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)

In a 10-year retrospective study, we evaluated the clinicopathologic features and renal immunofluorescence patterns of glomerulonephritis in 41 dogs. On the basis of results of histologic examinations, the dogs were segregated into 3 groups, including membranous (n = 12), mesangioproliferative (n = 15), or membranoproliferative glomerulonephritis (n = 14). No significant differences existed among groups in regard to age or duration of illness. Most dogs had been ill for one month or longer. The proportion of dogs with azotemia, anemia, and hyperphosphatemia were not different among the disease groups. Proportion of dogs with hypoalbuminemia and the severity of hypoalbuminemia were not different among groups. Highest urine protein losses and 24-hour urine protein/creatinine ratios developed in dogs with membranous glomerulonephritis. Although hypoalbuminemia and hypercholesterolemia were common (49%), the formation of edema or ascites was not (15%) and, therefore, few dogs had all of the classic features of the nephrotic syndrome. Few dogs suffered thromboembolic complications. Antinuclear antibody titers developed in 11 dogs, the highest titers developing in dogs with polyarthritis and systemic lupus erythematosis. Cellulose acetate electrophoresis detected alpha 2 and beta 1 globulin spikes in most dogs (87%). Results of renal immunofluorescence testing were positive in 36 dogs, using polyvalent antisera for immunoglobulins (Ig)G, IgA, IgM, and/or antisera for complement factor C3. When monovalent antisera for IgG, IgA, and IgM, and fibrinogen were used, immunofluorescence was not observed as often. The major fluorescent pattern was discrete multifocal segmental granular glomerular fluorescence, consistent with immune-complex deposition. Two dogs had linear glomerular staining patterns; however, antibodies directed against normal glomerular basement membrane were not found via elution studies. A high prevalence of glucocorticoid excess (treatment with glucocorticoids and spontaneous hyperadrenocorticism) (34%), chronic inflammatory skin disease (27%), neoplasia (17%), polyarthritis (12%), and systemic lupus erythematosis (7%) were observed as clinical problems concurrent with glomerulonephritis. In 5 dogs, treatment of glomerulonephritis with prednisolone (0.5 to 1.1 mg/kg) did not result in beneficial effects and in fact appeared to be detrimental, leading to azotemia and worsening proteinuria and physical condition in some of the dogs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinicopathologic, renal immunofluorescent, and light microscopic features of glomerulonephritis in the dog: 41 cases (1975-1985). 354 34

Effect of hypertension on progressive renal disease was examined in spontaneously hypertensive rats (SHR) with experimental focal glomerular sclerosis, produced by the intravenous administration of adriamycin (ADR). Serial changes of urinary protein, blood pressure and blood chemistry for 22 weeks after ADR-treatment, and renal histology at week 22, were compared between ADR-treated SHR (group ADR-HT) and ADR-treated SHR given antihypertensive drugs (group ADR-AH). Hypertension persisted in group ADR-HT, while blood pressure markedly decreased in group ADR-AH, after oral administration of antihypertensive drugs (guanethidine and hydralazine). Massive proteinuria, hypoalbuminaemia and hypercholesterolaemia were observed throughout the experiment both in group ADR-HT and in group ADR-AH. Urinary protein levels were significantly larger in the former at weeks 12 and 16. Blood urea nitrogen and serum creatinine levels increased progressively from week 16 in the ADR-treated rats. The increase was more rapid in group ADR-HT than in group ADR-AH. In group ADR-HT, 10 of 25 rats died between weeks 20 and 22, whereas all in group ADR-AH survived. Histologically, ADR-treated rats showed focal glomerular sclerosis with tubulointerstitial changes. The lesions were more extensive in group ADR-HT than in group ADR-AH. We conclude that hypertension influences the progress and prognosis of chronic progressive renal disease, as induced by adriamycin.
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PMID:Effect of hypertension on the progress and prognosis of experimental focal glomerular sclerosis. 370 73

Studies with two models of immunologically mediated glomerular disease in the rat, chronic serum sickness and Heymann nephritis, show that fluid retention can be dissociated from other signs of the nephrotic syndrome (excessive proteinuria, hypoalbuminemia, hypercholesterolemia). Clinical evidence of fluid retention (increased body weight, decreased hematocrit, ascites) was only detected in severe chronic serum sickness and coincided with an abrupt drop in urinary sodium concentration and sodium excretion. Severe proteinuria was not associated with sodium and water retention in moderate chronic serum sickness and in Heymann nephritis. These observations support the hypothesis that, in conditions of severe proteinuria, an intrarenal defect in sodium excretion rather than a systemic factor, leads to fluid retention.
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PMID:Absence of sodium and water retention in rats with severe proteinuria. 387 45

In order to determine the influence of hypertension on the progression of chronic glomerulonephritis, we studied the renal lesions in Heymann nephritis (autologous immune complex nephritis) produced in SHR. Nephritic SHR treated by AHD, normal SHR, nephritic WKYR, and normal WKYR served as controls. Induction of Heymann nephritis did not alter the blood pressure in either SHR or WKYR as compared with each untreated control group. Administration of AHD normalized the blood pressure of SHR. Proteinuria, hypoproteinemia, hypercholesterolemia, and reduction in body weight were significantly greater in nephritic SHR than in nephritic SHR treated by AHD or nephritic WKYR, whereas BUN and serum creatinine were unchanged in all the nephritic rats. Histological findings such as glomerular basement membrane thickening, IgG and C3 deposits along capillary walls, and subepithelial electron-dense deposits were similar in all nephritic groups. Glomerular sclerosis and tubulointerstitial changes were more marked in nephritic SHR than in the other nephritic groups. Severe vascular thickening and necrosis, intravascular thrombosis, and perivascular cell infiltration were frequently observed in nephritic SHR. These lesions are characteristic of malignant hypertension. However, they were not found in control SHR, which maintained elevation of blood pressure equivalent to that of nephritic SHR throughout the study. It was concluded that hypertension may aggravate nephritic manifestations such as proteinuria, hypoproteinemia, and hypercholesterolemia but not excretory renal function and that the hypertensive vascular lesions are augmented by Heymann nephritis.
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PMID:Influence of hypertension on the progression of experimental autologous immune complex nephritis. 621 70

Advances in our understanding of the mechanisms of proteinuria in humans have depended on a variety of animal models. Most of these have been partially satisfactory because they require pretreatment of the animal with chemicals or toxins or they depend on an aging-related glomerular protein leakiness. The strain in this study was obtained by Koletsky after selective inbreeding of the offspring from a hypertensive Kyoto-Wistar and a normotensive Sprague-Dawley rat. The affected animals appear in 25% of the litters, indicating an autosomal recessive gene, and present with a spontaneous and progressive nephrotic syndrome detected as early as 3-5 weeks and associated with obesity, hypertension, hypoalbuminemia, hypercholesterolemia, and hyperlipidemia. Preliminary morphologic and immunofluorescence studies of their kidneys show progressive glomerular segmental sclerotic lesions and prominent mesangial deposition of IgM, a picture which resembles a steroid-resistant form of idiopathic nephrotic syndrome in humans, namely, focal glomerular sclerosis.
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PMID:Spontaneous nephrotic syndrome in a genetic rat model. 650 87

Experimental autoimmune glomerulonephritis with pulmonary hemorrhage was induced in rats by a single injection of soluble antigen obtained from bovine glomerular basement membrane. Groups of rats were injected with various amounts of the nephritogenic antigen with Freund's complete adjuvant and killed 10 weeks later. Glomerulonephritis with linear deposition of IgG along the glomerular basement membrane developed in 7 of 10 rats injected with 10 micrograms of the antigen and all 20 rats of other 2 groups with 100 or 1,000 micrograms of the antigen. Pulmonary hemorrhage was observed in 21 of 27 rats with nephritis, and it was particularly severe in those injected with 1,000 micrograms. Glomerulonephritis with pulmonary hemorrhage and the linear deposition of IgG along with the glomerular basement membrane suggests that this model resembles human anti-glomerular basement membrane antibody-induced glomerulonephritis including Goodpasture's syndrome. The nephritic rats showed symptoms of nephrotic syndrome such as hypoalbuminemia, hypercholesterolemia and hypertriglyceremia, and the severities of these symptoms clearly depended on the degree of proteinuria.
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PMID:Experimental autoimmune glomerulonephritis with pulmonary hemorrhage in rats. The dose-effect relationship of the nephritogenic antigen from bovine glomerular basement membrane. 652 75

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

We have examined the effects of various levels of dietary protein intake on the course of nephrotoxic serum nephritis in the rat by feeding low (4.6% casein), standard (23% casein), and high (57.5% casein) protein diets which were identical in calorie, mineral, and electrolyte content. Nephritic rats on a high protein diet manifested heavy proteinuria, hypoalbuminemia, hypercholesterolemia, azotemia, and elevated serum creatinine levels. In those subjected to dietary protein restriction, proteinuria remitted and azotemia did not develop. While mesangial widening, interstitial abnormalities, and segmental proliferation and sclerosis of glomeruli occurred regularly in nephritic rats fed high protein diets, histologic abnormalities were virtually absent in those on low protein intake. Animals on a standard protein intake manifested histologic and clinical features intermediate in severity. We conclude that the renal functional and histologic consequences of nephrotoxic serum nephritis can be averted by dietary protein restriction.
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PMID:Amelioration of experimental glomerulonephritis by dietary protein restriction. 666 81

Lipids of the blood serum were studied in 29 patients with untreated nephrotic syndrome (NS) and in 28 patients treated with corticosteroids or nonsteroid drugs. None of the patients had evidence of renal failure, either acute or chronic. The patients with untreated NS showed massive proteinuria, marked hypoproteinemia, considerable hypertriglyceridemia and hypercholesterolemia. Serum high-density lipoprotein cholesterol (HDL cholesterol) concentrations were lower in these patients than in the control group, including 35 normal subjects, and correlated with the total serum protein (r = 0.46, p less than 0.05) and serum albumin (r = 0.46, p less than 0.05). An inverse correlation was observed between HDL cholesterol and serum triglyceride levels (r = -0.58, p less than 0.01). In the treated patients the laboratory indices of NS were less pronounced. HDL cholesterol levels were within normal limits in 14 patients with NS treated mostly with nonsteroid drugs, while in the patients receiving the corticosteroids (14 subjects) they were significantly higher than in the control group.
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PMID:High-density lipoprotein cholesterol in patients with untreated and treated nephrotic syndrome. 671 5

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


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