Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With polyacrylamide gel electrophoresis (PAGE), we studied serum lipoprotein (Lp) abnormalities in patients with nephrotic syndrome (NS) caused by primary glomerulonephritis. Nineteen untreated nephrotic patients were studied. Seven patients of them were followed up with PAGE in the remitting course. Serum total cholesterol, triglycerides and beta-Lp concentrations were higher in untreated patients than those in normal control. Serum HDL-cholesterol concentration was lower in untreated patients than those in normal control. PAGE showed broad midband-Lp and increased pre-beta-Lp in 16 of 19 untreated patients. Those findings suggested that untreated nephrotic patients had impaired catabolism of VLDL to LDL in peripheral tissue or impaired hepatic catabolism of IDL and LDL. Furthermore, PAGE showed decreased alpha-Lp in all patients with untreated NS. Correlation was not found between histological classification of glomerulonephritis and broad midband or hyperlipidemia. After administration of prednisolone, PAGE revealed the appearance of chylomicron, and increased pre-beta-LP and alpha-Lp. After remission, broad midband-Lp and pre-beta-Lp were markedly decreased or dis appeared in all 6 patients with broad midband-Lp in untreated phase, and serum total cholesterol and beta-Lp concentrations were markedly decreased, and HDL- cholestrol was markedly increased. In the course of remission, serum total cholesterol, triglycerides and beta-Lp concentrations had negative correlation with serum albumin concentration. Furthermore, serum total cholesterol and beta-Lp concentrations were decreased along with decrease of urinary protein excretion. The results of the present study suggest that the loss of serum albumin and/or some other substances to the urine cause broad midband.
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PMID:[Serum lipoprotein abnormalities in patients with nephrotic syndrome and effects of steroid therapy]. 274 6

The effects of bezafibrate on hyperlipidaemia in experimental nephrotic syndrome in rats has been investigated. The treated group received bezafibrate 10 mg kg-1 p.o. daily. No significant differences in total serum cholesterol occurred, but a significant reduction in serum triglyceride (P less than 0.005) and elevation in HDL cholesterol (P less than 0.005) occurred. These findings may have implications for therapeutic intervention in severe hyperlipidaemia of the nephrotic syndrome in man.
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PMID:The effect of bezafibrate on hyperlipidaemia in experimental nephrotic syndrome in rats. 286 48

The efficacy, safety, and tolerability of simvastatin (20 mg twice a day) in the treatment of hyperlipidaemia due to unremitting nephrotic syndrome was compared with that of cholestyramine (8 g twice a day) in a crossover trial in ten patients. Two patients were taken off the protocol, one because he could not tolerate cholestyramine and one because of non-compliance with the cholestyramine regimen. No clinical or laboratory adverse experiences were noticed during the study in the other eight patients. Simvastatin was significantly more effective than cholestyramine in reducing the hyperlipidaemia--it produced a 36% decrease in total cholesterol and a 39% decrease in low density (LDL)-cholesterol, whereas cholestyramine reduced total cholesterol by 8% and LDL-cholesterol by 19%. With simvastatin the apolipoprotein B level decreased by 30%, whereas the apolipoprotein A level increased by 10%.
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PMID:Effects of simvastatin and cholestyramine on lipoprotein profile in hyperlipidaemia of nephrotic syndrome. 290 53

Nephrotic syndrome characterized by hypoalbuminemia and hyperlipidemia is associated with an increased incidence of thromboembolism and increased platelet hyperaggregability. Although plasma coagulation proteins are also abnormal, changes are too inconsistent to attribute thromboembolic complications to the coagulation cascade alone. Antithrombin III (ATIII) has been shown to be deficient in nephrotic syndrome. There is, however, an increase in alpha 2 macroglobulin. It is clear that platelet to platelet interactions require exposure of platelet fibrinogen receptors, the binding of fibrinogen to these receptors, platelet crossbridging, and subsequent platelet aggregation. Fibrinogen is consistently elevated in nephrotic syndrome. Hyperlipidemia and hypoalbuminemia in nephrotic syndrome increases the availability of thromboxane A2 (TxA2) by increasing the availability of TxA2 precursors and the removal of TxA2 inhibitors. Thromboxane A2 is a known inducer of platelet aggregation probably through the exposure of platelet fibrinogen receptors. Recently, fibronectins a group of adhesive proteins, were implicated in platelet to platelet interactions. Since thrombin increases the expression of platelet surface fibronectin, fibronectin may be involved in thrombus formation in nephrotic syndrome. Thromboembolic formation in nephrotic syndrome is a composite mechanism involving the coagulation cascade, platelet-platelet interactions, and platelet-surface interactions.
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PMID:Nephrotic syndrome: a platelet hyperaggregability state. 293 Sep 39

