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)

The progression of adriamycin-induced nephrotic syndrome in rats was studied over a 3-month period. The effect of an angiotensin-converting enzyme inhibitor, captopril, on this model of renal disease, was also studied. Two weeks following a single iv injection of adriamycin, rats were divided into two treatment groups: one received a daily po dose of captopril and the other received a placebo. Measurements of renal function were performed at 4, 8, and 11 weeks following the initiation of therapy. Necropsies and light microscopic evaluation of the kidneys were performed at the end of the treatment period. Functional and morphologic alterations in both groups of rats were compared to each other and to normal age/weight-matched control rats studied over the same time period. At 13 weeks following the administration of adriamycin, both treatment groups had significant renal dysfunction when compared to normal controls. In addition to severe proteinuria, rats receiving adriamycin exhibited polyuria, polydipsia, increased plasma urea nitrogen and plasma creatinine, and decreased endogenous creatinine clearance. They had severe generalized kidney lesions characterized by tubular dilation and atrophy, cast formation, interstitial fibrosis and lymphocytic infiltration, and focal, global glomerulosclerosis. The histopathologic ranking of the kidneys was correlated with some antemortem laboratory parameters but not with the degree of proteinuria. Captopril had no ameliorating effects on the progression of renal disease. Certain findings indicate that captopril may actually have promoted the deterioration of renal function. We conclude that adriamycin-induced nephrotic syndrome in the rat is a progressive disease resulting in generalized renal dysfunction, and that captopril, at the dose given in this experiment, is unable to slow the progression of the disease.
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PMID:The progression of adriamycin-induced nephrotic syndrome in rats and the effect of captopril. 351 65

Calves (n = 4) were given neomycin (2.25 or 4.5 mg/kg) twice daily IM and were compared with 2 calves given penicillin IM. The 2 hallmarks of aminoglycoside toxicosis, nephrotoxicosis and ototoxicosis, were seen with both dosages of parenterally administered neomycin. Nephrotoxicosis was confirmed by abnormal findings in urinalysis (granular casts, proteinuria, low specific gravity), renal biopsy results (tubular degeneration and necrosis), and increased 24-hour amounts of urinary enzymes (alanine aminopeptidase and gamma-glutamyltranspeptidase). Azotemia, decreased creatinine clearance, polyuria, and polydipsia also were documented in calves given neomycin. Clinically, deafness was suspected in 2 calves and was documented by electrical auditory-evoked response tests. Abnormalities in partial thromboplastin times and renal residues of neomycin were seen in all 4 calves that were given neomycin, but not in calves that were given penicillin.
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PMID:Neomycin toxicosis in calves. 611 66

The chronic administration of captopril to Sprague-Dawley rats was performed under the barrier system by feeding ad libitum with mixed diet in various concentrations of captopril with 3 months recovery period. The number of animals was 180 female and 180 male including 5 groups of control, 30, 100, 300 and 900 mg/kg/day. The maximum nontoxic dose was estimated as about 30 mg/kg/day for male but a little more than this for female rats. Body weight increase was significantly reduced in male but for the first 3 months in female rats. No death was ascribed to the toxic effect of captopril. Polydipsia and polyuria in male, and the significant increase in values of BUN and inorganic phosphate in both sexes were observed. The reduction in erythrocyte count, values of hemoglobin and hematocrit, hemosiderosis in reticulum cells of the spleen and Kupffer cells in the liver and the increase of erythropoieses indicated hemolytic anemia. Heart weight reduced while kidney weight increased. Pathological examination revealed hypertrophia and hyperplasia of JG cells and thickening of walls of afferent arterioles with hyperplasia of vascular smooth muscle cells and increase of collagen fibers. Thickening of walls extended to walls of the interlobular arteries which remained after withdrawal of captopril for 3 months though JG granules attenuated. The age-related increases of incidences of proteinuria and myocardial fibrosis were attenuated dose-dependently which are probably due to hypotension induced by captopril.
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PMID:[Twelve month studies on the chronic toxicity of captopril in rats]. 627 84

The nephrotoxic properties of the chemical N-(3,5-dichlorophenyl)-succinimide were investigated in rats with a view to establishing the usefulness of this chemically-induced nephritis as a model of chronic interstitial renal fibrosis. The compound was synthesized and given daily by gastric intubation as a suspension in arachis oil B.P. to male WAG-strain rats, for periods of up to 108 days. Polydipsia and polyuria resulted rapidly in all treated animals and persisted for the duration of the experiment. There was a progressive increase in the extent of proteinuria in all treated animals and, by the end of the experiment, there was an increase in the plasma levels of urea and creatinine. Short term treatment (up to 3 days) resulted in focal areas of necrosis of some proximal convoluted tubules. Treatment for 28 days resulted in patchy but severe tubular interstitial nephritis with which was associated a moderate interstitial fibrosis. By 108 days, the nephritis was more widespread and the interstitial fibrosis was severe. The activity of proline hydroxylase, a part of the intracellular sequence of collagen synthesis, showed progressive increase in the renal cortex throughout the experiment and there was an associated increase in the cortical hydroxyproline content, a measure of the amount of collagen present. Associated with this biochemical evidence of an active, chronic fibrosis, was an increased water content of the cortical tissue. The results indicate that this chemically-induced, tubular interstitial nephritis is indeed a good and reliable model of interstitial renal fibrosis.
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PMID:Experimental interstitial renal fibrosis in rats: nephritis induced by N-(3,5-dichlorophenyl)succinimide. 631 Dec 37

