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)

Proteinuria developed in six of 81 hypertensive patients given captopril for at least four months (protein excretion, greater than 200 mg/24 hr). Two had previously elevated protein excretion. In all patients the increased protein excretion occurred by the fourth month of treatment. It subsided in four after two to nine months, despite continued therapy. In two of the four, proteinuria cleared completely within seven months after onset, while in the other two it subsided to the range of 600 mg/24 hr. However, in the remaining two patients proteinuria persisted during captopril therapy and was associated with hypoalbuminemia and hypercholesterolemia. Renal biopsy specimens showed mild membranous nephropathy in two patients, one of whom had a remittance of proteinuria during continued captopril treatment.
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PMID:Proteinuria during long-term captopril therapy. 699

Accumulation of glomerular foam cells were seen in a kidney biopsy of a 59-years old patient with persistent proteinuria and mild renal insufficiency. Further investigations revealed hypercholesterolemia, hypertriglyceridemia, normal activity of LCAT, absence of lipoprotein x. Foam cells which were shown by histochemical methods to be loaded with intracytoplasmic cholesterol were found in bone marrow. These findings strongly suggest cholesterol-ester-storage disease with glomerular involvement.
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PMID:[Mesangial lipidosis associated with cholesterol polycoria]. 714 95

Twin and family studies have revealed genetic and maternal influences on plasma cholesterol. This study was designed to identify familial and environmental variables related to cholesterol levels in children. Volunteer families (n = 74) were obtained from a previous study of cord blood cholesterol. When the children were 2.5 years old, blood samples, dietary histories, heights, weights, and skinfold thicknesses were obtained. Dietary variables were significantly correlated with plasma cholesterol levels in children but not in their parents. Stepwise multiple regression was used to identify sets of variables predictive of plasma cholesterol fractions of these children. For plasma total cholesterol, the set included previous history of breast feeding (versus formula), child's current dietary poly-unsaturated/saturated fatty acid ratio, maternal alcohol and fat consumption, paternal cholesteryl esters, and maternal hematocrit (r = 0.53). Free cholesterol had a similar predictive variable set (r = 0.52). More variation in esterified cholesterol of children was predicted (r = 0.69) by history of breast feeding, child's current protein and caloric intake, maternal total and esterified cholesterol, and proteinuria during pregnancy. Cord blood cholesterol was not predictive of any later cholesterol measurement. These correlations of children's plasma cholesterol with multiple factors emphasize the importance of focusing on very early childhood for study of both the normal developmental pattern of human cholesterol and intervention to prevent adult hypercholesterolemia.
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PMID:Determinants of plasma cholesterol in children--a family study. 735 82

We investigated the effects of cyclosporin A (CyA) on accelerated passive Heymann nephritis, an experimental model of membranous nephropathy, that is characterized by immune complex deposition on the glomerular basement membrane. The nephritis was induced in rats by injection of antiserum against the antigen located in the renal tubular brush border membrane and sensitization with rabbit gamma-globulin. CyA was administered p.o. at the dose of 2.5, 10 or 20 mg/kg/day for 40 days after the injection of the antiserum. The administration of CyA resulted in marked suppression of proteinuria and hypercholesterolemia in the nephritic rats. In light microscopy, nephritic control rats showed thickening of the glomerular basement membrane and spike formation in the glomeruli. CyA significantly reduced the appearance of the glomerular alteration. The production of antibody was dramatically attenuated by CyA administration. However, CyA did not decrease the number of circulating white blood cells and platelets below the normal level. In conclusion, CyA suppressed the progress of accelerated passive Heymann nephritis in a dose-dependent manner. The effect of CyA is likely attributable to the powerful depression of antibody production.
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PMID:[Effects of cyclosporin A on experimental nephritis in rats (2): Cyclosporin A suppresses the development of accelerated passive Heymann nephritis]. 750 79

Activity of the renin-angiotensin system in the nephrotic syndrome was investigated in rats with acute nephritis induced by anti-glomerular basement membrane (GBM) antibody. Injection of anti-GBM antibody resulted in a transient 2-fold elevation of both plasma renin and angiotensinogen with a peak at 12 h. Angiotensinogen mRNA levels in the liver also rapidly and transiently increased 4-fold at 3 h. The manifestation of acute nephritis, indicated by proteinuria, hypoalbuminemia, hypercholesterolemia and an increase in serum creatinine, following injection of anti-GBM antibody, was inhibited by a single administration of the selective angiotensin II type 1 receptor antagonist TCV-116 (1 mg/kg, p.o.) 2 h before an injection with the antibody, but not by successive administration of this drug for 1 week from 3 d after the injection of antibody. These results suggested that the enhanced generation of angiotensin II by elevated levels of both renin and its substrate in the early phase of anti-GBM nephritis promotes the evolution of acute nephritis via angiotensin II type 1 receptor.
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PMID:Activation of the renin-angiotensin system in anti-glomerular basement membrane antibody-induced glomerulonephritis. 755 93

