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)

Renal histology in 163 Japanese children, aged 3 to 15, with proteinuria and/or haematuria showed that 11 had membranous nephropathy (M.N) and the rest had various other renal diseases. Hepatitis-B-virus surface antigen (HBsAg) was identified, by a reversed passive haemagglutination method, in the serum of all the patients with M.N. but in only 4.6% of the patients with other renal diseases. 6 of the 11 mothers of the children with M.N. were positive for HBsAg, and 1 was positive for antibody to HBsAg (anti-HBs). These findings suggest that M.N. in Japanese children is mainly, if not exclusively, caused by hepatitis-B virus and that in most instances the virus is transmitted from mother to child.
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PMID:Strong association between membranous nephropathy and hepatitis-B surface antigenaemia in Japanese children. 8 85

In 53 patients (19 women, 34 men), of them 41 patients with an intracapillary proliferative glomerulonephritis, 9 with membranous proliferative and 3 with a membranous glomerulonephritis under an indometacin therapy examinations concerning proteinuria were carried out, partly with determination of the index of selectivity and representation of the protein clearance. In patients with a moderate proteinuria of less than 3 g a day this treatment achieved a smaller antiproteinurie effect than in patients with a large proteinuria. When a large activity of the inflammatory process was present a therapeutic success was less frequently to be proved. An unequivocal correlation between the histological course of the disease and the change of the proteinuria could not be recognized. After cautious estimation of the findings the selectivity of the proteinuria may be regarded as a certain indicator for the application of indometacin. The protein clearance, however, proved less suitable for the judgment of the treatment performed.
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PMID:[Long-term treatment of glomerulonephritis with indomethacin with special regard to quantity and selectivity of proteinuria]. 9 29

The development of severe proteinuria or nephrotic syndrome as an adverse reaction to gold therapy in rheumatoid arthritis is well known. Morphologic examination reveals membranous glomerulonephritis in almost all cases. Since the beginning of 1978 there has been a striking increase in the number of such cases seen at this institute. 5 patients aged from 17 to 65 years who had been treated with sodium aurothiomalate for rheumatoid arthritis developed severe proteinuria. In all cases only minimal glomerular changes were observable by light microscopy. Electron microscopy demonstrated multiple electrondense, subepithelial deposits which were confirmed by fluorescence microscopy. In all cases characteristic lysosomes ("aurosomes") were demonstrated in the cytoplasm, mainly of the epithelial glomerular cells. This unusual accumulation of almost identical cases coincides with the introduction of a new gold preparation, Na-aurothiomalate (Tauredon), containing 46% metallic gold.
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PMID:[Conspicuous accumulation of membranous glomerulonephritis following gold therapy in chronic polyarthritis--a side effect of a new preparation?]. 10 66

The laboratory counterpart of tubular antigen-mediated membranous glomerulonephritis in humans was produced in rats by a single injection of homologous nephritogenic tubular antigen with adjuvant. The rat developed membranous glomerulonephritis with typical clinicopathologic features of human nephritis mediated by the tubular antigen, i.e., massive proteinuria and diffuse thickening of glomerular basement membranes due to deposition of tubular antigen-antibody complexes which were demonstrated by immunofluorescent technique. The nephritogenic tubular antigen was solubilized by pronase digestion, further purified by gel filtration, and demonstrated to have the same physicochemical properties as the human tubular antigen which was found in the deposits together with beta1C- and immunoglobulins in the glomeruli of patients with membranous glomerulonephritis.
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PMID:Laboratory model of membranous glomerulonephritis in rats induced by pronase-digested homologous renal tubular epithelial antigen. 12 17

