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)

Glomerulonephritis has been believed to be a rare complication in rheumatoid arthritis (RA). However, recent studies have revealed a focal segmental increase in mesangial cells and matrix in RA patients with hematuria. In our series, proteinuria, hematuria or both abnormalities were recognized in 74 (22%) out of 336 RA cases. Among 119 patients examined by renal biopsy, mild mesangial proliferative glomerulonephritis (GN) was found in 25 patients, of which 22 demonstrated mesangial IgA deposits, by immunofluorescent microscopy. Membranous nephropathy was noticed in 26 cases. Three cases of membranous nephropathy had no history of gold or D-penicillamine treatment. Electron microscopy revealed diffuse thinning of the glomerular basement membrane in 12 cases. The average thickness of the glomerular basement membrane was significantly thinner in RA patients than in normal subjects. The immunological processes associated with rheumatoid factor do not seem to be related to the renal lesions in RA patients.
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PMID:[Renal disorders in rheumatoid arthritis]. 158 51

Heymann's nephritis (HN), a rat model of the membranous glomerulonephritis in man, is thought to be mediated by auto-Ig with subsequent activation of C. Whether T cell mechanisms are involved in the mediation of HN, apart from CD4+ cells providing help for auto-Ig production, was examined by treatment with mAb specific for T cell subsets for 6 weeks after immunization to induce HN. Anti-CD4 mAb therapy totally prevented proteinuria, in that at 6, 8, and 12 week treated rats had less than 15 mg/day of protein compared to controls that all had greater than 260 mg/day. Ig and C deposition in the glomerulus was significantly less and auto-Ig titers in serum were partially suppressed by anti-CD4 therapy. Anti-CD8 mAb therapy markedly reduced proteinuria at all time points, for example at 6 weeks there was 51 +/- 40 mg/day compared to 183 +/- 120 mg/day (P = 0.0003), but had no effect on auto-Ig titers or on Ig and C deposition in the glomerulus. A non-specific effect of high dose mouse mAb therapy was excluded by the findings that a mAb that did not bind to rat cells had no effect on the induction of HN and that serum C was not depleted in any of the mAb treated animals. A role for T effector mechanisms was further supported by the finding that therapy with mAb to T cell receptor alpha/beta chain or with cyclosporine also markedly delayed the onset of proteinuria. Examination of renal biopsies showed a T cell infiltrate in glomeruli and the interstitium of the untreated HN controls that was not present in MRC Ox35 or MRC Ox8 treated groups. This infiltrate included CD4+ and CD8+ T cells and macrophages. These results suggest induction of proteinuria in HN was totally dependent upon CD4+ T cells, and that CD4+ and CD8+ cells may have a direct role in the mediation of glomerular dysfunction in HN.
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PMID:The role of T cells in the mediation of glomerular injury in Heymann's nephritis in the rat. 159 Dec 15

A distinct, hitherto unknown renal histopathological appearance, consisting of diffuse thickening of the glomerular basement membrane (GBM) with fine intramembranous electron-dense deposits, was observed in the renal biopsies from three patients with collagen diseases. In each case, proteinuria was mild with normal urinary sediment. On light microscopy there were no particular abnormalities but a mild thickening of the glomerular capillary wall. Immunofluorescence studies revealed faint linear or extremely fine granular IgG deposition along the capillary wall. On electron microscopy, the GBM was diffusely thickened with fine intramembranous electron-dense deposits without spike formation. No other deposits were seen in the glomerulus. These histological features resembled those of membranous glomerulonephritis (MGN), although the possibility of the early change of MGN is excluded by specific findings in these cases. Other GBM-thickening diseases such as diabetic glomerulosclerosis were ruled out clinically and histologically. Our cases have a singular renal histopathology which differs from any of the previously established classifications of glomerular lesions. It may be a specific change associated with some type of collagen disease.
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PMID:Intramembranous fine deposit disease associated with collagen disorders: a new morphological entity? 159 95

