Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

With puromycin aminonucleoside-induced nephrotic syndrome (NS) in rats, twofold elevated levels of lipoproteins were observed. These levels were not related to proteinuria or to plasma albumin levels. Ultrastructural lesions induced in the kidneys by puromycin aminonucleoside were consistent with NS, while there was little or no hepatic involvement. Apolipoprotein B (apo B) kinetic measurements using homologous 125I-labeled low density lipoproteins (LDL) demonstrated a higher synthetic rate in nephrotic rats relative to controls (6.18 +/- 1.86 micrograms x g-1 x d-1 v 3.94 +/- 0.66 micrograms x g-1 x d-1 respectively, P less than .005), while the fractional catabolic rate was only marginally reduced (1.64 +/- 0.28 pools x day-1 in NS v 1.83 +/- 0.37 pools x day-1 in controls, P less than 0.4). These results indicate that in rats with experimentally induced NS, the expanded apo B-LDL pool results from increased synthesis of this apoprotein while no significant role can be ascribed to alterations in its catabolism. These data are consistent with our preliminary findings in NS in humans.
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PMID:Low density lipoprotein metabolism in rats with puromycin aminonucleoside-induced nephrotic syndrome. 272 89

Lecithin:cholesterol acyltransferase (LCAT) and lysolecithin acyltransferase (LAT) are two activities carried out by the same plasma enzyme, but require different apoprotein activators. The LCAT reaction takes place primarily on high density lipoproteins (HDL) and is activated by serum albumin, whereas LAT takes place on low density lipoproteins (LDL) and is inhibited by albumin. In nephrotic syndrome (NS), the levels of serum albumin are reduced, whereas the LDL levels are increased, and therefore, the ratio of LAT/LCAT activities should be increased. To test this hypothesis, we estimated the lipid levels and the two enzyme activities in experimental NS induced in rats by the injection of anti-Fx1A antibody (passive Heymann nephritis). As found in other nephrotic conditions, the plasma lipid levels rose progressively as the proteinuria increased and the serum albumin concentration declined. In addition, the ratio of LAT/LCAT activities increased by about fourfold after nine days of induction of nephritis. The LCAT activity correlated positively and the LAT activity negatively with serum albumin levels. The esterified cholesterol correlated positively with LCAT activity in normal rats but negatively in nephrotic animals, indicating that most of the cholesteryl esters in NS may be non-LCAT derived. The free cholesterol/lecithin ratio, a known risk factor for atherosclerosis, increased significantly in nephrotic rats. Furthermore, since the increase in the LAT activity produces more disaturated lecithins, another putative risk factor, the cumulative risk of coronary heart disease may be increased in long-term NS.
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PMID:Plasma lipids and acyltransferase activities in experimental nephrotic syndrome. 277 94

We investigated lipoprotein profiles in 24 children with normal renal function at different stages of the idiopathic nephrotic syndrome (NS). Four groups of patients were studied: (I) steriod-resistant NS with persistent proteinuria; (II) untreated steroid-sensitive NS during a relapse; (III) steroid-sensitive NS in remission induced by steroid-treatment; (IV) steroid-sensitive NS in long-term remission without therapy. Triglycerides (TG), cholesterol (CHOL), and phospholipids (PLP) were measured in plasma as well as in the lipoprotein fractions of very low (VLDL), intermediate (IDL), low (LDL) and high density (HDL). Apoproteins (Apo) AI, AII, B and C-apoproteins were measured in patients of groups I and IV. Results were compared to those obtained in 24 healthy control subjects. All patients with active NS (groups I-III) had significantly elevated CHOL levels. TG and CHOL in the VLDL, IDL, LDL, and CHOL in HDL2, but not HDL3 were inversely correlated with the serum albumin level. Patients with active NS had increased concentrations of TG and CHOL in lipoprotein fractions of lower density. Total and fractionated HDL-CHOL was not significantly different from control levels in any group. Patients in group I had significantly reduced Apo AI levels, whereas an increase of Apo AI and Apo AII in HDL3 and of most C-apoproteins in both HDL fractions was observed in patients of group IV. While changes in HDL apoprotein composition during long-term remission are of yet unknown clinical significance, our data indicate an increased risk of atherosclerosis only in those paediatric patients with persistent steroid-resistant NS.
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PMID:Lipoprotein profiles at different stages of the nephrotic syndrome. 339 Dec 17

