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)

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

We determined whether the serum lipoprotein levels in insulin-dependent diabetic patients (IDDM) with nephropathy and in patients on haemodialysis or continuous ambulatory peritoneal dialysis were affected by beta-blocker therapy. A case control study was performed in 18 IDDM patients with diabetic nephropathy, in 18 patients receiving chronic haemodialysis (HD) and 16 patients undergoing continuous ambulatory peritoneal dialysis (CAPD). In IDDM patients with diabetic nephropathy very low density lipoprotein-cholesterol (VLDL-CHOL) (0.680 +/- 0.17 vs 0.197 +/- 0.04 mmol/l, p = 0.004), total triglycerides (1.71 +/- 0.23 vs 0.808 +/- 0.14 mmol/l, p = 0.004) and very low density lipoprotein triglyceride (VLD-TG) were higher in the beta-blocker therapy group. In haemodialysis patients, beta-blocker therapy caused no significant changes in the serum lipoprotein profiles compared to the control group. In patients receiving continuous ambulatory peritoneal dialysis VLDL-CHOL was significantly higher (1.47 +/- 0.24 vs 1.08 +/- 0.21 mmol/l, p = 0.042) and cholesterol-high density lipoprotein (HDL-CHOL) was lower in the beta-blocker therapy group. The elevated VLDL-CHOL level (0.96 +/- 0.12 vs 1.24 +/- 0.14 mmol/l, p = 0.021) was correlated with the duration of CAPD in patients receiving beta-blocker therapy. Antihypertensive therapy with beta-blockers in IDDM patients with persistent proteinuria and in patients on continuous ambulatory peritoneal dialysis appears to adversely effect serum lipoproteins which may add to their cardiovascular risk.
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PMID:Effect of beta-blocker therapy on serum lipoprotein profiles in patients on renal dialysis and in diabetic nephropathy. 771 87

Lecithin:cholesterol acyltransferase (LCAT) deficiency is a genetic disorder associated with low levels of serum HDL cholesterol. The proband of the Finnish LCAT-deficient family had corneal opacities, proteinuria, anemia with stomatocytosis, low serum HDL cholesterol (0.27 mmol/L), and low LCAT activity. Sequence analysis of his LCAT gene revealed compound heterozygosity for two different mutations: a C insertion in exon 1 between nucleotides 932 and 937 and a C-to-T point mutation in exon 6 at position 4976. The C insertion in exon 1 is predicted to result in premature termination and a truncated polypeptide containing only 16 amino acids. The C-to-T point mutation in exon 6 substitutes cysteine for arginine at residue 399. The functional significance of the Arg399-->Cys mutation was examined by expressing the mutated and wild-type LCAT cDNAs in COS cells. COS cells transfected with mutated and wild-type cDNAs showed comparable levels of mature LCAT mRNA. However, LCAT activity in the cell media of COS cells transfected with the mutant LCAT cDNA was significantly lower than that of COS cells transfected with the wild-type cDNA (1.4% versus 12.0% cholesterol esterified, respectively). A polymerase chain reaction-based duplex assay, in which both mutations can be detected simultaneously, was used for preliminary screening of Finnish subjects with serum HDL levels below 0.9 mmol/L; two additional individuals heterozygous for the Arg399-->Cys mutation were identified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Two different allelic mutations in a Finnish family with lecithin:cholesterol acyltransferase deficiency. 774 57

The aim of this study was to evaluate Lp(a), total, HDL and LDL cholesterol, triglycerides, Apo A and Apo B100 plasmatic concentrations in patients affected by nephrotic syndrome that is known able to increase the ratio of the risk of cerebral and cardiovascular events, in comparison with a group of healthy patients homologous for sex and age. In the group of patients with nephrotic syndrome we have compared the variables between diabetic mellitus type I patients and non diabetic patients. All the variables, in exception of HDL cholesterol, were significantly increased in the group of patients with nephrotic syndrome compared with the control group. HDL-cholesterol concentration was significantly higher in controls than in nephrotic patients. Diabetic and nephrotic patients showed increased levels of Lp(a) concentration than non diabetic patients and the difference was statistically confirmed. These data suggest that Lp(a) acts really like a risk factor for atherosclerotic disease, being elevated in patients characterized for increased risk for cerebral and cardiovascular events because of the presence of nephrotic syndrome. Moreover we can suppose that elevated plasmatic Lp(a) levels in nephrotic patients could be linked to increased synthesis of proteins in the liver as physiological reaction to severe proteinuria.
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PMID:[Plasma Lp(a) levels: a comparison between diabetic and nondiabetic patients with the nephrotic syndrome and control subjects]. 775 72

