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)

Chronic progressive membranous nephropathy (MN) in humans is characterized by thickening of the glomerular basement membrane (GBM) with formation of spikes which contain laminin and other extracellular matrix (ECM) proteins. We have utilized two models of MN in the rat (active and passive Heymann nephritis, AICN, PHN) to define the sequential changes in composition of GBM as they relate to changes in glomerular gene expression for ECM components, altered permeability and morphological changes. Renal biopsies obtained during the course of AICN and PHN were immunostained for various ECM proteins and total glomerular RNA was hybridized with cDNA probes specific for laminin B2-chain, s-laminin, and types I and IV collagen. In addition, the ability of anti-glomerular epithelial cell (GEC) antibody and complement on rat GEC in culture to induce laminin release or laminin and s-laminin mRNA expression was determined. The results demonstrate that at weeks 12, 16, and 20 of AICN, immunostaining for laminin, s-laminin, fibronectin, entactin, and heparan sulfate proteoglycan increased in the GBM in a spike-like pattern. Concomitantly, glomerular mRNA levels of laminin B2-chain and of s-laminin increased. Type IV collagen protein and gene expression remained unchanged or decreased. No glomerular immunostaining for type I collagen occurred during AICN despite increased expression of mRNA for this collagen type. In contrast to AICN, in PHN no pronounced changes of the glomerular ECM occurred, except for transient expression of type I collagen mRNA in whole glomerular RNA and type I collagen protein the GEC cytoplasm. Stimulation of GEC in culture with anti-GEC antibody and complement also failed to induce transcription of laminin or s-laminin mRNA or the release of laminin protein. These findings suggest that the polyantigenic expansion of GBM which occurs in chronic experimental MN may be stimulated by factors different from the C5b-9 mediated processes that cause the initial proteinuria.
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PMID:Altered glomerular extracellular matrix synthesis in experimental membranous nephropathy. 138 96

This study was carried out in rats with nephrotoxic serum nephritis after autologous phase proteinuria was well established to determine the effect of tubule fluid iron chelation on the course of this disease. Deferoxamine administration caused a reduction in urinary iron potentially capable of catalyzing hydroxyl radical (.OH) formation and kidney iron uptake (224 +/- 60 vs. 398 +/- 152 mg/kg). This was associated with a decrease rate of progression of renal failure over the 21-day study period (creatinine clearance -0. 199 +/- 0.152 vs. -0.509 +/- 0.336 ml/min, P < 0.05) and improved survival (8/8 vs. 4/8, P < 0.05). In addition deferoxamine caused a reduction in urinary transferrin excretion (32 +/- 15 vs. 74 +/- 16 mg/day) and fractional excretion of transferrin (2.01 +/- 1 vs. 5.9 +/- 3.7%) and an increase in serum transferrin levels (229 +/- 36 vs. 139 +/- 45 mg/dl, all P < 0.05). It is suggested that iron presented to the tubule fluid as a result of the glomerular leak for transferrin is dissociated from transferrin. In turn the iron is available in a form capable of catalyzing .OH formation, resulting in lipid peroxidation of tubule cell membranes. Deferoxamine chelation of tubule fluid iron retards the development of both tubulointerstitial injury and superimposed glomerular sclerosis in this model of membranous nephropathy.
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PMID:Toxicity of tubule fluid iron in the nephrotic syndrome. 138 59

A 58-year-old fisherman was admitted because of an abnormal chest X-ray shadow on the right side. Bronchoscopic examination revealed tumor of right B7. Transbronchial biopsy showed squamous cell carcinoma. He was treated with four courses of CDDP and PEP. Two years later, he developed nephrotic syndrome and relapse of lung cancer. Proteinuria and pedal edema continued. Renal biopsy revealed the characteristic light and immunofluorescent microscopic features of membranous nephropathy. Oral administration of low dose etoposide resulted in reduction of the carcinomatous lung lesion and a decrease in proteinuria as well as pedal edema.
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PMID:[A case of nephrotic syndrome associated with bronchogenic carcinoma]. 140 14