Lecithin-cholesterol acyltransferase (LCAT) deficiency was first described in a Norwegian family as an inborn error of metabolism. Altogether, 35 patients in 18 families have been identified. The authors report the first German patient, who presented with the characteristic clinical features of corneal opacity, proteinuria, and mild anemia. Renal biopsy revealed foam cells and an increased mesangial matrix in the glomeruli. Confirmation of the clinical diagnosis of LCAT deficiency was obtained by plasma enzyme and lipid analyses. Functional LCAT activity was not detected in incubated plasma by chemical or radiochemical methods, although rocket immunoelectrophoresis indicated that the patient had about one-third of normal LCAT mass. In keeping with other reports of LCAT deficiency, apoE-rich discoidal particles were seen in the patient's high-density lipoprotein fraction by electron microscopic examination.
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PMID:Hereditary lecithin-cholesterol acyltransferase deficiency. Case report of a German patient. 366 2

Although lipoprotein abnormalities of the nephrotic syndrome are assumed to be related to the presence of proteinuria, this topic has not been investigated extensively. We measured lipoproteins from 19 nonuremic patients during and after remission of the nephrotic syndrome in an effort to determine the extent of their putative atherogenicity. As expected, disturbances involved primarily the apoprotein B-containing lipoproteins. No patient showed serum lipoprotein(a) [Lp(a)] < 300 mg/L during the acute phase. Lp(a) concentrations correlated significantly with those of apoprotein B, and both values decreased dramatically with the remission of the nephrotic syndrome. Surprisingly, despite the resolution of proteinuria, concentrations of intermediate-density lipoproteins and Lp(a) remained above normal in hypertriglyceridemic patients, suggesting a residual effect of nephrosis in the overall lipoprotein transport. Accumulation of atherogenic remnants should be considered a characteristic of the hyperlipidemia of the nephrotic syndrome, and aggressive treatment to reduce proteinuria is mandatory.
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PMID:Accumulation of atherogenic remnants and lipoprotein(a) in the nephrotic syndrome: relation to remission of proteinuria. 776 11

It has been reported that focal and segmental glomerulosclerosis (FSGS) with pronounced proteinuria rapidly develop in Dahl salt-sensitive hypertensive (DS) rats fed a high-salt diet. We found that even when they are fed a standard rat chow (0.3% NaCl), DS rats, especially males, exhibit marked proteinuria, hypoalbuminemia, and hypertriglyceridemia without marked hypertension at 32 to 38 weeks of age. The nephrosis was associated with spontaneously developed FSGS. We therefore investigated the mechanism of hypertriglyceridemia in nephrotic animals. Plasma triglyceride (TG) and apoprotein (apo) B levels were markedly increased in DS rats compared with Sprague-Dawley (SD) rats, and this was mainly attributable to an increase in the concentration of very-low-density lipoprotein (VLDL). The TG secretion rate estimated by the Triton WR1339 method was significantly greater in DS rats. VLDL-TGs isolated from both the DS and SD rats were endogenously radiolabeled with different isotopes, and a mixture of these was then injected into DS and SD recipients. The half-life of VLDL-TG was about three times longer in DS recipients, regardless of the source of VLDL. In SD recipients, VLDL from DS rats was cleared at a slower rate than VLDL from SD rats. The activity of lipoprotein lipase in postheparin plasma was substantially decreased in DS rats. Isoelectric focusing gel electrophoresis (IEF) showed that the ratio of apo E/C or apo C-II/C-III in VLDL was markedly decreased and the ratio of apo E or apo C to apo A1 in high-density lipoprotein (HDL) was slightly decreased in DS rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of hypertriglyceridemia in Dahl salt-sensitive rats, an animal model of spontaneous nephrotic syndrome. 812 10

Elevated plasma levels of total cholesterol and increase in the hepatic synthesis of some apo B-containing lipoproteins have been noted in the nephrotic syndrome. Apoprotein (a), the apolipoprotein distinguishing lipoprotein (a) [Lp(a)] from low-density lipoprotein, is equally of hepatic origin, and Lp(a) recently has been shown to possess both atherogenic and thrombogenic activities. However, little is known of Lp(a) levels in nephrotic patients. We measured plasma Lp(a) concentrations in 11 patients with primary nephrotic syndrome in the absence of hematuria, hypertension, and renal insufficiency. Histologic lesions were minimal-change disease in five cases, membranous glomerulopathy in four cases, and focal and segmental glomerulosclerosis in two cases. Mean levels of Lp(a) (98 +/- 92 mg/dL [mean +/- SD]) were markedly elevated in the nephrotic patients as compared with the controls (14 +/- 13 mg/dL). No correlation was noted between plasma Lp(a) and proteinuria, albuminemia, total cholesterolemia, low-density lipoprotein cholesterol, apoprotein B100, or plasminogen. Furthermore, there was no correlation between Lp(a) levels and apoprotein (a) isoform size. In four patients, the level of Lp(a) decreased approximately fourfold after remission of the nephrotic syndrome under corticosteroid treatment. Our observation that Lp(a) levels are elevated in the nephrotic syndrome is consistent with the hypothesis that these patients may be at an increased risk of cardiovascular and thrombotic complications.
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PMID:Elevated lipoprotein (a) levels in primary nephrotic syndrome. 825 27

