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)

Mesangial proliferative glomerulonephritis (MsPGN) induced by chronic serum sickness in rabbits coincide with the human chronic progressive glomerulonephritis resulted from repeated infection, which is similar to pathologic changes of Dampness-Heat Syndrome. The experimental model of MsPGN was treated by Abelmoschus manihot. which could remove the Dampness-Heat. The amount of proteinuria in treating and control group were 62.68mg/24hr and 121.94mg/24hr respectively (P < 0.05), the number of cells in glomeruli were 61.54 and 80.39 respectively (P < 0.01), and diameters of glomeruli were 102.43 microns and 121.13 microns respectively (P < 0.01). It suggested that the drug could alleviate circulating immune complex (CIC) mediated renal injury.
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PMID:[Pathogenic factor (Dampness-heat) of glomerulopathy]. 147 99

The presence and extent of focal-segmental glomerulosclerosis/hyalinosis (FSSH) was determined in 79 autopsy cases of analgesic nephropathy and correlated with the levels of proteinuria, serum creatinine and arterial blood pressure. FSSH was present in 77% of cases. The extent of FSSH correlates positively with increasing proteinuria and serum creatinine. The widely scattered pattern suggests a multifactorial pathogenesis for FSSH in analgesic nephropathy, including, for example, glomerular overload and arterial hypertension. Mesangial proliferative glomerulonephritis was observed in only two cases.
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PMID:[Focal-segmental glomerulosclerosis in analgesic nephropathy]. 648 41

Twenty-six cases of Mesangial Proliferative Glomerulonephritis and diffuse IgM deposits were studied. Nine had nephrotic syndrome; 8 minimal urinary abnormalities; 7 asymptomatic proteinuria; 2 recurrent haematuria. Immunofluorescence revealed granular mesangial deposits in 14 cases and interrupted linear deposits in the others, chiefly along the capillary walls. In the latter group the clinical picture was mainly nephrotic syndrome or asymptomatic proteinuria. The clinical course is favourable: 7 cases recovered; 12 improved; 7 did not show any change. No progression of renal lesions was observed. Despite uniform histological features, this nephropathy is unlikely to be a unique disease, but in our opinion it should be considered separately from other glomerulopathies.
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PMID:Long term study of mesangial proliferative glomerulonephritis with IgM deposits. 732 78

Mesangial proliferative glomerulonephritis without IgA deposition (non-IgA MesPGN) is commonly detected in biopsy specimens, but the clinicopathological correlation with the long-term prognosis still remains obscure. The aim of our study is to elucidate the long-term prognosis and the clinicopathological prognostic factors in patients with non-IgA MesPGN. We mailed questionnaires to 122 patients with primary glomerulonephritis who were biopsied between 1963 and 1975. Information was obtained from 109 of these 122 patients and 55 were histologically rediagnosed as having non-IgA MesPGN. The histological alterations of glomeruli and tubulointerstitium were classified into five grades. The mean period between the biopsy and the questionnaires was 20.5 years. Six of the 55 patients with non-IgA MesPGN developed end-stage renal failure and histopathological alterations of renal biopsies from these six patients were classified into grade IV or V. The presence of hypertension, heavy proteinuria of over 2+ or renal insufficiency at the biopsy was related to the severe histological changes, a grade of IV or V and to a poor prognosis. The renal survival rate of all the 55 patients was 88.3% at 20 years after the biopsy, while that of the 12 patients with severe histological changes was 48.6%. Although non-IgA MesPGN is considered to be a heterogeneous disease, we cannot ignore the incidence of this disease and thus consider it to be one of the important primary glomerulonephritides that occur in childhood.
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PMID:Long-term prognosis and prognostic factors of Japanese children with mesangial proliferative glomerulonephritis without IgA deposition. 757 45