A total of 126 (99 males, 27 females) serologically confirmed hospital-treated adult cases of nephropathia epidemica (NE) were studied. The initial diagnosis suggested by the referring physician was correct in only 28%. Some rare clinical manifestations of NE were observed; acute myopericarditis in 3 patients and encephalitis in 1. Pulmonary involvement due to vascular congestion was observed in 16% and liver involvement in 34% of the patients. Thrombocytopenia was present in 75%, leukocytosis in 50% and anemia in 50%. Erythrocyte sedimentation rate (ESR) was 2-108 (mean 38) mm/h and C-reactive protein (CRP) 0-126 (mean 52) mg/l. Proteinuria was observed in 94%, hematuria in 58% and pyuria in 28%. Electrolyte abnormalities (hyponatremia, hypokalemia, hypocalcemia, hyperphosphatemia) were all common but rarely serious. Serum lipid changes caused by the acute infection and renal failure included very low total and HDL-cholesterol as well as high triglyceride levels. Renal function was transiently impaired in 94% of the patients and 7 needed transient dialysis therapy. All recovered.
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PMID:Nephropathia epidemica in Finland: a retrospective study of 126 cases. 791 Jul 5

To evaluate long-term benefits and risks of CyA therapy in renal transplantation, we analyzed the 10-year experience with all 59 patients who had received a first cadaveric renal graft until August 1983 and were immunosuppressed with CyA. We compared their actual graft survival with that of all 213 patients who had received a first cadaveric graft from 1967 until August 1983, but were immunosuppressed initially with azathioprine and prednisone (AzaP). For comparison of p-creatinine, proteinuria, blood pressure, lipids, uric acid and skin malignancies we evaluated the patients staying unchanged on initial therapy for 10 years (CyA = 12, AzaP = 53). RESULTS. (1) Actual graft survival at 10 years was 34% (20/59) with CyA and 27% (58/213) in AzaP treated patients (intention to treat) (P = .09 = ns). At 1 to 5 years, graft survival was 15% superior with CyA, but after 7 years the survival curve of the CyA-group has closely joined the chronic decline seen in the AzaP group. This behaviour could neither be explained by chronic CyA-nephrotoxicity nor by chronic rejection after switching from CyA to AzaP. (2) P-creatinine at 10 years was significantly (P < .03), but mildly elevated under CyA (130 +/- 52; AzaP = 109 +/- 65). (3) Proteinuria (g/d) at 10 years was not significantly different (CyA = 0.41 +/- 0.58, versus AzaP = 0.83 +/- 1.61). (4) Systolic blood pressure was higher at 10 years under CyA (152 +/- 19) than under AzaP (136 +/-) (P < .02), but diastolic pressure was not (89 +/- 10 versus 84 +/- 12; ns). Antihypertensive drug/patient was twice as high under CyA (1.25 versus 0.64 P < .02). (5) Cholesterol, triglyceride, HDL were not different. 75% of the CyA-patients were steroid free at 10 years, none of the AzaP-patients. (6) P-uric acid was not significantly different in both groups (494 +/- 192 vs 400 +/- 124), but 42% of CyA-patients were on uric acid lowering drug (given after at least one gout attack) as compared to 9% under AzaP (P < .006). (7) Seventeen percent of patients under CyA for 10 years had at least one skin cancer, not different from 15% of AzaP-patients. CONCLUSIONS. The main benefit of CyA was the better graft survival up to 5 years and the chance to stay free of steroids. The main risks of CyA were nephrotoxicity, hypertension and symptomatic hyperuricemia. No difference was found for hyperlipidemia and skin-malignancies.
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PMID:Long-term benefits and risks of cyclosporin A (sandimmun)--an analysis at 10 years. 794 Jul 65

The lipid and lipoprotein profiles including apolipoprotein A1 and B100 are measured in 50 idiopathic nephrotic patients (males 26, females 24) with mean age of 32 + 13.6 yrs, serum creatinine 1.32 +/- 0.43 mg/dl compared with 50 age matched normal controls. The renal histology consist of IgM nephropathy 70 per cent, membranous 12 per cent, and IgA 2 per cent. The serum cholesterol, triglycerides, LDL- cholesterol, VLDL-cholesterol, apolipoprotein B (521.6 +/- 201.6, 291.4 +/- 156.2, 438.8 +/- 207.4, 58.3 +/- 31.2, 265.1 +/- 119.8) are statistically significantly higher than controls (p < 0.001). The HDL-cholesterol (30.2 +/- 16.1) is also significantly lower than controls (p < 0.001) but apolipoprotein A is not different from normal subjects. The most common hyperlipoprotein type is type IIb (66%), less common are type IIa (22%), IV (6%) and III (4%) respectively. There is no correlation between serum lipids, lipoproteins and urinary protein, serum albumin, and histological diagnosis. The ratio of cholesterol: HDL, LDL: HDL and Apo A1: B are all significantly higher than normal control (p < 0.001) and correlate with urinary protein levels. This study shows that the nephrotic patients who have persistent heavy proteinuria have dyslipidemia which is highly atherogenic and probably increases the incidence of coronary heart disease.
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PMID:Lipoprotein abnormalities in adult nephrotic syndrome. 796 58

