Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-four children with steroid-responsive nephrotic syndrome relapsing within 6 months of their initial response were randomly allocated to receive two different regimens of prednisone therapy. The test regimen differed from the standard prednisone relapse regimen used by the International Study of Kidney Disease in Children in that the total dosage was about double, and the duration of daily therapy (8 weeks vs. a mean of 12 days) as well as the total duration of treatment (8 weeks vs. a mean of approximately 6 weeks) was longer. The proportion of patients relapsing during treatment was significantly smaller (8% vs. 40%) and the length of remission following treatment was significantly longer (3.27 vs. 1.48 months) in the test group. All patients in both groups relapsed by 8 months. During a period of approximately 6 months after this relapse, neither the frequency of relapses nor the mean number of days of proteinuria differed significantly. Opinions of participants in this multicenter trial varied concerning whether these statistically significant differences clinically justified exposing patients to the more intensive treatment regimen. However, all agreed that neither form of treatment was satisfactory in terms of preventing subsequent relapses.
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PMID:Nephrotic syndrome in children: a randomized trial comparing two prednisone regimens in steroid-responsive patients who relapse early. Report of the international study of kidney disease in children. 10 98

Diacetylbenzidine was used to induce a nephrotic syndrome in female rats. Enzymes involved in glycoprotein metabolism were evaluated during an early stage of induced renal disease before extensive histologic changes occurred. The results show that lysosomal acid hydrolases are not activated or released to any measurable degree during the early stages of the disease. Minimal differences in the composition of glomerular basement membrane of nephrotic rats were found despite heavy proteinuria. Glomerular specific activities of certain glycoprotein:glycosyl transferases were depressed in nephrotic animals. A new viewpoint to explain the pathology of glomerular proteinuria is presented based on the phenomenon of sublethal autolysis affecting cell surface structure and function, of which activity levels of glycoprotein:glycosyl transferases are an example. Increased activities of glycosyl transferases and Na-D ATPase were noted in the cortex from nephrotic animals. These studies involving cortex indicate that the pathologic process is not confined to the glomerulus and may contribute information concerning Na+ transport in the nephrotic rat.
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PMID:Studies of enzymes involved in glycoprotein synthesis and degradation in diacetylbenzidine nephrosis. 12 59

The pathogenesis of focal glomerular sclerosis (FGS) and its relation to proteinuria and idiopathic nephrotic syndrome are unknown. Urine protein excretion in Sprague-Dawley rats increased with age. Fifty per cent of 12-month and 90 per cent of 24-month-old animals were proteinuric (greater than 20 mg. per day). Heavily proteinuric old rats manifested biochemical changes characteristic of nephrotic syndrome without significant loss of renal function. Three-month, 6-month, and nonproteinuric 12-month-old animals had mesangial deposits of IgM in occasional lobules of some glomeruli and slight mesangial hyperplasia. Four proteinuric 12-month-old rats had diffuse 4+ deposits of IgM in the mesangium of most glomeruli, basement membrane thickening and epithelial cell foot process fusion without FGS. The mesangial IgM deposits eluted in acid buffer and did not fix complement. Six proteinuric 12-month-old rats had focal and segmental areas of glomerular sclerosis with adhesions to Bowman's capsule, foamy cells, intraluminal eosinophilic deposits and capillary wall wrinkling and collapse. These lesions were more advanced in 24-month-old animals. Nonproteinuric 24-month-old rats did not have detectable FGS. Mesangial uptake of colloidal carbon was normal in proteinuric and nonproteinuric animals without FGS. Mesangial uptake of colloidal carbon was normal in proteinuric and nonproteinuric animals without FGS and reduced in proteinuric animals with FGS. In the aging rat the development of proteinuria and mesangial IgM deposition apparently precede development of a focal sclerotic glomerular lesion with histologic and ultrastructural features similar to FGS in man. The generalized impairment of mesangial phagocytic function in proteinuric rats with FGS suggests that this lesion may result from mesangial overload and dysfunction consequent to the persistent increase in glomerular permeability and proteinuria.
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PMID:Mesangial lesions and focal glomerular sclerosis in the aging rat. 12 75