Two adult patients with mesangial proliferative glomerulonephritis with diffuse IgM deposition in the glomeruli are reported. Case 1 was a 25-year-old female with nephrotic syndrome who showed complete remission after treatment with prednisolone (PSL). Case 2 was a 46-year-old male with asymptomatic proteinuria who showed incomplete remission (0.5-1.0 g/24 hr) of urinary protein without any medication. In light microscopy, these patients revealed minimal or slight proliferation of glomerular mesangial cells without glomerular sclerosis and crescent formation. Deposition of IgM and C3 was observed in the glomerular mesangial areas and capillary walls by immunofluorescence. Electron-dense deposits were observed in the glomerular mesangial areas in these patients. Mesangial proliferative glomerulonephritis associated with diffuse IgM deposition in the glomeruli appears to have a benign clinical course. It has also been suggested that this disease has variant clinical courses since we recently experienced two other patients with mesangial proliferative glomerulonephritis with focal IgM deposits who showed renal tubular dysfunction or chronic renal failure.
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PMID:Two adult cases of IgM-associated mesangial proliferative glomerulonephritis. 793 71

Persistent proteinuria and tubulointerstitial lesions are important signs of progressive renal disease. The purpose of this study was to assess the role of complement in the development of tubulointerstitial lesions in rats with proteinuria due to primary glomerulonephritis. Mesangial proliferative glomerulonephritis was induced in mononephrectomized rats by intravenous injection of monoclonal antibody (mAb) 1-22-3 (Clin Exp Immunol 102: 181-185, 1995). As early as 24 h after the injection, proteinuria became evident, persisted throughout the observation period, and was associated with mesangial cell proliferation and tubulointerstitial lesions when examined at 7 and 14 d after mAb administration. Deposition of rat C3 and C5b-9 was observed at the luminal surface of proximal tubules and in cellular debris present in the tubular lumen (group I). Rats injected with mAb 1-22-3 and depleted of complement by injections of cobra venom factor starting at day 3 developed glomerulonephritis and proteinuria comparable to rats of group I, but complement deposition in the tubules and the tubulointerstitial lesions were markedly reduced (group II). Rats in group III were injected with mAb and, from day 3, with soluble complement receptor type 1, which became detectable at the luminal surface of proximal tubules and in the urine. Deposition of C5b-9 in tubular cells was not detectable, and the severity of tubulointerstitial lesions was reduced compared with rats in group I. These results indicate that, in this model of primary mesangial proliferative glomerulonephritis with proteinuria, the development of tubulointerstitial lesions is associated with activation of serum complement at the level of tubular brush border, and tubulointerstitial lesions can be reduced by inhibition of complement activity.
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PMID:The role of complement in the pathogenesis of tubulointerstitial lesions in rat mesangial proliferative glomerulonephritis. 929 27

The effects of chitosan-coated dialdehyde cellulose (chitosan DAC), a newly developed oral adsorbent for urea and ammonia, were examined in a glomerulonephritis model in rats. Mesangial proliferative glomerulonephritis accompanied with proteinuria was induced by an intravenous injection of anti-rat Thy-1.1 monoclonal antibody (OX-7). The proliferation of mesangial cells and an accumulation of extracellular matrix components such as type I collagen and fibronectin were observed in the glomeruli 9 days after OX-7 injection; these were improved in rats fed a diet containing chitosan DAC (10% content) for 9 days compared with those in rats fed a normal diet. Chitosan DAC treatment decreased the elevated urinary protein and blood urea nitrogen at days 8-9 to the normal levels; the increased fecal excretion of nitrogen might participate in this phenomenon. In addition, chitosan DAC treatment showed an increase in fecal water content associated with a decrease in urinary volume. These therapeutic effects may be due to the reduction of proteinic factor expression and the compensational function of chitosan DAC for kidney. These results suggest that chitosan DAC treatment may be useful for ameliorating mesangial proliferative glomerulonephritis.
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PMID:Effects of chitosan-coated dialdehyde cellulose, a newly developed oral adsorbent, on glomerulonephritis induced by anti-Thy-1 antibody in rats. 957 70

