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)

1. The primary aim of this study was to assess the impact of renal haemodynamics on the pharmacokinetic behaviour of ibuprofen enantiomers. Thirty-two patients and ten age-matched healthy volunteers participated in this study. These patients had at least one of the following risk factors for cardiovascular disorders: hypertension, diabetes mellitus, hyperlipidaemia and hyperuricaemia with or without consequent complications such as coronary artery disease, congestive heart failure, cerebral vascular disease, and chronic renal failure. Renal function in these patients was thus characterized by unstable renal haemodynamics that might render them susceptible to ibuprofen-incurred renal damage. 2. Each subject received a single oral dose of 800 mg of racemic ibuprofen. The pharmacokinetic parameters of (S)- and (R)-ibuprofen, t 1/2(S), t 1/2(R), AUC(S), AUC(R), V/F(R), and CL/F(R), for each individual were determined from respective plasma concentration-time curves. To assess the effect of individual clinical conditions on the disposition of ibuprofen enantiomers, the arithmetic means of these pharmacokinetic parameters for each disease group were compared with those of the healthy volunteers by a t-test. 3. All of these disease groups showed elevated AUC(S) and higher (S)/(R) AUC ratios. These disease states along with gender and age were analyzed by multiple linear regression to discern significant factors for elevating AUC(S). Of these, advanced age (P = 0.02) and hypertension (P = 0.03) were identified as independent factors contributing to AUC(S) increase in this population. Thus, patients with these two clinical conditions are at particular risk from the adverse renal effect of ibuprofen.
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PMID:Stereoselective disposition of ibuprofen in patients with compromised renal haemodynamics. 852 70

Hypertension, diabetes and hyperlipidemia are risk factors for life-threatening complications such as end-stage renal disease, coronary artery disease and stroke. Why some patients develop complications is unclear, but only susceptibility genes may be involved. To test this notion, we studied crosses involving the fawn-hooded rat, an animal model of hypertension that develops chronic renal failure. Here, we report the localization of two genes, Rf-1 and Rf-2, responsible for about half of the genetic variation in key indices of renal impairment. In addition, we localize a gene, Bpfh-1, responsible for about 26% of the genetic variation in blood pressure. Rf-1 strongly affects the risk of renal impairment, but has no significant effect on blood pressure. Our results show that susceptibility to a complication of hypertension is under at least partially independent genetic control from susceptibility to hypertension itself.
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PMID:Renal disease susceptibility and hypertension are under independent genetic control in the fawn-hooded rat. 852 50

A functioning kidney transplant provides the uraemic diabetic patient a greater survival with greater rehabilitation than does either CAPD or maintenance haemodialysis. There are no reports, however, of prospective controlled studies of dialysis versus kidney transplantation in diabetic patients whose therapy was assigned randomly. For the minority ( < 10%) of diabetic ESRD patients who have insulin-dependent diabetes mellitus (IDDM), serious consideration should be devoted to performance of a combined pancreas and kidney transplant to cure diabetes. No matter which ESRD therapy has been elected, optimal rehabilitation in diabetic ESRD patients requires that effort be devoted to recognition and management of co-morbid conditions. Uraemia therapy, whether CAPD, haemodialysis or a kidney transplant should be individualized to the patient's specific medical and family circumstances. Attention to control of hypertension and hyperlipidaemia may slow the course of macrovascular disease, particularly of the coronary arteries, which threatens long-term survival of diabetic kidney recipients. Pretransplant cardiac evaluation is mandatory to identify and correct silent coronary artery disease that may be severe and life threatening. Survival is continuously improving in treating ESRD in diabetes by dialytic therapy, renal transplantation, and in IDDM, by combined pancreas and kidney transplantation. This inexorable progress in therapy reflects multiple small advances in understanding of the pathogenesis of extrarenal micro- and macrovasculopathy in an inexorable disease, coupled with safer immunosuppression.
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PMID:Management choices in diabetic end-stage renal disease. 857 82

In patients with diabetic nephropathy retinopathy is always present and proliferative retinopathy is common. Retinopathy tends to deteriorate as renal failure develops particularly in patients with poorly controlled blood pressure and in patients in whom no retinal treatment has been given before development of renal failure. Treatment of hypertension and of end stage renal failure will improve macular edema and stabilize vision. As the progression of diabetic retinopathy is independent of diabetic nephropathy and not reversed by treatment of nephropathy, further follow-up and treatment of diabetic retinopathy are imperative. In recent years medical treatment of arterial hypertension and facilities for dialysis and kidney transplantation have become available, and patients are now treated at a much earlier stage of their renal disease. Consequently, were are seeing fewer patients with renal failure and severe hypertensive fundus changes. Nevertheless, arterial hypertension is still a very important problem in diabetic patients with and without nephropathy and complications of atherosclerosis are common as a result of chronic hypertension and hyperlipidemia.
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PMID:[Eye fundus of the diabetic patient with nephropathy and hypertensive retinopathy. Macroangiopathic complications]. 858 Dec 31