A variety of renal structural and functional abnormalities have been associated with sickle cell disease. To define the relationship between the hemoglobinopathy and glomerular disease, clinicopathologic correlations, renal morphologic, ultrastructural immunohistologic and functional studies were performed on seven patients with clinical and laboratory evidence of glomerular disease. In addition, immunologic studies including isolation and characterization of cryoprecipitable immune complexes, and determination of immunoglobulin, total complement and complement component levels, and antibody titers to several antigens were performed in an attempt to define the etiologic and pathogenic mechanisms of the renal disease and its relationship to sickle cell anemia. Proteinuria was presnet in all patients. The nephrotic syndrome, hypertension, hematuria and renal insufficiency were found in more than one half the patients. All patients had membranoproliferative glomerulonephritis of varying degree; glomerular basement membrane splitting, electron dense deposits in the glomerulus; interstitial fibrosis, tubular atrophy and hemosiderin deposits were frequent. Immunoglobulin complement components (classif complement pathway) and renal tubular epithelial antigen were distributed in a granular pattern along the glomerular basement membranes of all patients studied by these methods. Cyroprecipitable complexes of renal tubular epithelial antigen-antibody to renal tubular epithelial antigen as well as antibody to renal epithelial antigen were detected in the circulation of some patients. There was no serologic evidence of activation of the alternate complement pathway. These studies demonstrated an immune deposit normocomplementemic nephritis associated with sickle cell anemia; they further support our hypothesis that the relationship is more then coincidental, and is mediated by glomerular deposition of immune complexes of renal tubular epithelial antigen-antibody to renal tubular epithelial antigen, the antigen possibly released after tubular damage secondary to oxygenation and hemodynamic alterations related to sickle cell disease.
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PMID:Nephropathy associated with sickle cell anemia: an autologous immune complex nephritis. II. Clinicopathologic study of seven patients. 12 92

A nephrotic syndrome caused by immune-complex glomerular disease was diagnosed in a 4-year-old male Great Dane. The syndrome was characterized by proteinuria, hypoproteinemia, hypoalbuminemia, hypercholesterolemia, and subcutaneous edema. Renal biopsy revealed segmental membranous glomerular disease. The edema underwent complete remission 18 days after admission. Two months after admission, there was no clinical or laboratory evidence of glomerular disease. Periodic reevaluation of the dog during the next 2 years revealed recurrence of proteinuria, but no other clinical or laboratory abnormalities. Serial renal biopsies revealed persistence, but no appreciable increase, in the severity of the segmental membranous glomerular disease. The natural course of the nephrotic syndrome and immune-complex glomerular disease has been associated with unpredictable variability. It was concluded that the widespread use of corticosteroid or immunosuppressant therapy in dogs with immune complex glomerular disease should be withheld until the natural course of the disease has been evaluated in a significant number of patients and until the results of well-controlled clinical studies confirm or deny their therapeutic value.
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PMID:Natural remission of nephrotic syndrome in a dog with immune-complex glomerular disease. 12 46

The course of disease of a patient with membranoproliferative glomerulonephritis and partial lipodystrophy is described. The case is further characterized by a deficiency of C3 and C3- activator, by normal values of C4, by evidence of the nephritogenic factor, by raised fibrin degradation products and by an unselective proteinuria. The course of the glomerulonephritis runs parallel to a pronounced susceptibility to infection (at first varicella, tonsillitis and measles, later pneumonia, meningitis, encephalitis and hepatitis). On account of a nephrotic syndrome and an initative impairment of the renal function, a cytostatic treatment was begun, which although raising the C3 level did not influence the further course of the disease. As the patient has a healthy identical twin sister without lipodystrophy, who shows no reduction in C3 and no nephritogenic factor, this case proves that these diseases are acquired and not genetically determined.
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PMID:Membranoproliferative glomerulonephritis with partial lipodystrophy: discordant occurrence in identical twins. 12 86