The most recent studies, using the actuarial life-table technique, of the problem of long-term renal outcome and the factors that influence it in adult patients with one of the three most common types of chronic idiopathic immune complexes-mediated glomerulonephritis (IgA nephropathy [IgAN], membranous nephropathy [MN], and type I membranoproliferative glomerulonephritis [MPGN]) are reviewed. In the last decade, renal survival 10 years after onset has become similar to adult patients with idiopathic IgAN (80% to 87%) and idiopathic MN (75% to 83%), because of improvement of the renal survival of patients with MN. Renal survival at 10 years is worse for adult patients with idiopathic type I MPGN (60% to 64%). There is no substantial difference in the average renal survival times between different geographical regions, with the exception of a better prognosis for idiopathic MN in Japan. The presenting clinical factors that most strongly predict subsequent poor outcome are similar for the three types of glomerulonephritis and are rather nonspecific: (1) severe proteinuria, (2) impairment of renal function, and (3) arterial hypertension. As for the histological features, the most powerful predictor of subsequent progression in all three types of glomerulonephritis is tubulointerstitial damage, suggesting that a cell-mediated immune process believed to occur there may independently influence outcome in glomerular diseases.
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PMID:Influence of clinical and histological features on actuarial renal survival in adult patients with idiopathic IgA nephropathy, membranous nephropathy, and membranoproliferative glomerulonephritis: survey of the recent literature. 141 98

We developed an approach in quantifying the risk of developing chronic renal insufficiency (CRI) based on a cohort of 184 patients with idiopathic membranous glomerulonephritis (IMGN), prospectively followed by the Toronto Glomerulonephritis Registry between 1974 and 1988. After a mean follow-up period of 5.8 years, 26% of patients developed CRI (defined as persistent reduction of creatinine clearance (CCr) less than or equal to 60 ml/min/1.73 m2 for greater than or equal to 12 months). We found that when compared to the baseline probability of the unselected patients, the severity of proteinuria at kidney biopsy added only marginally to the prediction of CRI. We introduced a special test condition: persistent proteinuria (PP) (that is, duration of proteinuria, g/day, above different cut-off levels). We examined the positive predictive value (PPV) and sensitivity (SEN) of 15 arbitrarily chosen levels of PP (that is, proteinuria greater than or equal to 4, 6 or 8 g/day persisting for greater than or equal to 6, 9, 12, 18 or 24 months) to select levels with optimal predictive characteristics. We found that PP greater than or equal to 8 g/day for greater than or equal to six months was a simple and useful predictor of CRI with a PPV and SEN of 66%. To further improve our prediction, we tested the following parameters: age, sex, initial SCr and CCr, proteinuria, serum albumin, hypertension, rate of change of CCr over time, and therapy (steroids +/- immunosuppressive drugs) in a multivariate analysis. Proteinuria, initial CCr, and rate of change of CCr were most important in predicting CRI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Predicting chronic renal insufficiency in idiopathic membranous glomerulonephritis. 145 88

We performed two trials. The former was a multicentric trial on 24 untreated patients with nephrotic syndrome due to membranous nephropathy to ascertain whether or not a long-term reduction of protein intake reduces urinary protein loss. In a randomized cross-over design the patients ate sequentially each for 3 months a normal protein diet (1.1 +/- 0.3 g/kg/day of proteins) and a low-protein diet (0.7 +/- 0.1 g/kg/day). Both diets were low in fat (< 30% of total calories). Neither urinary protein excretion nor serum albumin concentration were significantly different at the end of the low protein diet period or the normal protein diet period. We found that after 6 months of dietary manipulation serum total and LDL-cholesterol were reduced by 24 and 27% from the values at the beginning of the run-in period, also the mean 24 h proteinuria was significantly lower. In the later trial, after a baseline control period of 2 months on free diet, 20 untreated nephrotic patients were fed for two months a vegetarian soy diet, low in fat (28% of total calories) and in proteins (0.71 +/- 0.36 g/kg ideal body weight/day). At the end of the diet period all patients ate the same free diet as in the baseline period for 2 more months. The soy diet induced highly significant decreases in total serum cholesterol (28%). LDL-cholesterol (33%), apolipoprotein B (19%), urinary protein excretion (32%), that reversed on discontinuation of the diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary manipulation on the lipid abnormalities and urinary protein loss in nephrotic patients. 146 59

On the basis of 1263 observations a relative incidence and clinical manifestations of main morphological forms of primary glomerulonephritis (PGN) are studied. Alterations in the clinical and morphological structure of primary glomerulonephritis are noted with nephrotic forms becoming more frequent and mesangiocapillary glomerulonephritis among patients with nephrotic and nephrotic-hypertension syndrome becoming somewhat less frequent. A bimodal pattern of distribution of patients with membranous nephropathy depending on the age at the beginning of the disease indicating possibly the change of etiological factors in the age groups was established. Minimal alterations, focal-segmentary glomerulosclerosis, membranous nephropathy manifested most frequently by nephrotic syndrome or subnephrotic proteinuria. Mesangioproliferative and mesangiomembranous glomerulonephritis manifested by nephrotic, proteinuric-hematuric syndrome and were the main cause of the PGN hematuric form. The highest incidence of pronounced tubulointerstitial changes in mesangiocapillary and diffuse fibroplastic glomerulonephritis is noted this explaining a considerable lowering of the kidney function in these two forms of PGN.
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PMID:[Characteristics of primary glomerulonephritis (on the basis of kidney biopsies of the Pathology Department, I. M. Sechenov Moscow Medical Academy, from 1980 to 1989)]. 147 30

We report a case of endstage renal disease due to simultaneous occurrence of membranous nephropathy and crescentic glomerulonephritis associated with anti-GBM antibodies. The patient was a 60-year-old male and was hospitalized for prolonged anorexia and general malaise. On admission, his body temperature was 38.5 degrees C. Urinalysis revealed 3+ proteinuria and the sediment contained abundant erythrocytes. The urea nitrogen was 142.4 mg/dl, the creatinine 19.5 mg/dl, the potassium 6.47 mEq/dl and CRP 10.1 mg/dl. Anti-GBM antibodies were 1000EU/ml. Immediately after initiating hemodialysis, pulse steroid therapy, plasma exchange and continuous heparinization were performed. However, renal function had been impaired and maintenance hemodialysis was required. Histological examination of the renal specimen revealed marked epithelial crescent formation, whereas thickening of basement membrane and mesangial proliferation were not observed. By immunofluorescent staining, both bright linear and fine granular fixation of IgG and fine granular fixations of C3 along the glomerular capillary walls were observed. Electron microscopy showed subepithelial electron lucent deposits and thickening of the glomerular basement membrane, diagnostic of the advanced membranous nephropathy (stage IV).
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PMID:[A case of anti-GBM nephritis (crescentic glomerulonephritis) associated with membranous nephropathy]. 147 22

Little information is available about the clinical status and outcome of patients with a long history of lupus nephritis. We have reviewed the dossiers of 25 patients (23 women and two men) who have been monitored by our Unit for more than 10 years after the diagnosis of lupus nephritis. At presentation the mean age was 28.5 +/- 10.33 (SD) years, the mean plasma creatinine was 136.1 +/- 144.7 (SD) nmol/l, the mean proteinuria was 3.02 +/- 2.7 (SD) g/day. At initial renal biopsy 18 patients showed diffuse proliferative glomerulonephritis, six patients showed membranous glomerulonephritis and one showed focal proliferative glomerulonephritis. All patients but one were treated with corticosteroids and 18 were also given immunosuppressive agents. At the last observation (16 +/- 4.6 (SD) years after presentation), 19 patients have normal plasma creatinine (11 of them show proteinuria less than 0.2 g/day) and six patients show increased plasma creatinine (mean 203.3 +/- 61.9 (SD) mmol/l). Eleven patients have been without any treatment for 88 +/- 64 (SD) months. The incidence of lupus flare-ups fell significantly after the tenth year (0.31/patient/year between 0 and 10 versus 0.11 between years 11 and 27; p = 0.01). No case of pericarditis or cerebritis occurred after the tenth year. Only one case of cerebral thrombosis occurred before the tenth year, but ten severe atherosclerotic cardiovascular and cerebrovascular complications were seen after the tenth year (two cardiac infarcts, three angina pectoris, four cerebral thrombosis, one cerebral haemorrhage). Two cases of cancer (thyroid and lung) occurred after the tenth year. The professional rehabilitation was good in most patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical status of patients after 10 years of lupus nephritis. 148 Jul 42

A 64-yr-old man presented with diabetes mellitus, proteinuria, hypertension and moderate renal dysfunction. Renal biopsy revealed diabetic glomerulosclerosis (diffuse lesion), IgA nephropathy and membranous nephropathy (stage 2). Both mesangial IgA and subepithelial IgG deposits were demonstrated by immunofluorescence and immunoelectron microscopy. Electron microscopic studies by immunogold method showed localization of IgA (diameter 15nm gold particles) within mesangial dense deposits and IgG (diameter 15nm gold particles) within subepithelial dense deposits. Overlapping IgA and membranous nephropathy was revealed in the same diabetic glomeruli with functional and biochemical alternations.
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PMID:[A case of superimposed renal lesions of IgA and membranous nephropathy with diabetic nephropathy]. 148 12


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