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)

Analgesic abuse is a major public health hazard in Australia, and analgesic nephropathy with consequent terminal renal failure is the underlying cause in 20% of the patients requiring dialysis and transplantation. Analgesics are invariably taken in the form of compounds and mixtures. In the aspirin-phenacetin-caffeine (APC) mixture, aspirin appears to be the major nephrotoxic agent and phenacetin appears to play a secondary and synergistic role. The renal disease associated with abuse of analgesics is characteristic and is part of a much wider clinical syndrome, the analgesic syndrome, which includes peptic ulcer disease (35%), anemia (60 to 90%), hypertension (15 to 70%), ischemic heart disease (35%), psychological and psychiatric manifestations, pigmentation, and possible gonadal- and pregnancy-related effects. The primary lesion in analgesic nephropathy is renal papillary necrosis (RPN), and this is a nephrotoxic effect common to all nonsteroid antiinflammatory agents. The most important factor in the management of patients with analgesic nephropathy is the cessation of analgesic abuse, and this leads to improvement and stabilization of renal function. A small proportion of patients will, however, deteriorate in relation to accelerated hypertension, persistent proteinuria, ischemic heart disease, and complications leading to nephrectomy. Patients with analgesic nephropathy are poor risk patients and have a poor prognosis, even after dialysis and transplantation.
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PMID:Analgesic nephropathy: etiology, clinical syndrome, and clinicopathologic correlations in Australia. 36 34

A human proximal renal tubular epithelial antigen (designated HRTE-1) was isolated and purified from a crude tubular preparation (Fx1A) by a process of salt fractionation, DEAE anion-exchange chromatography, and Sephadex G-200 gel filtration. Utilizing 125I-HRTE-1 and a rabbit antiserum specific for the proximal tubular brush border, as determined by immunofluorescent microscopy, a radioimmunoassay by competitive protein-binding was developed. HRTE-1 was demonstrated in serum and urine and in extracts of a variety of body organs. A range of concentrations for normal random urine samples and 24-hr urine excretion rates were determined. Random urine samples from 36 patients with a variety of functional and pathologic renal disorders were assayed for the HRTE-1 antigen. Twenty-three of 24 patients with either chronic nephropathy or pre-renal azotemia had normal urinary antigen concentrations, despite wide differences in urine flow rates, the degree of existing renal function, and the amount of proteinuria. Ten of 12 patients with acute tubular necrosis, however, had statistically abnormal HRTE-1 concentrations (high in eight patients, undetectable in two). These findings suggest that HRTE-1 antigen can be detected in both normal and pathologic urines, that altered antigen concentrations can be documented in at least one renal disorder, and that quantitation of HRTE-1 in urine may have clinical value as a marker of acute rubular injury.
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PMID:Radioimmunoassay for urinary renal tubular antigen: a potential marker of tubular injury. 36 38

Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) was shown to be reproducible in random urine specimens when expressed as the ratio of NAG to milligrams of urinary creatinine. The enzyme/creatinine ratio in 815 healthy people was relatively constant throughout childhood and adult life except for the first two years after birth and in individuals 56 years or greater. High ratios in the young children may be explained by low urinary creatinine excretion probably related to small body mass and reduced glomerular filtration rate at this age. The ratio was increased in adult uremic patients and children and adults with a variety of neurologic and obstructive lesions of the voiding mechanism. The presence of bacteriuria did not appear to increase the ratio. Significant enzymuria (greater than 2 SD above the mean for age and sex) was detected in 38 of 81 children with well-characterized renal disease. Among patients with predominantly glomerular disorders there was a close relationship between activity of the disease and enzymuria. In patients with tubulointerstitial disease enzymuria was frequent even in the absence of proteinuria. One of the highest enzyme/creatinine ratios was observed in a child with cystinosis. These studies indicate that NAG enzymuria is a sensitive indicator of activity of renal disease and may prove to be a suitable screening test for significant renal disease or injury in childhood.
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PMID:Enzymuria as a marker of renal injury and disease: studies of N-acetyl-beta-glucosaminidase in the general population and in patients with renal disease. 36 92

