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)

A study was made of urine lipids and their fractions in chronic glomerulonephritis (CGN) and renal amyloidosis with nephrotic syndrome (NS). 91 patients suffering from NS were examined. 2 subgroups were distinguished among these patients: with CGN of the nephrotic type and with the nephrotic stage of renal amyloidosis. The reference groups were made up of patients with latent CGN and healthy subjects. Measurements were made in the blood and urine of total lipids (TL) and their fractions--phospholipids (LP), free cholesterol (FC), mono- and diglycerides, triglycerides (TG), and cholesterol esters (CE). The presence of the NS was attended by a rise in the blood of TL concentration, relative content of FC, TG and by a decline of RL and CE, with the decrease of the relative content being more manifest in amyloidosis. Nephrotic lipiduria was largely characterized by an increase of the concentration of TL and of the relative content of PL, with the changes of the latter parameter being mostly characteristic of CGN patients. Thus, NS was associated with a high excretion of lipids with urine which is likely to reflect their elevated filtration under nephrotic hyperlipidemia. Still, in nephropathies whose pathogenesis is determined by an important role of inflammatory and membrane-destructive processes, of definite role is also the local (renal) formation of PL.
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PMID:[Lipiduria in the nephrotic syndrome]. 144 Mar 28

One of the most prominent manifestations of the nephrotic syndrome is hyperlipidemia. Lipoprotein synthesis is increased and catabolism is reduced in nephrotic patients and animals. The observation that infusion of either albumin or dextran reduces lipid levels suggests that oncotic pressure (pi) may regulate lipogenesis. It has been postulated that prolonged plasma half-life of lipoproteins in nephrosis is a consequence of saturation of catabolic sites and is secondary to the hyperlipidemia that results from increased lipogenesis. However, the absolute rate of triglyceride catabolism is reduced in nephrotic rats in comparison to normal suggesting that defective lipid catabolism may be a cause rather than a consequence of hyperlipidemia. Furthermore, chylomicrons (CM) and very-low-density lipoproteins (VLDL) are cleared normally in rats with hereditary analbuminemia despite increased lipid synthesis. When we cause proteinuria in analbuminemic rats, the clearance of CM and VLDL becomes greatly prolonged, suggesting that proteinuria, and not reduced serum albumin or pi, is responsible for defective lipoprotein catabolism. Maneuvers that reduce proteinuria, such as administration of an angiotensin-converting enzyme inhibitor, reduce lipid levels in nephrotic patients and animals even when plasma albumin concentration is unchanged supporting a hypothesis that proteinuria may lead to reduced catabolism of lipoproteins.
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PMID:Nephrotic hyperlipidemia: primary abnormalities in both lipoprotein catabolism and synthesis. 146 61

Both increased synthesis and decreased catabolism of lipoproteins may account for the severe hyperlipidemia which frequently occurs in patients with the nephrotic syndrome (NS). Nevertheless the complex relation between hyperlipidemia and proteinuria remains unclear and still debated. Increased levels of serum total cholesterol, of low-density lipoprotein and of apolipoprotein B are the most characteristic reported abnormalities placing these patients at high risks for atherosclerotic vascular disease. Moreover recent experiments have suggested that hyperlipidemia may also play a role in the progression of renal disease. Thus the reasons for using hypolipemic treatment are now growing in number and recent trials with lipid lowering medication have been successful without major side effects.
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PMID:[Disturbances of lipid metabolism during nephrotic syndrome: physiopathology and treatment]. 147 Feb 93

Post-prandial lipaemia was investigated in a group of nine subjects with nephrotic syndrome by following the concentrations of triglyceride and retinyl palmitate in the d < 1.006 g ml-1 fraction of plasma after a standard oral fat load containing vitamin A. Lipoprotein lipase and hepatic triglyceride lipase activities were measured in post-heparin plasma. Subjects with other renal disease but insignificant proteinuria acted as controls. The time course of the lipaemic response was similar in both groups although individual patients demonstrated a prolonged lipaemia. Overall, there were no significant differences in the rise in triglyceride at 6 h (nephrotic--median 2.53 mmol l-1; range 0.87-4.76 vs. control 1.88; 0.38-4.12, P = 0.34), the peak concentration of retinyl palmitate (nephrotic 0.87 mg dl-1; 0.27-2.16 vs. control 0.65; 0.24-1.89, P = 0.97) or the areas under the curve from 0-24 h for triglyceride (nephrotic 10.5 mmol. h l-1; 2.9-43.6 vs. control 9.7; 4.3-27.0, P = 1.0) or retinyl palmitate (5.5 mg.h dl-1; 1.0-23.4 vs. 4.3; 1.5-12.4, P = 0.7). At baseline, the particles in the d < 1.006 g ml-1 fraction of plasma from nephrotic subjects had a higher free cholesterol:phospholipid ratio but this difference was no longer apparent 6 h after the test meal. There were no differences in total heparin-releasable lipase, lipoprotein lipase or hepatic triglyceride lipase activities between the two groups. These data suggest that impaired clearance of chylomicrons is not a major contributor to nephrotic hyperlipidaemia in man.
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PMID:Post-prandial lipoprotein metabolism in nephrotic syndrome. 147 53