A 64-year-old man with renal artery thrombosis (RAT) associated with nephrotic syndrome (NS) is reported. Although this patient was diagnosed as NS due to membranous glomerulonephritis (MGN) and treated with prednisolone, RAT occurred as a result of unknown mechanisms and caused mild renal dysfunction. Creatinine clearance has been about 70 ml/min for 9 years since the onset of RAT. The renal scintigraphic image has not changed since the onset. NS responded to prednisolone therapy initially and at the time of the relapse. Recent data have shown proteinuria levels of less than 0.2 g/day.
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PMID:Renal artery thrombosis in a patient with membranous glomerulonephritis. 160 Feb 82

40 patients with idiopathic membranous glomerulonephritis were randomized to receive either no treatment or a regime of cyclophosphamide for 6 months, and warfarin and dipyridamole for two years. During the two years of the trial there was no significant deterioration in renal function in either group. A significantly greater improvement in urinary protein excretion was, however, observed at all time points in the treatment group. Plasma albumin was also significantly higher in the treatment group at 18 and 24 months. As progressive deterioration in renal function in membranous glomerulonephritis is associated with persistent heavy proteinuria these results suggest a beneficial effect of treatment.
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PMID:Randomized controlled trial of cyclophosphamide, warfarin and dipyridamole in idiopathic membranous glomerulonephritis. 160 72

Of 103 patients with membranous glomerulonephritis proved by renal biopsy, 11 (10.7%) had rheumatoid arthritis. Nine of these 11 patients received systemic treatment with anti-rheumatic remedies including gold, D-penicillamine and bucillamine. Two others were administered only token of nonsteroidal antiinflammatory drugs. Renal function of the patients was well maintained and within normal limits. Four patients showed nephrotic syndrome, while mild to moderate proteinuria was found in the other 7. Hematuria was minimal to mild, and it was not a major symptom. Six patients resolved proteinuria completely and 2 patients incompletely after discontinuation of chrysotherapy. Nine cases of the membranous lesion in patients with rheumatoid arthritis were stage 1. Thus it was often difficult to identify the glomerular change only by light microscopy. IgA nephropathy and AA amyloidosis were associated in one patient respectively. Our data lead us to conclude that chrysotherapy would cause membranous lesions, but rheumatoid arthritis itself also induce membranous glomerulonephritis.
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PMID:[Clinicopathological study of membranous glomerulonephritis in patients with rheumatoid arthritis]. 163 32

We examined the effect of a selenium-deficient diet on two experimental models of glomerular disease, the puromycin aminonucleoside (PAN)-induced nephrotic syndrome, a model of minimal change disease, and passive Heymann nephritis, a complement-dependent and neutrophil-independent model that resembles membranous nephropathy. The specific activity of selenium-dependent glutathione peroxidase was markedly reduced in the liver, the kidney cortex, and in glomeruli in weanling male Sprague-Dawley rats placed on a selenium-deficient diet for 6 wk compared with rats fed a selenium-replete diet, with no significant differences in the specific activities of superoxide dismutase or catalase. PAN-injected selenium-deficient rats had a marked and significantly greater proteinuria throughout the course of the experiment compared with PAN-injected selenium-replete rats with no significant histological differences. In the passive Heymann nephritis model induced by injecting anti-Fx1A immunoglobulin G, rats fed a selenium-deficient diet had significantly higher urinary protein (day 5: 91 +/- 16 mg/24 h, n = 10) compared with rats fed a selenium-replete diet (52 +/- 5 mg/24 h, n = 11) with no differences in the amount of antibody deposited in the kidney. The most likely explanation for the effect of a selenium-deficient diet is that selenium deficiency resulted in a marked reduction of glutathione peroxidase, thus indicating an important role of glutathione peroxidase in these models of glomerular injury.
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PMID:Effect of selenium-deficient diet in experimental glomerular disease. 163 44

We carried out a retrospective study to investigate the clinical and pathological findings in 31 patients with rheumatoid arthritis (RA). In clinical findings, 17 patients showed nephrotic syndrome, five had isolated proteinuria, two had proteinuria and hematuria and seven had renal failure. In pathological findings, there were 16 patients with membranous nephropathy (MN), two with proliferative glomerulonephritis (DPGN), two with minor glomerular abnormality (MGA), six with amyloidosis, 2 with tubulointerstitial nephritis, and three patients had accompanying lupus nephritis. Eleven of 16 with MGN had been treated with gold, bucillamine or D-penicillamine, so they were diagnosed as drug induced MGN. In the other five patients, we could not decide which drugs induced the nephropathy. The 2 cases of MGA were associated with nephrotic syndrome and acute renal failure, which were caused by non-steroidal antiinflammatory drugs. There were two cases of non-Ig A DPGN, which was regarded as the native nephropathy in RA. The three cases with lupus nephritis were diagnosed as systemic lupus erythematosus by the criteria of the American Rheumatism Association (ARA). In conclusion, the nephropathy in patients with RA was varied and renal biopsy was a useful examination.
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PMID:[Clinicopathological study of nephropathy in patients with rheumatoid arthritis]. 167 90