We evaluated serial measurements of serum lipid levels in 68 patients aged 12.6 +/- 4.7 years undergoing treatment with continuous ambulatory peritoneal dialysis/continuous cycling peritoneal dialysis (CAPD/CCPD). Fasting mean levels of triglycerides (TG) and cholesterol (C) were elevated above the 95th percentile of published normal values by 102% and 19%, respectively, at the start of dialysis. Except for a short-term decrease in TG levels at 6 and 9 months, no significant change in mean lipid levels was observed during a follow-up period of 2 years. At initiation of dialysis, elevated TG and C levels were present in 90% and 69% of the patients, respectively. The prevalence of hyperlipidemia (HL) varied between 63% and 88% (TG) and 61% and 93% (C), respectively, during the follow-up period. TG and C levels were not correlated with caloric intake (evaluated in 17 patients), serum albumin levels, treatment modality (CAPD or CCPD), a history of the nephrotic syndrome, or previous treatment with hemodialysis or transplantation. However, a significant inverse correlation was observed between age and serum lipids at the initiation of dialysis treatment and after 1 year (TG: r = -0.40; C: r = -0.44). Our data indicate a high prevalence of HL but no significant change of serum lipid levels during 2 years of treatment with CAPD/CCPD.
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PMID:Hyperlipidemia in pediatric patients undergoing peritoneal dialysis. 315 58

The nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, and hypercholesterolemia. Hypertriglyceridemia often is present as well. In this study, the kinetics of plasma lipoproteins were investigated in four patients with nephrotic hyperlipidemia, and repeat studies were carried out in three of these patients during therapy with lovastatin. Before lovastatin therapy, the patients had an extremely delayed catabolism of very low density lipoproteins (VLDL) without evidence of overproduction of lipoproteins in this fraction. Three of four patients had elevated levels of low density lipoprotein (LDL) that were due mainly to increased production rates for LDL. In the three patients treated with lovastatin, the drug therapy lowered plasma concentrations of total cholesterol, triglycerides, VLDL-cholesterol, and LDL-cholesterol, and raised high density lipoprotein (HDL)-cholesterol. Lovastatin therapy decreased VLDL-triglycerides primarily by enhancing their catabolism, and lowered LDL-cholesterol levels mainly by reducing input rates for LDL. Overall, lovastatin appears to be an effective drug for the treatment of hyperlipidemia in the nephrotic syndrome.
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PMID:Lovastatin therapy in nephrotic hyperlipidemia: effects on lipoprotein metabolism. 316 83

Modern views of the pathogenesis and natural history of nephrotic syndrome have changed substantially since the early studies by Cotugno and Bright. Contrary to beliefs held 20 years ago, we do not possess a unique satisfying explanation for the induction, maintenance, and resolution of nephrotic edema, and many concepts firmly established as "classic" are now being revised or reconsidered. These include the relationship between urinary protein losses and hypoalbuminemia, which is complicated by several factors such as daily protein intake, albumin catabolism, and the possible role of albumin loss at extrarenal sites. The influence of lowered plasma albumin on the decrease in plasma volume is also quite complex, due to technical difficulties in measuring plasma volume and turnover of radio-labeled albumin. The most contentious areas are how sodium and water retention are initiated and maintained and the relationship between hypoalbuminemia, plasma oncotic pressure, and edema. While aldosterone excretion and plasma concentrations are elevated in nephrotic patients, data on the renin-angiotensin system are controversial and the renal handling of sodium is related to a host of factors including glomerular filtration rate, altered proximal tubular reabsorption, and the role of vasodilators or vasoconstrictors. The complications of nephrotic syndrome are protean and relatively common. Among those are acute renal failure, thrombosis, infections, and hyperlipidemia. Since the introduction of percutaneous biopsy, the spectrum of lesions underlying nephrotic syndrome has widened considerably, the most common being minimal change, especially in children. There are very few prognostic indicators by which response to treatment may be predicted and these include persistent microscopic hematuria.
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PMID:The nephrotic syndrome and its complications. 330 94