A 45-year-old male was admitted to the hospital because of polyuria and polydipsia. After admission, proteinuria and hematuria were found. The kidney function deteriorated and necessitated the initiation of chronic hemodialysis. Examination of the bone marrow revealed multiple myeloma and kappa light chains were found in the urine. The kidney biopsy showed membranoproliferative glomerulonephritis with dense deposits in the glomerular basement membrane.
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PMID:Multiple myeloma presenting as dense deposit disease. Light chain nephropathy. 640 20

Oligomeganephronia (OMN) is characterized by a reduced number of nephrons, with compensatory hypertrophy of the remaining glomeruli and tubules. The clinico-pathological features of six cases seen at The Hospital for Sick Children, Toronto were reviewed. One patient presented in infancy (10 days of age), the others between 12.8 and 14.5 years (mean 13.7 years), with long-standing polydipsia and polyuria, enuresis, and growth retardation. All patients had proteinuria which tended to increase as the disease progressed. At renal biopsy, four patients showed significant proteinuria (greater than 1.3 g/24 hr). Biopsies from these patients showed focal segmental glomerulosclerosis (FSGS) and all have rapidly progressed to dialysis/transplantation. The two remaining patients had lesser degrees of proteinuria (less than 0.3 g/24 hr) and no evidence of FSGS on biopsy; however, they are currently in chronic renal failure (mean serum creatinine 2.8 mg/dl). We conclude that increasing proteinuria in patients with OMN heralds the development of FSGS, presumably due to functional overload of the reduced nephron number. This is associated with a rapid decline in renal function.
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PMID:The significance of focal segmental glomerulosclerosis in oligomeganephronia. 649 Mar 19

Ochratoxin A was isolated from a culture of Aspergillus ochraceus grown on a cornmeal substrate. The mycotoxin was added to a grower ration for 14 kg young pigs at 2, 4, 8 and 16 mg/kg and fed to groups of 3 for periods ranging from 6 to 20 days. The highest dose rate group only became sick, with loss of appetite, weight loss, polydipsia, polyuria, proteinuria, glucosuria, elevation of serum creatinine, pale swollen kidneys, renal tubular degeneration and cortical fibrosis. The pigs on the 2 mg toxin/kg of diet appeared unaffected with only slight renal tubular degeneration present in one animal. Feeding diet contaminated with the intermediate doses of 4 and 8 mg toxin/kg diet lead to reduction of weight gain and/or reduced feed intake and feed conversion efficiency as well as mild renal lesions. Ochratoxin A has recently been reported on mould-affected grain in Queensland and some local strains of A. ochraceus in culture have been shown to be able to produce levels of ochratoxin A of up to 4000 mg/kg of substrate. Rare episodes of nephrotoxicity in pigs seen at slaughter in Queensland may thus be due to prior contamination of the diet with ochratoxin A.
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PMID:Experimental ochratoxicosis A in pigs. 649 7

Chronic renal failure was diagnosed in 6 young Standard Poodles from 2 related litters. Clinically, the disease was characterized by polydipsia, polyuria, anorexia, lethargy, vomiting, and bony deformities suggestive of fibrous osteodystrophy. Laboratory evaluation revealed azotemia and hypercholesterolemia in all 6 dogs and nonregenerative anemia in 3 dogs. Two dogs had hyperphosphatemia and another 2 were hypercalcemic. Isosthenuria and proteinuria were found in both dogs for which urinalyses were available. The kidneys were characterized pathologically by interstitial fibrosis, variable interstitial infiltrates of lymphocytes and plasma cells, tubular atrophy, tubular dilatation, tubular basement membrane mineralization, cystic glomerular atrophy, and immaturity of glomeruli, with inconspicuous capillary lumens.
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PMID:Juvenile renal disease in related Standard Poodles. 662 80

Renal failure was diagnosed in 22 young Doberman Pinscher dogs. The clinical findings were anorexia, weight loss, vomiting, lethargy, polydipsia, polyuria, and dehydration. Laboratory findings were azotemia, hyperphosphatemia, lymphopenia, nonregenerative anemia, hypercholesterolemia, and proteinuria. The kidneys were characterized pathologically by glomerular sclerosis, cystic glomerular atrophy, tubular dilatation, tubular atrophy, mononuclear interstitial inflammation, interstitial fibrosis, interstitial mineralization, and hyperplasia of the collecting duct epithelium.
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PMID:Juvenile renal disease in Doberman Pinscher dogs. 683 84

Nephronophthisis is a chronic interstitial nephropathy which in childhood may lead to terminal renal failure. Between January 1975 and July 1980, 41 children with terminal renal failure were seen in our service, of which 10 (21.9%) presented with nephronophthisis. Age of the patients ranged from 3.5-18 years, boys were in the majority (8/2). Three cases were isolated and 7 were familial (3 families). Onset was during the first year of life in 8 patients, and polydipsia-polyuria were the first symptoms. Retarded growth and anemia proportionate to the degree of renal failure were present in all patients. When diagnosed, 5 patients (50%) presented terminal renal failure, and the other 5 had renal failure of different degrees. Moderate proteinuria was found in 4 patients, without changes in urine sediment. Sodium depletion in urine was high in 5 cases and maximal urine osmolarity was less than 500 muOsm/l after hydropenia in all cases. Four had associated mental deficiency with cerebellar ataxia associated in two and congenital hepatic fibrosis (confirmed histologically) in one. The diagnosis was confirmed by biopsy in 8 and in two of these on frozen section during nephrectomy prior to kidney transplantation. At present, five of the patients are in maintenance hemodialysis, two died at home due to cardiovascular complications in terminal renal insufficiency and the remaining ones presented different degrees of renal insufficiency. Time elapsed between onset of the symptoms and inclusion in hemodialysis or death ranges form 6 months to 13 years (mean 6.7 years).
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PMID:[Nephronophthisis: study of 10 cases. Incidence, natural history and associated pathology (author's transl)]. 732 36


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