An extracellular matrix (collagens I, III, IV) was studied in the glomeruli of patients demonstrating glomerular low density lipoproteins (LDL) and free of them. These two patients' groups were not found significantly different by age, nephropathy duration, blood pressure, serum concentrations of creatinine, triglycerides, HDL cholesterol. The LDL deposit group differed by longer duration of the nephrotic syndrome, higher 24-h proteinuria, lower serum albumin levels, higher total cholesterol in the serum and the proportion VLDL and LDL cholesterol to HDL cholesterol. They had noninflammatory nephropathies more frequently, collagen IV accumulated in the glomerulus more actively, there appeared interstitial collagens I and III. The discussion concerns the role of hypercholesterolemia with the above proportion of cholesterols, its duration, a type of cells dictating mesangial proliferation, in the development of LDL-deposit-induced glomerulosclerosis.
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PMID:[Hyperlipidemia and glomerulosclerosis in nephropathies: clinicomorphological comparisons]. 798 38

Eight patients with biopsy-proven primary nephrotic syndrome were included in an open, prospective, two-year study of lovastatin. One patients was withdrawn after 6 months due to an asymptomatic rise in creatinine phosphokinase, which was rapidly reversed after interruption of lovastatin. In the remaining patients, treatment was well-tolerated and produced no side effects. After 2 years of treatment, these 7 patients had decreases in total cholesterol from 446 +/- 165 to 250 +/- 57 mg/dl (p < 0.001), LDL cholesterol from 343 +/- 121 to 174 +/- 49 mg/dl (p < 0.001), Apo B lipoprotein from 162 +/- 60 to 108 +/- 42 mg/dl (p < 0.05), triglycerides from 336 +/- 273 to 182 +/- 71 mg/dl (p < 0.04). There was no change in HDL cholesterol. The LDL/HDL cholesterol and the total/HDL cholesterol ratios fell from 15.0 +/- 12.1 and 19.1 +/- 17.2 mg/dl before the study to 4.4 +/- 1.2 and 6.3 +/- 1.6 mg/dl, respectively, at 2 years. A decrease in proteinuria from 8.6 +/- 4.6 to 5.0 +/- 3.7 g/24 h (p < 0.02) was noted in 4 patients on concomitant ACE inhibitor therapy. Renal function remained stable in all patients throughout the study, except for one whose moderate impairment progressed to end-stage renal failure requiring dialysis 3 months poststudy. We conclude that long-term lovastatin in patients with primary nephrotic syndrome is an effective and generally safe treatment for accompanying dyslipidemia.
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PMID:Long-term effect of lovastatin on lipoprotein profile in patients with primary nephrotic syndrome. 805 Feb 7

Low-density lipoprotein apheresis (LDL-A) was performed for nine episodes of steroid-resistant nephrotic syndrome in eight patients. The clinical and immunohistological findings were analysed retrospectively. Six of the patients had focal glomerular sclerosis (FGS), one had minimal-change nephrotic syndrome (MCNS), and one had membranous nephropathy (MN) with FGS. The LDL-A treatment, carried out 2-13 times (mean 7.33 +/- 4.05) for one nephrotic episode, at average intervals of 3-16 days (mean: 8.5 +/- 5.1 days) and combined with steroid pulse therapy and the administration of an antihyperlipidaemic agent in some cases, led to rapid amelioration of hyperlipidaemia. In six nephrotic episodes (5 patients) more than 50% reduction of proteinuria occurred (less than 3.5 g/day) (response-group). A significant elevation of serum albumin (more than 3.0 g/dl) was obtained in five of these episodes. The other three patients were resistant (resistant-group). The number of and intervals between LDL-A treatments in the response group (5 +/- 2.8 times and 5.8 +/- 4.1 days) were significantly less than those in the resistant-group (12.0 +/- 0.8 times and 13.2 +/- 1.8 days) (P < 0.05). After LDL-A, significant reductions were observed in the serum total cholesterol (T-CHO), phospholipid (PL), triglyceride (TG), free-CHO (F-CHO), and beta-lipoprotein (beta-lipo) (P < 0.05). HDL-cholesterol (HDL-C) increased somewhat after LDL-A. Further, Ccr was elevated in all nephrotic episodes, except in one patient who manifested renal failure after 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does LDL-apheresis in steroid-resistant nephrotic syndrome affect prognosis? 805 31


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