Hyperlipidemia is a prominent feature of the nephrotic syndrome. Lipoprotein abnormalities include increased very low and low density lipoprotein (VLDL and LDL) cholesterol and variable reductions in high density lipoprotein (HDL) cholesterol. We hypothesized that plasma cholesteryl ester transfer protein (CETP), which influences the distribution of cholesteryl esters among the lipoproteins, might contribute to lipoprotein abnormalities in nephrotic syndrome. Plasma CETP, apolipoprotein and lipoprotein concentrations were measured in 14 consecutive untreated and 7 treated nephrotic patients, 5 patients with primary hypertriglyceridemia, and 18 normolipidemic controls. Patients with nephrotic syndrome displayed increased plasma concentrations of apoB, VLDL, and LDL cholesterol. The VLDL was enriched with cholesteryl ester (CE), shown by a CE/triglyceride (TG) ratio approximately twice that in normolipidemic or hypertriglyceridemic controls (P < 0.001). Plasma CETP concentration was increased in patients with untreated nephrotic syndrome compared to controls (3.6 vs. 2.3 mg/l, P < 0.001), and was positively correlated with the CE concentration in VLDL (r = 0.69, P = 0.004) and with plasma apoB concentration (r = 0.68, P = 0.007). Treatment with corticosteroids resulted in normalization of plasma CETP and of the CE/TG ratio in VLDL. An inverse correlation between plasma CETP and HDL cholesterol was observed in hypertriglyceridemic nephrotic syndrome patients (r = -0.67, P = 0.03). The dyslipidemia of nephrotic syndrome includes increased levels of apoB-lipoproteins and VLDL that are unusually enriched in CE and likely to be atherogenic. Increased plasma CETP probably plays a significant role in the enrichment of VLDL with CE, and may also contribute to increased concentrations of apoB-lipoproteins and decreased HDL cholesterol in some patients.
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PMID:Increased concentration of plasma cholesteryl ester transfer protein in nephrotic syndrome: role in dyslipidemia. 147 91

Membranous nephropathy is a worldwide problem that accounts for about 20% of the cases of the adult-onset nephrotic syndrome. This disease places many patients at risk for both end-stage renal failure and the complications of hyperlipidemia. Immune-mediated injury to the glomerular capillary wall in patients with membranous nephropathy is characterized by subepithelial immune complex formation and generation of the membrane attack complex of complement. Glomerular capillary hypertension, hyperlipidemia, and possibly cytokines could contribute to the glomerular sclerosis seen in the advanced stages of the disorder. In some cases, production of pathogenic antibody can be suppressed by treating the underlying condition. The mechanisms of action of immunosuppressive agents are being investigated and treatments are being tested in clinical trials to optimize the balance of efficacy and toxicity. Alternate-day treatment with corticosteroids is often recommended for nephrotic patients with idiopathic membranous nephropathy, but this approach has not been proved beneficial. Ongoing studies are evaluating whether cytotoxic drugs or cyclosporin A combined with prednisone is more effective than treatment with corticosteroids alone. Lipid-lowering drug therapy is warranted in cases of the persistent nephrotic syndrome to avert the cardiovascular sequelae of hyperlipidemia.
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PMID:NIH conference. Membranous nephropathy. 154 69

Serum concentrations of apolipoprotein(a) [apo(a)], the unique glycoprotein of lipoprotein(a), are increased in patients with end-stage renal failure. We prospectively studied serum apo(a) and other lipoproteins in 20 consecutive patients, ages 46 +/- 11 years, before and for six months after successful renal transplantation. All patients received cyclosporine, and no patient was treated for hyperlipidemia. The mean creatinine clearance increased from 7.5 mL/min before transplant surgery to 40.9 mL/min six months afterwards (P less than 0.001). Apo(a) decreased from a median of 403 units/L before transplantation to 184 units/L at one week (P less than 0.001) and was 170 units/L (P less than 0.001) at six months. For the assay used, 1 unit of apo(a) is equivalent to 1 mg of lipoprotein(a). In contrast, from baseline to six months, increases were found for low-density lipoprotein (LDL) cholesterol (P = 0.03), high-density lipoprotein cholesterol (P = 0.06), apo B (P = 0.07), and apo A-I (P = 0.01). The decrease in apo(a) in individual patients was significantly correlated with the increase in creatinine clearance (r = -0.48, P less than 0.001). The single patient who developed nephrotic syndrome after renal transplantation had marked increases in apo(a) (693-1595 units/L), apo B, and LDL cholesterol, which paralleled the degree of proteinuria. These findings suggest that abnormal renal function affects the regulation of lipoprotein(a) metabolism.
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PMID:Decreases in apolipoprotein(a) after renal transplantation: implications for lipoprotein(a) metabolism. 154 51