The concentrations of two components of the complement system (C1q and C3) were measured in the urine and blood in 10 normal subjects and 134 patients with primary and secondary glomerulonephritis by using a highly sensitive enzyme immunoassay. The values of urinary excretion of C1q and C3 were well correlated to the ratios of fractional clearance of these complement proteins to that of neutral dextran of 55 A, which was used to minimize the influences of glomerular sieving because of their comparable molecular size to these complement components. The rate of renal tubular reabsorption of C1q and C3 were at least 89.2 and 93.4% of filtrated C1q and C3, respectively. Urinary C1q and C3 were excreted significantly in cases of membranoproliferative glomerulonephritis (MPGN), membranous glomerulonephritis, IgA nephropathy with both mesangial and capillary immune complex (IC) deposit and also in case of active lupus nephritis. On the other hand, the concentrations of these complement components were low in case of minimal lesion nephrotic syndrome, mild proliferative glomerulonephritis, inactive lupus nephritis and diabetic nephropathy without any immune staining. There was a significant correlation between the urinary excretion of C1q or C3 and intraglomerular IC deposition, especially IC deposition along the glomerular capillary wall. However, the degree of the excretion of these proteins was not correlated to the degree or permselectivity of proteinuria. The correlations between urinary C1q and C3 were observed in cases of IgA nephropathy with both mesangial and capillary deposit and MPGN, although we couldn't see the correlation in the other glomerular diseases. It is suggested that urinary excretion of such complement components represents the fixation of complement by deposited intraglomerular IC. The measurement of urinary concentration of these complement components provides a new clue to investigation or diagnosis of glomerular diseases.
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PMID:Significance of urinary complement components in various glomerular diseases. 169 33

We examined the effect of a fish oil-enriched diet on the development of experimental membranous nephropathy in the rat induced by administration of cationic bovine gamma globulin (CBGG). Rats were placed on a fish oil-enriched diet and control rats received a diet containing an equivalent amount of beef tallow. After 6 weeks on either diet, rats were pre-immunized and injected with CBGG. Proteinuria was significantly reduced in the fish oil-fed group as compared to the control group (160 +/- 40 mg/24 hours, n = 15, versus 280 +/- 36 mg/24 hours, n = 17, p less than 0.02). Glomerular filtration rate was also significantly higher in the fish oil-fed rats than in controls (0.91 +/- 0.07 ml/minute, n = 11, versus 0.60 +/- 0.05 ml/minute, n = 10, p less than 0.005). Glomerular production of prostaglandin E2 and thromboxane B2 the stable product of thromboxane A2, were inhibited by 68% and 70%, respectively, by the fish oil-enriched diet (n = 8, p less than 0.01 versus control). Glomerular leukotriene B4 was also inhibited by 50% in the fish oil-treated rats (n = 6, p less than 0.01), but inhibition of leukotriene B4 by the specific inhibitor L-663,536 in control rats did not ameliorate proteinuria. There was no difference in the amount of distribution of glomerular immune deposits as demonstrated by immunofluorescence and electron microscopy between the experimental and control groups. Moreover, comparable amounts of glomerular IgG deposits were present in the two groups. The specific immune response, assessed by measuring anti-BGG antibody levels, was not different between the two dietary groups, while more than 85% suppression of the splenic T- and B-cell mitogenic response to concanavalin-A and lipopolysaccharide was noted in rats fed the fish oil-enriched diet. We conclude that a fish oil-enriched diet reduces proteinuria and preserves the glomerular filtration rate in rats with CBGG-induced membranous nephropathy. Its mechanism of action remains to be established.
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PMID:Effects of dietary fish oil on the induction of experimental membranous nephropathy in the rat. 170 5


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