Autologous immune complex (AIC) nephritis is a form of chronic renal disease with remarkable similarities to idiopathic membranous nephropathy occurring in man. AIC nephritis was induced in 160 gram Lewis rats with a single footpad injection of tubular brush-border antigen (FxIA) in complete Freund's adjuvant. When killed at 8 weeks, 85 per cent of the rats demonstrated typical diffuse glomerular deposits of immunoglobulin G and B1C (C1/3 component of complement) by immunofluorescent microscopy, and subepithelial electron-dense deposits by electron microscopy. Both immune complex disease and significant proteinuria occurred in two-thirds of these animals. An attempt to modify the natural course of established AIC nephritis using large doses of potent glucocorticoids (methyl-prednisolone), anti-inflammatory agents (acetylsalicylic acid, indomethacin, and cyproheptadine), and immunosuppressive drugs (cyclophosphamide, azathioprine) was begun 4 weeks after initial immunization and continued for 4 more weeks. None of the single drug nor multiple drug protocols employed was of demonstrable benefit in ameliorating the immune events operating in AIC nephritis. Cyclophosphamide and indomethacin, when used singly, were associated with significant mortality in the animals studied. All combined drug protocols involving glucocorticoids and antimetabolites were associated with unacceptable mortality as well. Of interest, immune complexes could not be demonstrated in the vascular choroid plexus of any rat with AIC nephritis. This failure to modify the course of established renal disease (AIC) in an experimental animal with generally available pharmacologic agents, is similar to the usual results of such treatment in chronic renal disease (idiopathic membranous nephropathy) in man. It is possible that new and more potent anti-inflammatory agents employed singly or in various combinations, will permit more successful manipulation of the host's immunologic system to prevent or modify immune injury of the renal glomerulus.
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PMID:Single and multiple drug therapy in autologous immune complex nephritis in rats. 12 75

There is considerable circumstantial evidence relating neoplasia to glomerular injury. Recently, more convincing evidence has been derived from the demonstration of tumor-associated antigen or antibody to such antigen, in relation to glomerular basement membranes in four patients with glomerular injury and cancer. The most common form of glomerulopathy reported in patients with carcinoma has been membranous glomerulonephritis. However, increased mesangial cells and matrix have also been found in some patients with hematuria and progressive renal failure. In contrast, most patients with Hodgkin's disease and glomerulopathy have had the minimal lesion-type nephrotic syndrome, which has usually responded to successful treatment of the Hodgkin's disease. Glomerular abnormalities have also been reported with chronic lymphocytic leukemia, lymphosarcoma, Waldenstrom's macroglobulinemia, and benign tumors. When there is no apparent cause, proteinuria with or without hematuria or impaired renal function should suggest the possibility of associated neoplasia, particularly in elderly patients.
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PMID:Glomerular injury in patients with neoplasia. 18 Aug 69

The incidence and early recurrence after transplantation prove the specificity of the appearance of an electron dense alteration of kidney basement membrane often called dense intra-membranous deposit disease. Three new cases with dense deposit disease affecting the original kidneys have been followed-up after transplantation for periods ranging from 4 to 8 years and illustrate the natural history of the recurrence. Serial kidney biopsies showed the predominance of dense deposits near the mesangial area and the vascular pole. These deposits were also seen in some tubular basement membranes. Absence of cell proliferation was noted in all biopsies performed. Immunofluorescence studies revealed fixation of C3 alone. Histological signs of recurrence are compatible with the absence of clinical and biological signs. Transient or permanent proteinuria and microhematuria were common findings. Serum complement levels, measured after transplantation, were low in all three cases. Despite recurrence of the original glomerulonephritis, long-term survival of the graft was commonly observed, two cases being followed-up for 7 and 8 years. Patients with dense intra-membranous deposits glomerulonephritis should not be excluded from a transplantation program. One of the three cases reported here illustrates the exceptional association of recurrence of dense intramembranous deposits, de novo membranous glomerulonephritis and chronic rejection.
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PMID:Dense deposit disease: long term follow-up of three cases of recurrence after transplantation. 31 48