Cerebrovascular and cardiovascular diseases are important predictors for survival in patients undergoing continuous ambulatory peritoneal dialysis (CAPD), and account for about half the deaths in these patients. Lipoprotein(a) [Lp(a)] is known to show high values in diabetics with proteinuria, and albuminuric renal disease. The purpose of this study was to determine Lp(a) levels and to investigate the association of Lp(a) and atherosclerotic risk factors in patients treated by CAPD. Lp(a) concentration were measured in 20 CAPD patients in the age range 31 to 83 years. Mean (+/- SD) levels of serum Lp(a) were elevated in the CAPD patients compared to age, sex matched 17 controls (49.5 +/- 27.7 vs. 15.5 +/- 12.4 mg/dl, p < 0.001). The levels of Lp(a) were significantly higher in the diabetic CAPD patients than in non-diabetics. There were significant positive correlations between serum Lp(a) concentrations and fasting blood sugar. However, when the above two groups were matched for age, sex, body mass index and FBS, Lp(a) concentrations were also significantly higher in CAPD patients than those in normal controls. We found no statistically significant correlations of Lp(a) with either age, body mass index, blood pressure, serum lipoprotein, apoprotein, glycated hemoglobin, BUN, creatinine or serum protein levels. There were no correlations between serum Lp(a) levels and albumin and LP(a) concentrations in the dialysate in all CAPD patients. Along with assessment of other known established cardiovascular risk factors such as elevated blood pressure, atherogenic abnormalities of plasma lipids and lipoproteins, and impaired glucose tolerance, we suggest that elevated levels of Lp(a) may lead to the accelerated atherosclerosis in these patients.
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PMID:[Alterations of Lp (a) lipoprotein in patients with chronic renal failure treated by continuous ambulatory peritoneal dialysis]. 837 89

Hyperlipidemia has been implicated in the pathogenesis of experimental progressive glomerulosclerosis, but its role in human renal injury is controversial. This report describes a 12-yr-old boy presenting with massive proteinuria, hepatomegaly, anemia, severe mixed hyperlipidemia, and progressive renal failure. The initial renal biopsy disclosed large numbers of foam cells that were shown to be monocytes. Evidence is presented suggesting that apoprotein-E2 homozygosity in our patient, together with an 88% reduction in plasma lipoprotein lipase activity associated with severe nephrotic syndrome, is responsible for the atypical clinical features, lipoprotein phenotype III with chylomicronemia, and renal lipidosis. A regimen of dietary lipid restriction, gemfibrozil, and niacin resulted in significant but partial improvement of the dyslipidemia and resolution of the hepatomegaly and ascites. This report stresses the importance of characterizing unique lipid disorders in patients with nephrotic syndrome in order to prescribe effective lipid-lowering strategies. Moreover, the striking resemblance of the clinical and nephrohistologic features of this patient to those occurring in experimental models of coexisting glomerular injury and hyperlipidemia led to the speculation that, in this setting, the hyperlipidemia may contribute to the development of progressive glomerulosclerosis.
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PMID:Atypical hyperlipidemia and nephropathy associated with apolipoprotein E homozygosity. 858 83

Fasting plasma cholesterol, triglycerides, high-density lipoprotein (HDL) and apoprotein (apo) B were elevated in 214 nondiabetic renal transplant recipients when compared to a reference group. Apo (a) was slightly but not significantly lower in transplant recipients (median 118 mg/dl, range 16-1680 vs 130 mg/dl, 10-1176) and this difference could be predicted from Lp (a) isoform analysis. Cholesterol, triglyceride, apo B and apo (a) concentrations correlated negatively with creatinine clearance but none of these parameters showed a significant association with proteinuria. Patients treated with steroids had higher plasma HDL concentrations than those receiving cyclosporin monotherapy (P < 0.01). The use of diuretics was associated with raised triglycerides (P < 0.001) and cholesterol (P < 0.01) and with reduced HDL (P < 0.01) whilst patients receiving beta-blockers had significantly higher triglycerides (P < 0.01) and lower HDL levels (P < 0.02). In multiple regression analysis, age (P < 0.01), creatinine clearance (P < 0.05) and diuretic therapy (P < 0.005) were independent risk factors for increased cholesterol whilst apo (a) levels correlated negatively with creatinine clearance (P < 0.005). These results suggest that impaired renal function, steroids and non-immunosuppressive drugs contribute to lipid abnormalites in renal transplant recipients.
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PMID:Factors influencing plasma lipid profiles including lipoprotein (a) concentrations in renal transplant recipients. 872 90


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