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)

Nephrotoxic nephritis was induced in Sprague-Dawley and Munich-Wistar rats by the injection of rabbit antirat kidney serum. A biphasic pattern of proteinuria was induced: the heterologous phase with a peak of proteinuria occurring at 10 to 16 hours, and the autologous phase with a peak at 10 to 15 days. For morphologic studies, glomeruli were fixed by perfusion, or by drip-fixation during good blood flow. In the heterologous phase, glomerular endothelial detachment or loss and leukocytic infiltration were prominent. In the autologous phase, focal detachment of glomerular endothelium and epithelium was commonly found. At sites of endothelial loss, in both phases, endogenous albumin (demonstrated by an ultrastructural immunoperoxidase technique), but not intravenously injected ferritin, showed abnormally deep penetration into the glomerular basement membrane. At sites of epithelial loss, found in the autologous phase, both albumin and ferritin were detected throughout the glomerular basement membrane. It is proposed that, in glomerular disease, leakage of plasma proteins may occur across the glomerular basement membrane at sites of endothelial or epithelial detachment.
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PMID:An ultrastructural study of the mechanisms of proteinuria in rat nephrotoxic nephritis. 32 69

Proteinuria was studied in ten renal allograft recipients; it was defined as: (a) glomerular--characterized by predominant albumin excretion; (b) tubular--significant excretion of both albumin and low molecular weight (LMW) proteins; and (c) glomerulo-tubular or mixed type, a combination of the two. LMW protein and albumin were quantitated by polyacrylamide gel electrophoresis with sodium dodecyl sulfate. In the immediate posttransplant period, LMW protein and albumin excretion, expressed as a percentage of creatinine clearance, were high, revealing a mixed pattern, and excretion of both protein classes was higher than during both acute tubular necrosis and acute rejection crisis. Tubular proteinuria was observed in acute tubular necrosis; a glomerulo-tubular or mixed pattern of protein excretion in acute rejection crises.
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PMID:Proteinuria following renal transplantation. 32 83

One month following a cadaver renal transplant for obstructive uropathy, a 27-year-old man developed diabetes mellitus. Two years later, marked proteinuria and decreased renal function were detected. Eight months later, a second decline in function occurred. Light microscopy of graft biopsy specimens obtained after each decline in renal function showed increased mesangial cells and matrix, thickening of Bowman capsule, and tubular atrophy with basement membrane thickening. Vascular changes, interstitial infiltrate, and fibrosis were not prominent. Electron microscopic studies of the second biopsy specimen confirmed the light microscopic changes; subepithelial dense deposits were also detected. Immunofluorescent studies of both biopsy specimens demonstrated linear staining of glomerular and tubular basement membranes and Bowman capsule for IgG and albumin. Antikidney antibodies were not detected in the patient's serum. These observations suggest development of the diffuse form of diabetic nephropathy in a renal homograft following steroid-induced diabetes mellitus.
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PMID:Development of a lesion resembling diabetic nephropathy in a renal homograft. 32 61

During the initial 50 days following transplantation of a cadaver kidney into 8 patients, determinations of 7 individual protein clearances were performed twice a week. This, the first posttransplantation investigation of single protein clearances utilizing unconcentrated urine, was made possible by the highly sensitive electroimmunodiffusion method of LAURELL [24]. The following results were obtained: 1. Kidney implantation was immediately followed by glomerulo-tubular proteinuria. In patients exhibiting good transplant tolerance the tubular proteins disappeared from the urine by the 43rd day at the latest; on the other hand, excretion of the glomerular proteins transferrin and albumin continued. In patients without complications the proteinuria was already highly selective by the 7th day (70 degrees). 2. In 5 of 8 patients there was a change in the proteinuria pattern during the rejection crisis: glomerulo-tubular proteinuria occurred three times and glomerular proteinuria twice. In two of these cases there was a change in the selectivity. 3. Patients with good tolerance showed plasma prealbumin levels which increased as a function of the time lapse since transplantation. 4. The plasma concentration of retinol-binding protein did not vary following transplantation and remained at 16.8 +/- 2.8 mg% in patients with uneventful course and at 18.5 +/- 4.9 mg% in patients with transplant rejection reactions, both values being markedly above the norm (4.7 +/- 1.1 mg%, [1 SD]).
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PMID:[Proteinuria and kidney transplantation. A quantitative immunochemical study of 7 protein clearances during the first 50 days following implantation of cadaver kidney]. 33 96

A mesangial glomerulonephropathy, characterized by the deposition of rat IgG, IgM, and C3 in the glomerular mesangium, was produced in Wistar rats by a prolonged administration of mercuric chloride (HgCl2). The HgCl2 was dissolved in sterile distilled water (0.2 mg. per ml.), and a group of 15 male Wistar rats was given injections subcutaneously three times a week on alternate days at a dosage of 0.15 mg. per 100 gm. of body weight for 27 weeks. A control group of nine rats was given injections of distilled water only. Mesangial glomerulonephropathy developed in 12 of 15 rats injected with HgCl2 and was characterized by the following: (1) coarse granular and nodular deposition of rat IgG, IgM, and C3 in the mesangium of all glomeruli, (2) absence of staining for rat albumin, IgA, and fibrin, (3) presence of electron-dense deposits in the mesangium, (4) focal and segmental proliferation of the mesangial matrix, (5) interstitial inflammation, (6) tubular atrophy, and (7) deposition of periodic acid-Schiff-positive material in the medulla adjacent to the thin limbs of the loops of Henle. Glycosuria and a slight increase in proteinuria were observed transiently in some rats. The blood urea nitrogen levels were normal in all rats. Eluates from the kidneys with heavy mesangial deposits contained rat IgG. However, the eluted antibody failed to react with normal rat kidney tissue components. None of the above findings were present in the control rats. The study provides a model of a mesangial nephropathy that seems to be immunologically induced; however, the mechanism for the formation and deposition of the immune deposits containing rat IgG, IgM, and C3, and the nature of the antigen(s) have not been elucidated.
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PMID:Mesangial glomerulonephropathy with deposition of IgG, IgM, and C3 induced by mercuric chloride: a new model. 37 39

