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)

Mice undergoing prolonged (5 to 8 weeks) immunization with cadium-free feeritin were studied 1 to 32 days following the last ferritin injection. Urine protein was measured and renal tissue examined by light, immunofluorescence, and electron microscopy. Immunized animals developed significant proteinuria and circulating antibody to ferritin.by light microscopy, proetinuric animals had a proliferative glomerular lesion with mesangial hypercellularity and martrix increase, focal and segmental necrosis, fibrin deposits, and occasional crescents. Iron stains revealed prominent mesangial iron deposition. In immunized animals, IgG and C3 deposits were localized mainly in the mesanglium. Electron microscopic studies revealed marked deposition of ferratin complexesexpanded mesangial matrix and mesangial interposition. Ferratin immune complexes were also visualized in epithelial spaces. In the latter location ferritin immune complexes occasionally formed characteristic electron-dense subepithelial deposits. In this model, mesangial and subepithelial localization of autologous ferritin immune complexes is associated with development of glomerulonephritis and characteristic mesangial lesions resembling those seen in some types of human glomerulonephritis.
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PMID:Experimental glomerulonephritis in the mouse associated with mesangial deposition ofautologous ferritin immune complexes. 12 61

A study was conducted on the disease susceptibility of inbred strains of rats to experimental autologous immune complex glomerulonephritis (AIC). Three strains representing two different H-1-haploytpes developed severe glomerulonephritis within 3 months in response to a single injection with equal doses of an autologous primary tubular epithelial fraction and complete Freund's adjuvant (Lewis, AS (H-11)) and Lew.BDV (H-1d)).By contrast, two strains of the H-1 haplotype H-1n (BN and Lew.BN) showed no proteinuria and no immunohistologic findings during that time. Hybrids of Lew.BN and Lewis, subjected to the same immunizing procedure, showed a later onset of the disease as compared to the responder parent. The possible relationship between responder status and the major histocampatibility complex is discussed.
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PMID:Genetically controlled autologous immune complex glomerulonephritis in rats. 12 58

Anticoagulation has been reported to ameliorate antiglomerular basement membrane glomerulonephritis (anti-GBM-GN) while its effect on chronic immune complex glomerulonephritis (IC-GN) as studied in the NZB mouse is unclear. Chronic serum sickness IC-GN was induced in rabbits by injecting bovine serum albumin (BSA) daily. Anti-GBM-GN was induced by i.v. injection of a known amount of heterologous anti-GBM antibody. Heparin was administered beginning at two to six weeks after the first BSA injections or before the administration of anti-GBM antibody, on various schedules from 5000 U every 12 hr to 8000 U every 8 hr. With this dosage the partial thromboplastin time remained greater than 1-1/2 to 2-1/2 times the control at the time of the subsequent heparin injection. Heparinized and nonheparinized groups were matched according to duration of disease, maximum anti-BSA concentrations or anti-GBM antibody dosage--and no significant differences were found in proteinuria; severity of the glomerular histologic lesions; or immunofluorescence patterns of immunoglobulin G (IgG), third component of complement (C3), BSA or fibrinogen-related antigen(s) (FRA). Crescent formation was not prevented. This study shows that heparin in the maximum permissible dosage is ineffective in preventing glomerular FRA deposition or altering the progression of experimental IC-GN or anti-GBM-GN in rabbits.
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PMID:Failure of heparin to affect two types of experimental glomerulonephritis in rabbits. 12 30

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

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 quantity of urinary proteins and their molecular weight composition was analyzed in different experimental glomerulopathies using the SDS-PAA-electrophoresis. Masugi nephritis, heterologous and autologous immune complex nephritis as well as D-penicillamine induced glomerulonephritis were studied in rabbits, guinea pigs and rats. The procedure allows (1) to distinguish physiological from low grade glomerular proteinuria by their respective characteristic patterns in early disease stages (2) to follow up the disease course of individual animals without sacrifice and (3) to discriminate species specificity of physiological urinary proteins. It is recommended to use this technique of urinary protein analysis in experimental conditions, where mild glomerular damage is expected.
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PMID:Molecular weight analysis of proteinuria in experimental glomerulopathies. 13 32

Autologous immune-complex glomerulonephritis developed in rats injected s.c. with HgCl2 2 days before the injection of anti-tubular fraction 3 antibody. The glomerulonephritis was progressive and characterized by granular deposition of IgG and C-3, with proteinuria from the eighth week onwards. Granular densities and severe glomerular basement membrane changes were observed when the experiment was terminated after 9 months. A possible mechanism of the glomerular lesion is discussed.
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PMID:Induction of an autologous immune-complex glomerulonephritis in the rat by intravenous injection of heterologous anti-rat kidney tubular antibody IV: Effect of injection of HgCl2 prior to the antibody. 13 79

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

A 22-year-old man with a ventriculojugular shunt had edema, hematuria, proteinuria, hypocomplementemia, azotemia, and S epidermidis bacteremia. Initial percutaneous renal biopsy showed a diffuse proliferative glomerulonephritis. Subendothelial and intramembranous deposits were seen on electron microscopy. Immunofluorescent studies were positive for IgG and C3. A repeat percutaneous renal biopsy six weeks after cessation of antibiotic therapy revealed a mild proliferative glomerulonephritis with some evidence of resolution. No deposits were seen on electron microscopy and immunofluorescent studies were negative. At elective shunt revision three months after cessation of therapy, culture of the jugular portion of the removed shunt revealed S epidermidis. Early recognition of immune complex glomerulonephritis occurring with an infected ventriculovascular shunt should permit early treatment (antibiotic therapy and removal of the infected foreign body) and a favorable outcome.
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PMID:Immune complex disease associated with an infected ventriculojugular shunt: a curable form of glomerulonephritis. 14 64


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