During 1984 to 1991, 54 out of 569 lupus nephritis patients at Siriraj Hospital were male (F:M sex ratio = 10:1). Mean age of the males was 29.8 +/- 14.6 years, range 12 to 69. The three most common extrarenal manifestations were anemia, cutaneous, and musculoskeletal involvement (74.5, 51.1, and 43.9%, respectively). The major renal manifestations were edema (75.9%) with heavy proteinuria over 3.5 g/day in 62.2% and nephrotic/nephritic findings in 51.9% of cases. Hypertension was found in 35.2%. Mean serum creatinine was 2.0 +/- 1.4 mg/dl while 60.5% of cases had creatinine clearance below 50 ml/minute. Mean serum albumin was 2.6 +/- 0.8 g/dl, cholesterol 262.8 +/- 129.5 and triglycerides 343.2 +/- 244.6 mg/dl. Interestingly, hypercholesterolemia (> 250 mg/dl) was found only in 44.8% of cases with nephrotic syndrome. Antinuclear antibody was demonstrated in 91.5%, anti-dDNA antibody in 64.4% and LE cells in 40.4% of cases. Renal biopsy was done in 45 patients and 30 cases (66.7%) were classified as diffuse proliferative nephritis (WHO type IV), 15.6% of type II, 6.7% each of type III and V, with the rest of type V plus IV (4.4%). Tubulointerstitial inflammation was found in 77.3% of cases. During the follow-up period (42 +/- 35.8 months), 6 patients died. The cause of death were uremia in 3, infection in 2, and cardiac failure in 1. By life-table analysis, the probabilities of survival for 1 and 5 years were 89.5 and 80.6%, respectively. In comparison between sexes, except for a higher amount of urinary protein excretion (4.5 +/- 3.1 vs 3.5 +/- 3.0 g/day, p < 0.05), there were no statistically significant differences in clinical and pathological parameters, and probability of survival.
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PMID:Lupus nephritis in males: 8-year experience at Siriraj Hospital. 761 14

The Strong Heart Study, a study of cardiovascular disease among American Indians, was conducted to determine cardiovascular disease rates and the prevalence of risk factors among members of 13 tribal groups in South Dakota/North Dakota (SD/ND), southeastern Oklahoma, and Arizona. From 1989 to 1992, 4,549 tribal members aged 45-74 years (62% of eligible participants) were surveyed and examined for cardiovascular disease and its risk factors. Mean total cholesterol concentrations were over 20 mg/dl lower among the men and 27 mg/dl lower among the women than national mean levels for the same age groups. Cholesterol levels varied by tribal group; Arizona Indians had mean levels more than 20 mg/dl lower than those of SD/ND Indians. The prevalence of hypercholesterolemia was almost twice as high among SD/ND Indians as among Arizona Indians, but the rates for all three groups were much lower than total US rates (all races). Mean levels of high density lipoprotein cholesterol were lower among Indian men and women than in the US population as a whole. The prevalence of hypertension among Arizona and Oklahoma Indians was higher than that for the entire United States. SD/ND Indians had significantly lower mean blood pressures and prevalence rates of hypertension than Oklahoma and Arizona Indians and the United States as a whole. The prevalence of cigarette smoking was higher for all Indian groups except Arizona women in comparison with US rates. Smoking rates were highest in SD/ND and lowest in Arizona. Indian smokers smoked fewer cigarettes per day than the average US smoker. Arizona Indians had the highest prevalence of diabetes mellitus; over 60% of those participants were diabetic. In Oklahoma and SD/ND, one third of the men and over 40% of the women were diabetic. In addition, 13-20% of the participants had impaired glucose tolerance. Proteinuria was also a common problem; almost half of the Arizona Indians had micro- or macroalbuminuria, and 20% of Oklahoma and SD/ND Indians had significant proteinuria. The prevalence of obesity was high in all three groups, with Arizona Indians having the highest rates and the highest mean body mass indices. The prevalence of current alcohol use was lower among Indians than in the nation as a whole, but binge drinking was common among those who used alcohol. These results indicate that cardiovascular disease risk factors vary significantly among tribal groups. Prevention programs tailored toward decreasing the prevalence of risk factors are recommended for long-term reduction of cardiovascular disease rates in American Indian communities.
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PMID:Cardiovascular disease risk factors among American Indians. The Strong Heart Study. 763 31