The pathogenesis of chronic membranous glomerulonephritis induced in rats by passive immunization with heterologous antibodies to rat renal tubular epithelial (RTE) antigens was investigated. This model is designated as "passive Heymann nephritis" (PHN) in order to contrast it with classical Heymann nephritis induced by active immunization with homologous RTE in adjuvant. A single i.v. injection of heterologous (rabbit) antibody to RTE evoked chronic proteinuria after a latent period of one to three days. The onset of proteinuria was accompanied by the granular deposition of rabbit IgG and rat beta1C globulin along the glomerular capillary wall. Renal isografts developed PHN only when transplanted within the first three days following injection of the heterologous anti-RTE antibodies. The data suggest that the heterologous antibodies form immune complexes with RTE antigens preexisting in the circulation, and these complexes subsequently deposit in the glomerular capillary walls. Chronic proteinuria is then perpetuated by a host reaction to the foreign protein in the deposits (i.e., rabbit IgG), in a fashion analogous to that seen in the autologus phase of nephrotoxic serum nephritis. These studies indicate that continued glomerular deposition of preformed circulating immune complexes may not always be a requisite for the perpetuation of glomerular injury in immune complex disease.
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PMID:Chronic nephritis induced by antibodies reacting with glomerular-bound immune complexes. 32 57

Forty-seven SLE patients with severe renal disease characterized by renal biopsy documentation of diffuse proliferative or membranous glomerulonephritis or the nephrotic syndrome have been treated with azathioprine and prednisone in combination and followed for up to 12 years. Survivorship was 82% +/- 6% for five years and 74% +/- 8% for 10 years. There have been eight deaths and two patients have gone on hemodialysis. Five of the eight deaths are attributable to superinfection. Improvement in creatinine clearance was documented in 21 and decreased proteinuria in 35 of the patients. A therapeutic program, which included high dose corticosteroids initially, the combinations of azathioprine with corticosteroids chronically, and the rapid reduction in corticosteroid dosage to an alternate day schedule, appears to contribute to improved survivorship.
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PMID:Longterm survival of lupus nephritis patients treated with azathioprine and prednisone. 37 23

The role of circulating immune complex deposition versus in situ complex formation in membranous nephropathy is controversial. Passive Heymann nephritis in rats resembles membranous nephropathy in man and was induced by injection of sheep antibody to rat proximal tubular epithelial cell brush border antigen (anti-Fx1A). Minutes after injection of 1 ml. of anti-Fx1A, subepithelial immune deposits were seen by immunofluorescence and electron microscopy, and proteinuria appeared within 5 days. The effects of alterations in the dose of administered antibody, corticosteroid therapy, and vasoactive amine blockade on the development of subepithelial deposits and consequent proteinura were studied. Variation of the dose of anti-Fx1A from 0.25 ml. to 1 ml. resulted in a progressive increase in the size and number of glomerular capillary wall deposits, but no alterations in their distribution. Only those rats which received 1 ml. became proteinuric within 5 days. Corticosteroid therapy and vasoactive amine blockade, begun 24 hours prior to the induction of passive Heymann nephritis and continued until termination of the study 5 days later, had no effect on the amount or site of immune complex formation, nor on the extent of proteinuria as compared to untreated controls. In contrast, in rats with unilateral proteinuria produced by the selective perfusion of one kidney with aminonucleoside of puromycin 7 days prior to the induction of passive Heymann nephritis, there was a marked reduction of subepithelial deposits in the perfused kidney as compared to the nonperfused contralateral kidney. In this model of membranous nephropathy, systemic factors play little role in the development of subepithelial deposits, whereas local factors are critical. These findings are consistent with the hypothesis that subepithelial immune deposits form locally.
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PMID:Determinants of glomerular localization of subepithelial immune deposits: effects of altered antigen to antibody ratio, steroids, vasoactive amine antagonists, and aminonucleoside of puromycin on passive Heymann nephritis in rats. 37 41


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