We designed a short-term randomized controlled study in 12 adult patients with chronic renal failure to assess the metabolic effects of a low-protein diet (LPD) supplemented or not with ketoacids (Cetolog, Clintec Corp., France). Dietary survey included a monthly 3-day food record and a 24-hour urinary urea measurement. After a baseline period (1.11 g protein, 31.7 kcal/kg BW/day), patients reduced their protein intake (PI) to 0.71 g/kg BW/day. Energy intake (EI) was kept constant (31.4 kcal/kg BW/day) during the 3-month period. Baseline plasma lipids did not show overt hyperlipemia. After reducing PI, a significant increase in apolipoprotein AI and the Apo-AI/Apo-B ratio was observed. Plasma Lp(a) levels were elevated at baseline and did not change during the 3-month LPD period. There was no difference between groups receiving ketoacids or not. Thus, in adult chronic renal failure, under a sufficient EI, reducing PI by 40% had a beneficial effect on plasma lipid profile. This improvement in lipid profile might reduce the high cardiovascular risk in these patients.
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PMID:Effects of low-protein diet supplemented with ketoacids on plasma lipids in adult chronic renal failure. 867 7

In children with steroid-resistant nephrotic syndrome (SRNS) hyperlipidaemia may in the long term be associated with progressive renal insufficiency and increased risk of coronary heart disease. We have assessed the efficacy and tolerability of diet prior to and in combination with a hydroxymethylglutaryl CoA reductase inhibitor, simvastatin, in seven children with SRNS with a mean age of 8 years (range 1.8-16.3 years). Dietary advice to maintain adequate energy and protein intakes with reduced saturated fat and cholesterol intake had little impact on lipid levels pre treatment (mean reduction in cholesterol 1 mmol/l, triglyceride 1.1 mmol/l) but was maintained throughout the study duration. The mean cholesterol and triglyceride concentrations pre treatment were 12.1 +/- 2 (SEM) mmol/l and 8 +/- 2.1 (SEM) mmol/l, respectively. On a median simvastatin dose of 10 mg/day (range 5-40 mg) there was a 41% reduction in cholesterol to 6.6 +/- 0.77 (SEM) mmol/l and a 44% reduction in triglyceride to 3.9 +/- 1.38 (SEM) mmol/l at 6 months which was sustained at 12 months in five patients. The drug was well tolerated with no clinical side effects being noted. Over 6 months the mean plasma albumin concentrations increased from 18.2 +/- 1.26 (SEM) g/l to 23 +/- 2.51 (SEM) g/l, accounted for by three patients (1 complete remission, 1 partial remission, 1 end-stage renal failure). Plasma creatinine concentrations remained stable in five patients with two having progressive chronic renal failure. Growth parameters for both weight and height were maintained. Simvastatin has a beneficial effect on abnormal lipid levels in SRNS but the effectiveness of long-term therapy needs to be evaluated.
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PMID:Hyperlipidaemia, diet and simvastatin therapy in steroid-resistant nephrotic syndrome of childhood. 870 4

Lipoprotein abnormalities are common in patients with chronic renal failure (CRF) on either dialysis or conservative therapy. In order to investigate the changes in lipid and apolipoprotein pattern from early CRF to dialysis treatment, plasma lipids with apoproteins AI, B, E, CII, CIII, CII/CIII ratio, E/CIII ratio, parathyroid hormone (PTH) and insulin levels were examined in 72 patients with different degrees of CRF and 31 patients on hemodialysis (HD), and compared the values of 28 controls. A significant decrease in the Apo CII/CIII ratio was the earliest lipoprotein abnormality to occur in CRF. Hypertriglyceridemia (HTG) with reduced high-density lipoprotein cholesterol levels, increased Apo CIII and decreased Apo E/Apo CIII ratio only occurred in more advanced renal failure (creatinine clearance < 31 ml/min). HD patients showed a general worsening of the lipoprotein profile with elevated Apo E levels and indirect evidence of remnant accumulation. While PTH did not have any significant influence on lipoprotein pattern, increased insulin levels during HD might partly account for the HTG of these patients. Our results point to elevated Apo CIII, reduced Apo CII/Apo CIII and Apo E/ Apo CIII ratios as typical features of uremic hyperlipidemia and show that a defective triglyceride removal is the major pathogenetic mechanism of uremic HTG. HD treatment seems generally to worsen the lipid and apolipoprotein pattern observed in the predialytic stage of CRF.
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PMID:Lipoprotein abnormalities in chronic renal failure and dialysis patients. 873 41

The effect of hyperlipidemia on the progression of chronic renal failure was investigated in 104 chronic renal failure patients, aged 39.3 +/- 2.9 years. The follow up period was 4.1 +/- 2.9 years. The serum creatinine level was 2.1 +/- 1.1 (mean +/- SD) mg/dl at the beginning of study and increased to 8.7 +/- 4.4 mg/dl at the end of the study. The reciprocal serum creatinine concentration (1/Cr) was plotted against the observation time, and the slope was calculated. The absolute value of the slope was used as the progression rate of renal impairment. The progression rate was positively related to total cholesterol level or urinary protein score, while it was negatively related to total protein level. Without the influence of urinary protein score, the progression rate correlated with total cholesterol level. The result suggests that hypercholesterolemia may be an independent aggravating factor in the progression of renal dysfunction in chronic renal failure patients.
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PMID:Hypercholesterolemia and the progression of the renal dysfunction in chronic renal failure patients. 900 82

The efficacy and safety of hydroxymethylglutaric coenzyme A reductase inhibitor (statins) in the treatment of hyperlipidemia were evaluated in 12 infants and children with steroid-resistant nephrotic syndrome followed prospectively for 1 to 5 years. All patients experienced a hypolipidemic response with a marked reduction in their total cholesterol (40%), low-density lipoprotein cholesterol (44%), and triglyceride levels (33%), but no appreciable change in high-density lipoprotein cholesterol. