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)

We followed renal function through the natriuretic phase of 6 occasions of drug-induced recovery from minimal lesions nephrotic syndrome (MLNS). Protein excretion started to fall 1-3 days prior to the start of the natriuresis. The natriuresis was accompanied by a rise in glomerular filtration rate (GFR, inulin clearance). The filtration fraction, calculated from the GFR and the p-aminohippurate clearance, rose steadily in 5 subjects in whom it was low before therapy. Proximal and distal sodium reabsorption fractions, estimated from the changes in maximum free water clearance, fell, and fractional sodium, lithium, uric acid and free water clearance rose. At the time of these changes plasma protein had hardly risen, whereas renin activity was down. These results are in agreement with the notion that the sodium retention of MLNS is due to a renal defect. Repair of the glomerular filter, evident from the disappearance of proteinuria and the rise in filtration fraction, apparently normalizes the elevated tubular sodium reabsorption proximal to the macula densa, which leads to a fall in renin release.
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PMID:Renal function during recovery from minimal lesions nephrotic syndrome. 331 90

The effect of converting enzyme inhibition (CEI) by captopril (CAP, 500 mg/liter drinking water) on the development and progression of glomerulosclerosis (GS) was studied in six groups of male uninephrectomized (UN) Wistar rats. In group A, treated with CAP for four to five weeks after UN, a reduction in systolic blood pressure (SBP), filtration fraction and glomerular volumes was found as compared to control group B. Long-term treatment with CAP for eight months after UN (group C) resulted in lowering of SBP with 30 mm Hg, a low level of proteinuria and low incidence of GS (0 to 1.5%) as compared to control rats (group D), with SBP of 131 +/- 4 mm Hg, proteinuria up to 103 to 509 mg/day and 9.1 to 29.7% GS at eight months after UN. Groups E and F were followed without therapy up to seven months after UN, at which time a high level of proteinuria was present. CAP therapy then started in group E, did not reduce SBP, proteinuria and GS at 11 months after UN relative to control group F. This study shows that early CEI prevents progressive proteinuria and GS in rats after UN and is associated with a reduction in SBP, filtration fraction and glomerular volume. Once high levels of proteinuria and GS have developed in rats after UN, CEI has no effect on SBP nor on the progression of GS and proteinuria.
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PMID:Converting enzyme inhibition and progressive glomerulosclerosis in the rat. 332 1

Forty-six patients who developed a Hemolytic Uremic Syndrome (HUS) during the period 1970-1976, were examined ten years later. Thirty-two individuals had no signs of renal disease whereas fourteen showed at least one abnormality. In the latter group a urinary osmolality below 800 mosmole per kg water was the most frequent defect found (eight cases). Three adolescents had both hypertension and proteinuria, which are considered as important late sequelae.
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PMID:Hemolytic uremic syndrome in childhood: renal function ten years later. 335 1

Gentamicin doses of 40 mg/kg body weight/day were administered intravenously to 62 Wistar rats. Nineteen animals were also treated orally with an NaHCO3 solution in place of water. The gentamicin-treated animals showed increased albuminuria immediately after the 3rd day of treatment. The fact that this increase was marked and that it also occurred at similar intensity in the animals treated with gentamicin and NaHCO3 whose tubular lesions were less serious suggests that the proteinuria was of glomerular origin. Albumins with different electrophoretic mobilities were also detected in the urine of these animals. Therefore, the change in electrical charge of the albumin may have contributed to albuminuria and to the nephrotoxicity induced by gentamicin.
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PMID:Analysis of urinary albumin excretion in gentamicin-treated rats. 338 Feb 30

(2R,5R)-6-heptyne-2,5-diamine (MAP; MDL 72175), a potent irreversible inhibitor of L-ornithine decarboxylase (ODC), possesses immunosuppressive activities in vitro as the result of inhibition of lymphocyte polyamine biosynthesis. The effects of MAP were now studied in vivo in MRL-lpr/lpr female mice, an animal model for human systemic lupus erythematosus (SLE). Administration of MAP (0.2% in drinking water; drug intake: 0.25-0.35 g/kg body weight/day) to female mice for 15 weeks, starting 8 weeks after birth, reduced by 47% the number of spleen cells, retarded development of lymphadenopathy and, at that time, markedly prolonged the survival of the mice. At week 23, MAP reduced plasma IgG concentrations by 50% whereas, in contrast, those of IgM were elevated 1.5-fold. No statistically significant effects of MAP were observed on plasma levels of anti-DNA autoantibodies although serum anti-RNP and anti-Sm titres tended downwards during treatment. Neither glomerular lesions nor proteinuria were improved by MAP administration. Finally chronic administration of MAP for 45 weeks prolonged the median survival time from 29.75 to 35.5 weeks.
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PMID:Immunosuppressive effects of (2R,5R)-6-heptyne-2,5-diamine, an inhibitor of polyamine synthesis: II. Beneficial effects on the development of a lupus-like disease in MRL-lpr/lpr mice. 340 47

In adult rats influences of single doses of bendamustin (0.5, 1 or 5 mg/100 g b.wt. i.p.) on kidney function were measured (time of experimentation 8 d following administration). Bendamustin administration is followed by an increase of kidney weight caused by a higher water content of kidney tissue. An increase of plasma concentrations of creatinine and of urea following bendamustin (1 or 5 mg/100 g b.wt. i.p.) indicates a reduced excretion capacity of kidney. Bendamustin administration is not connected with a distinct proteinuria. The highest administered does (5 mg bendamustin/100 g b.wt. i.p.) caused an oliguric effect connected with a distinctly reduced renal excretion of osmotically active substances. There is a distinct diminution of renal excretion of sodium following bendamustin administration and a decrease of renal excretion of PAH can be stated. It is most likely that bendamustin can reduce the glomerular function: Following administration of 1 mg bendamustin/100 g b. wt. i.p. CIn is reduced whereas a statistically significant increase of tubular transport capacity for organic anions can be measured (TmPAH).
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PMID:[Renal actions of bendamustin (Cytostasan) in rats]. 341 16

The fawn-hooded (FH) rat develops hypertension spontaneously. Systolic blood pressure is already elevated at 5 weeks of age, increases with age, and the final range is 180-240 mmHg at the age of 1 year. Concomitantly with the rise in blood pressure proteinuria occurs and increases with age. Fawn-hooded rats reaching the accelerated phase of the hypertension are characterized by blood pressure values exceeding 220 mmHg, heavy proteinuria and increased heart, kidney, liver, adrenal and spleen weights. Those prone to malignant hypertensive disease show a period of increased water turnover for several weeks after weaning; during this period, they do not show the pronounced decrease in water intake upon fasting for 24 h as observed in FH rats of the same age prone to a milder form of hypertension, i.e. diuresis and drinking continue even when no food is consumed. The major cause of death for FH rats is malignant nephrosclerosis with the nephrotic syndrome and/or cardiac failure with chronic pulmonary congestion. Some animals die of bleeding from mesenteric vessels with periarteritis nodosa. In FH rats with malignant hypertension, heart, kidney, liver and spleen weights are significantly increased compared with FH rats of the same age with mild hypertension. Histopathology shows myocardial fibrosis and myocardial infarctions. Generalized arteriolosclerosis is common, sometimes accompanied with local fibrinoid degeneration and (peri)arteritis. Some major arteries show intimal proliferation. It is concluded that the FH rat provides an interesting model for the study of hypertension and its consequences.
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PMID:Spontaneous hypertension in the fawn-hooded rat: a cardiovascular disease model. 346 7