We produced an autoimmune glomerulotubular nephropathy in Swiss-Webster mice using human glomerular antigen in Freund's complete adjuvant. The disease is associated with circulating antibody to both mouse and human glomerular basement membranes (GBM) and tubular basement membranes (TBM). All mouse IgG subgroups are deposited initially in a linear pattern along the GBM and TBM. IgG deposition remains linear, while that of the other subgroups assumes a granular GBM pattern with continued linear TBM deposits. Despite tissue deposition of antibody capable of C-3 fixation, no C-3 is found in vivo along the GMB or TBM, nor is there C-3 fixation in vitro. This appears to be related to spatial limitations of IgG molecule attachment to basement membranes. A unique ultrastructural lesion of the GMB developed, characterized by periodic expansions of the lamina rara externa to form a beaded pattern. Eluate of nephritic kidneys contained all subgroups of IgG, but mainly IgG1 fixed in vitro to mouse kidney and in vivo when injected intravenously into normal mice. Fixation of other IgG subgroups in vivo may have resulted from antibody formation to abnormally formed GBM, thereby accounting for the peculiar ultrastructural findings and tissue fixation characteristics of the eluted immunoglobulin. Abnormal proteinuria without glycosuria or lysozymuria developed in test animals as compared to controls. Our model is similar in certain aspects to previously described models of Stebley nephritis, but differs because of the total involvement of TBMs, unique ultrastructural lesions, and dissimilarity to other reports of this model in mice.
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PMID:Autoimmune glomerulotubular nephropathy in mice. 36 49

Renal disease, particularly glomerulosclerosis, is a major cause of morbidity and mortality in patients with juvenile-onset diabetes mellitus. Signaled by the onset of proteinuria after 15 or more years of insulin therapy, progressive renal insufficiency due to glomerulosclerosis terminates in uremia within five years. Although some patients have benefited from chronic dialysis programs, the outcome in uremic diabetics has been considerably better if successful renal transplantation can be accomplished. Extrarenal complications of diabetes mellitus and recurrence of diabetic lesions in transplanted kidneys have hampered the recovery and rehabilitation of transplant recipients. Other renal diseases encountered in juvenile diabetics are reviewed.
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PMID:Grand rounds: Nashville VA Hospital--Vanderbilt University. Saturday conference: renal disease in the juvenile diabetic. 37 Oct 5

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

In a controlled trial, symptomatic treatment alone, or 12 weeks of cyclophosphamide or azathioprine were compared in Nigerian children with nephrotic syndrome (mainly quartan malarial nephropathy) and poorly selective proteinuria. Full remission in 2 patients in each of the two groups treated with drugs, and diminution of proteinuria in most patients in the cyclophosphamide group showed possible evidence of benefit. Infections during treatment were significantly more common in the drug-treated groups but were controllable. Mortality from renal failure in the 2nd year after treatment was significantly greater in the azathioprine-treated group than in the other two, suggesting that the drug may have exacerbated the nephritis. The 5-year survival rate was similar in the cyclophosphamide and the control group.
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PMID:A controlled trial of cyclophosphamide and azathioprine in Nigerian children with the nephrotic syndrome and poorly selective proteinuria. 37 45

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

Thirteen patients who had systemic lupus erythematosus were studied for the purpose of correlating the findings of light and electron microscopy and immunofluorescent studies with renal function and the presence of proteinuria. Subendothelial deposits of electron-dense material were found in all biopsy specimens, whereas mesangial and subepithelial deposits were not always present. IgG and beta 1c were constant findings in the glomerular membrane. The seven patients who were found to have extensive subendothelial deposits had moderate to massive proteinuria, and four of these patients had decreases in renal function. Most of the patients who had smaller subendothelial deposits had slight or insignificant proteinuria. Massive subendothelial deposits were mainly found in specimens showing histologic evidence of active lesions. Correlation was also found between proteinuria and the overall amount of deposits and their distribution. The prognosis was dependent on the severity of subendothelial deposits, the overall amount of deposits, and the morphologic form of lupus nephropathy.
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PMID:Lupus nephritis. Electron-dense and immunofluorescent deposits and their correlation with proteinuria and renal function. 38 26

Ten patients with familial Mediterranean fever (FMF) and histologically confirmed amyloidosis received cadaver kidney transplants for treatment of terminal renal disease. Colchicine, 1 mg daily, was included in the routine postoperative regimen from 1974 for amyloidotic patients. Graft and patient survival were compared with ten nonamyloidotic recipients of renal grafts matched for age, sex, type of allograft, and HLA compatibility. In the FMF group, five of ten grafts have survived from 20 to 64 months; in the control group, six of ten. While only recipients with functioning grafts survived in the FMF group, patient survival in the control group is eight of ten after one year. In all five FMF survivors, graft function is satisfactory, proteinuria is absent, and blood creatinine levels are normal. Amyloid involvement of an allograft was documented 16 months after transplantation in the only patient whose maintenance colchicine dosage had been reduced to 0.5 mg daily.
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PMID:Renal transplantation in the amyloidosis of familial Mediterranean fever. Experience in ten cases. 38 52


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