Malaria infection leads to renal involvement. Reversible proteinuria accompanies many plasmodial infections. Chronic malarial nephrotic syndrome is specifically associated with quartan malaria. Acute renal failure is restricted to infections with Plasmodium falciparum. The pathogenesis of renal involvement during malarial infections includes immunological mechanisms. It is now realized that there exist at least two types of immunological processes: acute transient immune-complex glomerulonephritis with reversible proteinuria and chronic immune-complex glomerulonephritis with irreversible nephrotic syndrome.
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PMID:[Renal involvement in malaria (author's transl)]. 13 74

The nephrotic syndrome presumably caused by an immune complex glomerulonephritis constitutes a major side effect attendant upon chronic administration of penicillamine. The possible induction of an immune-complex glomerulonephritis by penicillamine and its further development after stopping the drug was investigated in rats. --60 rats were fed perorally 2000 mg D-Penicillamine/kg BW/die resp. for a period of 8--44 days. Following unilateral nephrectomy the animals were observed for further 5 weeks. --Dependent to the time of penicillamine application there was an increasing deposition of IgG and C3 in a granular pattern along the glomerular basement membrane and within the mesangium. The IgG deposits initially were focal and segmental later on diffuse and global in distribution. 5 weeks after stopping the penicillamine the immune globulin deposits had disappeared completely or at least in part as did the mild focal glomerulonephritis and the moderate proteinuria which developed in some animals after a 44 day treatment with penicillamine. --The results confirm the hitherto presumed immune complex pathogenesis of the penicillamine induced nephropathy. The disappearance of the immunoglobulins deposited and of proteinuria stopping penicillamine alludes the good prognosis of this kind of nephropathy.
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PMID:[Nephrotic syndrome presumable caused by an complex glomerulonephritis (author's transl)]. 14 Oct 75

Proteinuria, with or without the nephrotic syndrome, developed in 8 patients with seronegative rheumatoid arthritis after the institution of gold therapy. Light microscope examination of renal biopsies showed normal findings in 7, and a focal increase in the mesangial matrix of one glomerulus in the eighth. In all patients immunofluorescence showed deposits of IgG and C3 along the glomerular basement membrane, indicative of immune complex nephritis. The renal biopsies of 5 patients were studied with the electron microscope and subepithelial deposits were detected in all. The Rose-Waaler test for the detection of IgM-rheumatoid factor (IgM-RF) was repeatedly negative in all patients. These results suggest that the development of gold nephropathy may be related to an absence of IgM-RF in serum.
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PMID:Gold-induced immune complex nephritis in seronegative rheumatoid arthritis. 14 32

We report light- and electron microscopic findings in glomerular amyloidosis (secondary amyloidosis), which occurred after recurrent empyema of the pleura. After healing of the empyema, the clinical symptoms disappeared, over a period of eight years. During the acute stage of the disease (grade II-III amyloidosis) when the nephrotic syndrome was present, amyloid deposits were seen in the mesangium and on both sides of the basement membrane of the glomerular capillaries. Furthermore, denuded basement membrane areas showing the passage of amyloid into the urinary space, and invaginations of the podocyte by straightened amyloid fibrils were found. After clinical recovery (except for a trace of proteinuria), the renal amyloidosis had electronmicroscopically transformed from an active into an inactive or resting form, while the amount of amyloid present was almost the same. In the areas of amyloid deposits, reparative changes were observed, espcially in the area of the mesangial cells and of the podocytes. The podocytes were separated from the persisting amyloid deposits by newly formed basement membrane material.
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PMID:Correlations between the morphological and clinical findings in a patient recovering from secondary generalised amyloidosis with renal involvement. Light- and electron microscopic investigations on serial biopsies. 15 Jun 92


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