Immediate and longer-term (five-day) effects of indomethacin on proteinuria and renal function were examined in a group of nephrotic subjects with glomerular filtration rates (GFR) that ranged from near normal to moderately impaired. The modifying role of the patients' sodium/volume (S/V) status on renal prostaglandin inhibition was systematically evaluated by renal clearance and balance studies. After patients were S/V-depleted for five days, indomethacin (75 mg/d) decreased protein excretion by 45%. The decrement in proteinuria was greater than 2 times greater than the fall in creatinine clearance and was unrelated to baseline clearance. In acute clearance studies, 75 mg indomethacin administered orally immediately reduced protein excretion, effective renal plasma flow (CPAH), GFR (C inulin), Na, K, and free water excretion. Indomethacin responsiveness (reduced proteinuria) correlated with the change in PGE2 excretion. The effect of indomethacin on protein excretion and renal hemodynamics was apparent, but blunted, when dietary Na intake was increased to 200 mEq/d. Mean BP increased during indomethacin therapy only when patients were S/V-expanded.
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PMID:Reduction of proteinuria by indomethacin in patients with nephrotic syndrome. 346 3

In this study, we examined the effect of an immunoregulatory antirheumatic agent, lobenzarit disodium (CCA), on spontaneously developing glomerulonephritis in MRL/Mp-lpr/lpr (MRL/l) mice. Starting from 6 weeks of age, mice were given CCA orally 5 days a week at a dose of 2 or 10 mg/kg. A control group was given the same volume of distilled water. The CCA treatment suppressed the excretion of protein in the urine. At 40 weeks of age, the incidence of proteinuria was 10/10 in the controls, 6/10 in the 2-mg/kg treatment group, and 5/10 in the 10 mg/kg group. The life span was prolonged dose dependently. The 50% survival time was 33 weeks for the controls, 35.5 weeks for the 2-mg/kg group, and 41 weeks for the 10-mg/kg group. The serum levels of anti-ssDNA antibody, anti-TNP antibody, and rheumatoid factor (RF) of the Ig G isotype and immune complex were reduced compared with control group. But the antibodies of Ig M isotype were not reduced. The serum Ig G1, Ig G2, and Ig G3 were significantly lower in the CCA-treated mice than in the controls. But again the serum level of Ig M was unchanged. These effects of CCA may be based on the suppression of lymphadenopathy. CCA may correct abnormal B-cell growth and differentiation factor release by the MRL/l abnormal T cells. These results show that CCA inhibits the development of lupus nephritis in MRL/l mice through the amelioration of the abnormal immune response, polyclonal B-cell activation.
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PMID:An immunomodulating anti-rheumatic drug, lobenzarit disodium (CCA): inhibition of polyclonal B-cell activation and prevention of autoimmune disease in MRL/Mp-lpr/lpr mice. 350 2

Diabetic ketoacidosis is often associated with a temporary increase in protein excretion, but the mechanisms are not completely known. The aim of the present study was to examine the effect of acute experimental moderate ketosis on kidney function and specifically on protein handling using an infusion of 3-hydroxybutyrate in healthy subjects. Seven young healthy males were infused with sodium 3-hydroxybutyrate, the peak blood level attained being 1.96 +/- 0.53 mmol/l (SD). The pH in blood and urine rose significantly from 7.40 +/- 0.03 to 7.45 +/- 0.05 (2p less than 0.01) and from 7.29 +/- 0.79 to 8.51 +/- 0.82 (2p less than 0.01), respectively. Urinary beta-2-microglobulin excretion rose significantly from 0.038 microgram/min x/ divided by 1.9 to 0.082 microgram/min x/ divided by 1.4 (geometric mean x/ divided by tolerance factor) (2p less than 0.01) but urinary albumin excretion was unchanged. No changes were seen in blood pressure, glomerular filtration rate and renal plasma flow. A marked reduction in urine flow from 15 to 5 ml/min was noted, but could not be attributed to changes in plasma arginine-vasopressin, which was reduced before and during infusion due to considerable oral water loading. It is concluded that moderate elevation in blood ketone body levels does not induce albuminuria. It is suggested that the temporary proteinuria present in diabetic ketoacidosis may be related to acidosis per se.
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PMID:Effect of 3-hydroxybutyrate infusion on urinary protein excretion in healthy man. 352 Jul 91


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