The hyperlipidemia of the nephrotic syndrome is often associated with elevated total and low-density lipoprotein (LDL) cholesterol levels and low or normal high-density lipoprotein (HDL) cholesterol levels. This pattern of hyperlipidemia has been associated with an increased risk of accelerated atherosclerosis in other populations. Despite extensive studies of diet and drug therapy in other populations, few such therapeutic studies exist in patients with the nephrotic syndrome. To investigate the effect of diet and lipid-lowering drugs on the lipoprotein-lipid profile of patients with unremitting nephrotic syndrome and marked hyperlipidemia, we conducted a controlled trial using two such drugs: colestipol and probucol. Colestipol lowered the mean total fasting plasma cholesterol of seven patients from 397 +/- 27 to 317 +/- 37 mg/dL, a 20.2% decrease, and lowered the LDL cholesterol from 398 +/- 28 to 203 +/- 18 mg/dL, a 31.9% decrease. It did not affect the HDL cholesterol level, and thus lowered the LDL-to-HDL cholesterol ratio. Probucol lowered the mean total cholesterol from 439 +/- 72 to 339 +/- 60 mg/dL, a 22.6% decrease, and the LDL cholesterol from 282 +/- 43 to 215 +/- 26 mg/dL, a 23.8% decrease. Although the HDL cholesterol was lowered from 49 +/- 9 to 43 +/- 7 mg/dL by probucol, a 12.2% decrease, the LDL-to-HDL cholesterol ratio still declined. Both drugs were well tolerated and proved safe in this short-term trial. Antihyperlipidemic therapy may well be indicated in certain patients with unremitting nephrotic syndrome.
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PMID:Treatment of the hyperlipidemia of the nephrotic syndrome: a controlled trial. 354 20

Hyperlipemia is a common manifestation of the nephrotic syndrome. Serum lipid concentrations have been observed by others to be negatively correlated with serum protein concentration. Hyperlipemia has been postulated to result from a coordinate increase in the synthesis of both albumin and lipoproteins, as well as from their decreased catabolism. Simultaneous measurements of serum lipid concentration and the rate of albumin synthesis have not been previously reported. We measured the rate of albumin synthesis, urinary albumin loss, serum albumin, protein, cholesterol and triglyceride concentration in 13 nephrotic patients. Changes in the rate of albumin synthesis and in urinary albumin excretion were induced in eight patients by alteration in dietary protein intake. The resultant changes in serum triglyceride and cholesterol were analyzed by multiple regression analysis. The rate of albumin synthesis measured while patients were eating a low protein diet was 12.61 +/- 1.20 g/1.73 m2/day, well within normal limits, yet both serum triglyceride and cholesterol concentrations were markedly elevated (265 +/- 65 mg/dl and 325 +/- 44 mg/dl, respectively). Albumin synthetic rate increased to 17.60 +/- 1.25 g/1.73 m2/day when dietary protein intake was increased, while serum triglyceride and cholesterol concentrations changed little; triglyceride concentration was 306 +/- 75 mg/dl and cholesterol 376 +/- 55 mg/dl. Serum cholesterol concentration, by multiple regression analysis, was dependent only upon the renal clearance of albumin P less than 0.0001, and changes in serum cholesterol concentration was dependent only upon changes in the renal clearance of albumin, P less than 0.001. Serum cholesterol concentration was completely independent of the rate of albumin synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Albumin synthesis, albuminuria and hyperlipemia in nephrotic patients. 361 8

The study was designed to investigate the hyperlipidaemia associated with the steroid responsive nephrotic syndrome in children and in particular to examine the mechanism for the delayed clearance of the circulating triglyceride-rich lipoproteins. The possibility that plasma from patients with steroid responsive nephrotic syndrome may contain an inhibitor of lipoprotein lipase activity was studied by examining the effect of the addition of plasma from patients, on normal postheparin lipoprotein lipase activity. Plasma from children with steroid responsive nephrotic syndrome significantly inhibited lipoprotein lipase activity (p less than 0.001), whereas that from patients with familial hypercholesterolaemia and normal children had no significant effect. The inhibition of lipoprotein lipase activity by plasma from patients with steroid responsive nephrotic syndrome correlated significantly with their increased plasma cholesterol and reduced plasma albumin concentrations (p less than 0.001 and less than 0.02, respectively), but there was no significant correlation with plasma triglyceride concentrations. Thus, the degree of inhibition probably reflected the severity of the condition at the time of study. Neither the cholesterol, albumin nor triglyceride concentrations appeared to directly influence the lipoprotein lipase activity of postheparin plasma.
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PMID:Inhibition of lipoprotein lipase by plasma from children with the steroid responsive nephrotic syndrome. 365 46


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