A prospective study was performed in order to evaluate the efficacy of oral cyclophosphamide and chlorambucil in inducing a remission in children with steroid-resistant primary nephrotic syndrome (NS). Out of 215 children with steroid-resistant primary NS, 164 had been followed from one to 10 years. The children had a mean age of 8.2 years, with a range from one to 16 years. Steroid resistance was more common in children over six years of age compared with the other age groups. Hematuria was seen in 68 of the 164 children (41%); hypertension in 41 (25%); and hyperlipidemia in 112 (68%). Hypocomplementemia was noted in 24 of the 65 (37%) children in whom complement concentrations were determined. Renal biopsy was performed in 117 of the children. Pathologic changes consisted of minimal change nephrotic syndrome (MCNS) in 14 children (12%), membranoproliferative glomerulonephritis (MPGN) in 45 (38%), focal segmental glomerulosclerosis (FSGS) in 20 (25%), mesangial proliferation (MP) in 23 (20%), and membranous glomerulonephritis in six children (5%). Cyclophosphamide (2 mg/kg/day) was given to 164 patients, with complete remission and partial remission rates of 20.7% (34 of 164 children) and 24.4% (40 of 164 children), respectively. In this group, sustained remission and sustained partial remission rates were found in 20% (32 children) and 13% (21 children), respectively. Chlorambucil was given to 40 children with steroid- and cyclophosphamide-resistant nephrotic syndrome, with total remission and partial remission rates of 20% (eight children), and 12.5% (five children), respectively. These rates did not change during the follow-up. Thus, cyclophosphamide is valuable in the treatment of children with steroid-resistant NS with a variety of histologic changes.
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PMID:Long-term follow-up in children with steroid-resistant nephrotic syndrome. 158 94

The nephrotic syndrome results from altered glomerular permselectivity, causing urinary protein loss, reduced albumin concentration, oncotic pressure (pi), and hyperlipidemia. Hepatic lipid and apolipoprotein synthesis increases and lipoprotein catabolism decreases. Decreased lipoprotein catabolism follows the onset of proteinuria but is not associated with hereditary analbuminemia [Nagase analbuminemic rat (NAR)] if proteinuria is absent. We measured plasma apolipoproteins (apo) AI, B, and E levels, their mRNA concentrations in liver, and the transcription rate of each mRNA in rats with Heymann nephritis (HN) or NAR to determine which alterations occurred in NAR alone without proteinuria. Plasma apo AI, B, and E were increased in both HN and NAR. Cholesterol and apo AI were inversely proportional to pi and independent of urinary protein loss or the presence of albumin in plasma. In contrast, triglycerides (TGs) were significantly greater in HN and were increased out of proportion to apo B. The concentration of apo AI mRNA increased in liver of both HN and NAR as did apo AI transcription. Apo E mRNA increased in neither HN nor NAR, whereas apo B mRNA increased only in HN. Transcription of neither apo B nor E increased. Plasma apo AI levels are likely to be regulated transcriptionally at the level of protein synthesis, whereas plasma apo B and E levels are regulated either posttranscriptionally, at the level of protein catabolism, or at both sites. Lipoproteins rich in TG and poor in apo B appear after the development of proteinuria but not as a consequence of analbuminemia alone. The accumulation of TG-rich apo B containing lipoproteins in rats with HN may result from impaired lipolysis occurring as a consequence of proteinuria.
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PMID:Apolipoprotein gene expression in analbuminemic rats and in rats with Heymann nephritis. 159 Apr 20

The nephrotic syndrome is often accompanied by hyperlipidemia associated with an increased risk of accelerated atherosclerosis. The present study was undertaken to evaluate the effects of pravastatin, a novel competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on the serum lipids and apolipoproteins in patients with this syndrome and marked hyperlipidemia. Eleven adult patients received 10 mg of pravastatin twice daily for 4 to 8 weeks. The total serum cholesterol decreased from 426 +/- 44 to 309 +/- 18 mg/dl (-27.4%, mean +/- S.E.; p less than 0.01) following administration of pravastatin. The serum triglyceride decreased from 332 +/- 122 to 229 +/- 50 mg/dl (-30.9%), although this change was not significant. Despite the fact that the HDL cholesterol level was barely changed (51 +/- 7 to 51 +/- 6 mg/dl), the LDL cholesterol fell from 313 +/- 30 to 211 +/- 16 mg/dl (-32.5%; p less than 0.005), and the LDL to HDL cholesterol ratio fell from 7.57 +/- 1.59 to 4.94 +/- 0.88 (-34.8%; p less than 0.05). These changes caused the atherogenic index to decline from 9.6 +/- 2.4 to 6.1 +/- 1.2 (-36.5%; p less than 0.05). No significant alterations could be found among apolipoproteins A-1, A-2, B, C-2, C-3, and E. During the present study period, pravastatin was well tolerated and did not affect the serum protein, albumin, serum urea nitrogen, creatinine levels, or urine protein excretion. Also, there were no serious adverse effects. Pravastatin appears to be effective for treating patients with hyperlipidemia of the nephrotic syndrome.
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PMID:Effects of pravastatin on serum lipids and apolipoproteins in hyperlipidemia of the nephrotic syndrome. 163 84


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