The 24-hour urinary excretion of albumin, transferrin, haptoglobin, IgG, IgA, IgM, free lambda and kappa light chains from immunoglobulin, lysozyme, and beta2-microglobulin has been investigated in 22 patients with febrile diseases, using an automated immunoprecipitin reaction. The average excretion of the 10 proteins was significantly increased in the patients compared with a control group. In patients with body temperature is greater than or equal to 38.5 degrees C the tubular type of proteinuria was significantly increased compared with those with body temperature is less than 38.5 degrees C. Sequential studies in 10 patients showed that the tubular type of proteinuria occurred in all, whereas the glomerular type was demonstrated in 8. when the fever had subsided, the tubular proteinuria disappeared rapidly i in all patients, while the glomerular proteinuria disappeared in only 4 out of 8. It was shown that tubular proteinuria was caused by fever per se, and it is suggested that glomerular prteinuria might be due to an immue response to antigens, derived from the infectious agents, producing a transient or permanent glomerular injury.
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PMID:Urinary excretion of ten plasma proteins in patients with febrile diseases. 40 46

Three electrophoretic techniques are usually available in the clinical laboratories for the qualitative investigation of urinary protein patterns: 1) acetate cellulose, 2) immuno-electrophoresis; and 3) SDS-polyacrylamide gel electrophoresis. Proteinuria (the excretion of proteins in excess of 150 mg/day or 100 microgram/min) usually signifies either increased permeability of the glomerular-capillary membrane of diminished tubular reabsorption. Since glomerular disease is associated with an increased clearance of albumin and higher molecular weight proteins, whereas tubular damage is associated with the predominant excretion of proteins of lower molecular weight than albumin, it seems logical to establish a classification of proteinuria according to the molecular weight of its constituents. One can thus basically distinguish 5 types of proteinurias: 1) physiological; 2) tubular; 3) selective glomerular; 4) non selective glomerular; and 5) mixed proteinurias. Additionally one must distinguish "myeloma proteinurias" where monoclonal complete or incomplete gamma-globulins are found in the urine. Clinically it may be useful to determine the qualitatively normal or pathologic character of a quantitatively normal proteinuria, especially in the following conditions: 1) for early diagnosis of nephropathy in patients, such as diabetics, which are particularly prone to suffer from renal complications; 2) to confirm the clinical cure or to predict the recurrence of renal diseases; and 3) in such situations as orthostatic, or myeloma proteinuria, or any elevation of the urinary protein output of unknown etiology.
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PMID:Clinical relevance of different electrophoretic methods for the analysis of urinary proteins. 44 73

From the urine of a patient with proteinuria, the albumin protein component was isolated and compared with human serum albumin. By comparing the amino acid composition of the original proteins and their large cyanogen bromide fragments, peptide maps and N-terminal sequences of 33 amino acid residues, the identity of both proteins was shown.
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PMID:Chemical characterization of human urine albumin in proteinuria. 44

Plasma and urinary antithrombin III (AT-III) was measured in 15 cases of nephrotic syndrome. Plasma AT-III correlated well with serum albumin, but poorly with proteinuria, whereas urinary AT-III correlated well to proteinuria. The plasma AT-III level had a mean similar to 25 healthy controls, but the range was significantly wider. A case with nephrotic syndrome and left renal vein thrombosis is reported. The urinary output of AT-III rose and the plasma level fell with the activity of the disease. Although AT-III and albumin have similar molecule weight, their renal clearance was found to be different. It is suggested that urinary loss of AT-III plays a role in the hypercoagulable state sometimes found in the nephrotic syndrome.
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PMID:Antithrombin III and the nephrotic syndrome. 47 63

The suppressive effect of dipyridamole on the proteinuria of aminonucleoside nephrosis and protamine-induced proteinuria, was investigated. Male Wistar rats were given puromycin aminonucleoside (80 mg/kg s.c.) or protamine sulfate (20 mg/kg i.v.), and the urine was collected in metabolic cages. The content of proteins in the urine was determined by using a continuous gradient microgel electrophoresis procedure. Dipyridamole (20 mg/kg p.o.) suppressed the excretion of albumin and proteins larger than albumin (HMP) in aminonucleoside nephrosis. But the excertion of proteins smaller than albumin (LMP) was not affected by dipyridamole. Dipyridamole also suppressed the excertion of HMP in protamine-induced proteinuria, though the excretion of albumin and LMP was not affected. Puromycin aminonucleoside and protamine sulfate were known to cause renal glomerular epithelial changes referred to as "fusion" of foot processes. Since dipyridamole was effective in suppressing the both types of proteinuria, this drug was considered to improve the damaged renal glomerular barrier for plasma proteins.
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PMID:Suppressive effect of dipyridamole on the proteinuria of aminonucleoside nephrosis in rat. 48 Apr 1


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