The existence of a human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) as a distinct disease entity characterized by glomerulosclerosis is well established in North America and Western Europe. Although the large number of HIV-infected cases overwhelm the Asian countries, no cases of HIVAN are documented in the literature. We studied 26 cases of HIV-infected Thai patients with proteinuria greater than 1.5 g/d of protein during 1995 and 1996. None of the patients were treated with antiretroviral drugs at the time of renal biopsy. Intravenous drug addiction and sexual transmission were risk factors in 11 and 15 patients, respectively. Pathological examinations were performed by light microscopic and immunoperoxidase study. Mesangial proliferative glomerulonephritis was found in 17 cases, immunoglobulin A (IgA) nephropathy in 2 cases, and diffuse proliferative glomerulonephritis and interstitial nephritis secondary to cryptococcal infection in 2 cases each. One case each had membranous glomerulopathy, membranoproliferative glomerulonephritis, and granulomatous interstitial nephritis secondary to tuberculosis. The renal pathological findings of HIVAN with the unique features described in previous literature were not evident in these patients. Although the data in this study are limited to 26 HIV-infected Thai patients, we believe that HIVAN is uncommon in the Asian HIV-infected population.
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PMID:Renal pathology and HIV infection in Thailand. 1002 39

There is a broad spectrum of renal involvement following snake envenomation. At the clinical level the renal manifestation may be absent or minimal. Mild proteinuria with abnormal urinary sediment may be observed. Significant proteinuria is uncommon. Hematuria and hemoglobinuria are seen in envenomation by vipers or crotalids, while myoglobinuria follows envenomation of sea snakes or elapids. Acute renal failure can occur in these snake bites. All renal structures can be involved. Mesangial proliferative glomerulonephritis is common. Tubular necrosis is the important pathological counterpart of acute renal failure. Three mechanisms including hemodynamic alterations, immunologic reactions, and direct nephrotoxicity are incriminated in the pathogenesis of renal lesions.
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PMID:Nephrotoxicity in snake envenomation. 1041 Mar 37

Glucocorticoids are widely prescribed for renal diseases. It is believed that glucocorticoids attenuate immune-mediated renal diseases by suppressing the cell-mediated immune system. However, there is evidence that glucocorticoids influence the expression of such growth factors as vascular endothelial growth factor (VEGF), transforming growth factor-beta1 (TGF-beta1), and connective tissue growth factor (CTGF), which are known to influence the development or progression of renal diseases. Therefore, we undertook this study to determine whether glucocorticoids regulate proteinuria or extracellular matrix (ECM) production by altering these growth factors. Mesangial proliferative glomerulonephritis was induced in rats by intravenous injection of monoclonal antibody (OX-7), and dexamethasone (20 mg/kg) was administered intraperitoneally from the third to seventh disease day. Glomerular expression of VEGF, TGF-beta1, and CTGF, the amount of urinary protein, and glomerular ECM were measured on the seventh disease day. The nephritic group showed proteinuria and greater VEGF, TGF-beta1, and ECM production. Dexamethasone aggravated proteinuria (protein, 0.4 +/- 0.1 mg/mg creatinine in the NC group, 6.3 +/- 2.0 mg/mg creatinine in the DC group, and 21.1 +/- 1.9 mg/mg creatinine in the D-Dex group; P < 0.05) and diminished VEGF release (22 +/- 3 pg/mg total protein in the NC group, 292 +/- 26 pg/mg total protein in the DC group, and 198 +/- 23 pg/mg total protein in the D-Dex group; P < 0.05). Expression of TGF-beta1, CTGF, and ECM was not altered significantly by dexamethasone treatment. We found that glucocorticoid diminishes VEGF release and at the same time exacerbates proteinuria in rats with this type of glomerulonephritis.
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PMID:Glucocorticoid diminishes vascular endothelial growth factor and exacerbates proteinuria in rats with mesangial proliferative glomerulonephritis. 1197 43


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