Effects of 12 months of simvastatin treatment were examined in 48 NIDDM patients with total serum cholesterol levels exceeding 220 mg/dl and were compared with those in 35 nondiabetic patients with hypercholesterolemia. In the diabetic group, 5-10 mg of simvastatin given once daily at bedtime significantly lowered total cholesterol (21%). LDL cholesterol (28%), apoB (15%) and triglycerides (8%) levels. These changes were identical to those in the nondiabetic group, except for triglycerides which did not change significantly. HDL cholesterol increased significantly in the nondiabetic group but not in the diabetic group. The reductions in LDL cholesterol and apoB in hypercholesterolemic patients with NIDDM were not influenced by gender, age, glycemic control, the presence or absence of systemic hypertension, obesity and overt proteinuria. In addition, the decrease in LDL cholesterol was not affected by the number of risk factors per patient. Simvastatin did not significantly alter hemoglobin A1c or fasting plasma glucose and was well tolerated in both groups. Simvastatin produced beneficial effects on serum lipids and apolipoproteins and neutral effects on glycemic control in hypercholesterolemic patients with NIDDM, whether or not they had an additional atherosclerotic risk factor.
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PMID:Long-term effects of simvastatin in hypercholesterolemic patients with NIDDM and additional atherosclerotic risk factors. Hyogo Simvastatin Study Group. 764 76

Lipid abnormalities have been implicated in the pathogenesis of glomerulosclerosis in experimental models of kidney disease. In previous studies it has been shown that Adriamycin-induced nephropathy is associated with reduced activities of glomerular proteinases. This observation led to the hypothesis that reduced proteolytic activities may be responsible for mesangial protein accumulation, which ultimately leads to global sclerosis of the glomerular tuft. The aim of the present study was to investigate whether lovastatin treatment, which prevents progressive glomerulosclerosis in experimental nephrotic syndrome, would also have an effect on glomerular proteinase activities. Adriamycin administration resulted in a persistent nephrotic syndrome with gross proteinuria (377 +/- 26 mg/24 h), hypoalbuminemia (2.1 +/- 0.12 vs. 2.8 +/- 0.02 g/dl), hypercholesterolemia (575 +/- 74 vs. 68 +/- 1.5 mg/dl) and elevated triglyceride levels (1,155 +/- 78 vs. 57 +/- 8 mg/dl). Glomerular azocaseinolytic activities both at pH 5.4 (-21%) and 7.4 (-37%) were significantly reduced. In contrast to human subjects, nephrotic rats that were treated with lovastatin displayed reduced triglyceride levels (767 +/- 134 mg/dl); their serum cholesterol, however, remained unchanged. In terms of glomerular proteolytic enzyme activities, the decline in azocaseinolysis at both pH values was, at least partly, prevented by lovastatin. On the basis of these data, it appears that the beneficial effect of lovastatin on the evolution of glomerulosclerosis in the nephrotic rat is associated with the conservation of glomerular proteolytic activities.
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PMID:Lovastatin ameliorates depressed intraglomerular proteolytic activities in experimental nephrotic syndrome. 771 42

Overt proteinuria is often accompanied by hypercholesterolemia and is associated with increased lipoprotein(a) levels. These lipid abnormalities are probably involved in the high incidence of macrovascular complications associated with diabetic nephropathy and possibly other kinds of non-diabetic proteinuric renal disease. Over the last decade many studies have shown that ACE inhibitors can reduce urinary protein excretion but little attention was paid to the impact of this form of therapeutic intervention on the lipid profile. In this article we review our recent data showing that fosinopril administration was associated with significant decreases in both urinary protein excretion, serum total cholesterol levels, and plasma lp(a) levels. The use of ACE inhibitors in patients with renal impairment can result in the development of hyperkalemia as a result of suppression of angiotensin II-driven aldosterone secretion by the adrenal gland. Inhibition of aldosterone secretion may depend on the degree of inhibition of angiotensin II formation in the circulation and also locally in the adrenal gland. Because the various ACE inhibitors exhibit different degrees of ACE inhibition at the tissue level, we have postulated that angiotensin II-dependent aldosterone production will be inhibited to a lesser degree by agents that have low tissue affinity for the adrenal gland. The implication of this theoretical concept for the development of hyperkalemia in patients with impaired renal function treated with ACE inhibitors is discussed.
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PMID:Selected aspects of ACE inhibitor therapy for patients with renal disease: impact on proteinuria, lipids and potassium. 775 17


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