easily overlooked.
(2) high blood pressure: some patients are hypertension symptoms to hospital for treatment, doctors want them to laboratory urine, chronic nephritis caused by high blood pressure. For patients with chronic nephritis, the incidence of hypertension is one sooner or later, their blood pressure can be continuous, intermittent, and diastolic blood pressure (higher than 12.7kPa) is characterized by high blood pressure there are greatindividual differences in the degree of light only 18.7-21.3/12.7-13.3kPa, severe casescan even be more than 26.7/14.7kPa.
(3) urinary abnormalities: abnormal urine is almost a must in patients with chronic nephritis, including urine output changes and microscopic abnormalities. Edema in patients with decreased urine output, and the more severe edema, decreased urine output, the more obvious, and no edema in patients with normal urine majority. Whenpatients with kidney serious damage, urine concentration - dilution of functional disorder, but also increased nocturia and urine specific gravity decreased. The urine of patients with chronic nephritis put under the microscope, you can find almost all of the patients had proteinuria, urinary protein content ranging from (±) to (). Urine can see the levelranging from red blood cells, white blood cells, granular casts, transparent tube. Whenthe acute attack, may have significant hematuria, or even gross hematuria. In addition,patients with chronic nephritis also dizziness, insomnia, anorexia Shenpi fatigue,impatience, and varying degrees of anemia and other clinical symptoms.
Sunday, April 1, 2012
Concrete manifestation of acute and chronic nephritis symptoms
Concrete manifestation of the symptoms of acute and chronic nephritis, a lot of people heard of this disease, but specific to the disease what the performance is not clear, which makes many people sick without knowing it, until the discovery condition is very serious? because they missed the best time for treatment to regret it.
Mainly acute and chronic nephritis symptoms: The disease before the onset of more than a history of scarlet fever, tonsillitis, streptococcal infection, 7 to 21 days after infection onset. Three major characteristics of the symptoms of acute and chronic nephritis
Edema: eyelid edema, a few days later the development of the lower limb and body swelling disappear after 2 to 4 weeks.
2, hematuria: the majority of the dark brown or brown. About two weeks after the disappearance of gross hematuria, microscopic examination of hematuria sustainable for several months.
Hypertension: the majority of mild to moderate blood pressure increases, the performance of headache, dizziness, vomiting, usually last for two weeks, then gradually decreased. In addition, it can also be associated with mild anemia, fatigue and low back pain. In the treatment, such as early detection, and complete bed rest, careful treatment, the prognosis is good.
Expert tips can also refer to the laboratory screening and diagnosis of acute and chronic nephritis symptoms
Urinary protein excretion daily 0.5 ~ 2g/m2; any urine protein / creatinine ratio may be <2 (normal 0.1 to 0.3). Urine contains a shaped red blood cells, white blood cells and renal tubular cells, casts, including red blood cell casts and hemoglobin tube characteristic, the more common white blood cell casts and granular casts (protein droplets).
Anti-pathogenic infectious agent antibody titers are usually 1 to 2 weeks rose. Antibody increase against streptococcal antigen products can be measured: the antistreptolysin prime-O (ASO) is upper respiratory tract infection the best instructions, and pyoderma anti-hyaluronidase and anti-DNase B. usually reduce the disease activity of C3 and C4.Return to normal complement levels in 80% of the PSGN cases 6 to 8 weeks, in fact, one case of mesangial proliferative glomerulonephritis (MPGN) is so. Cryoglobulinemia is often persist for several months, and circulating immune complexes can only be detected within a few weeks.
Tubular function is often due to changes in the disorder of interstitial inflammation, leading to decreased ability to concentrate urine and acid secretion capacity, solute exchange impairment of the renal unit. Has some intrinsic glomerular hypertrophy and the ability of tubular function defects is usually occurs before the GFR was significantly reduced. With the gradual progress of glomerular dysfunction, total filtration area was significantly reduced decline in GFR, azotemia appear. GFR can be cleared from the serum creatinine concentration or urine creatinine, estimated rate of GFR is usually returned to normal in 1 to 3 months, proteinuria may last 6 to 12 months, microscopic hematuria for several years. Short-term changes in the urinary sediment of mild upper respiratory tract infection could happen again.
Before the onset of 1 to 6 weeks of this syndrome, there is a history of streptococcal infection, sore throat, impetigo or culture confirmed and the increase can be helpful in the diagnosis of anti-streptococcal antibody titer. Red tube in any glomerulonephritis are visible, but when and clinical manifestations associated, strongly suggestive of acute nephritic syndrome. The ultrasound can help differentiate the acute disease (kidney volume is usually normal or slightly larger) and chronic diseases increased (decreased renal size).
The above symptoms on acute and chronic nephritis, specific to each person will have a gap.
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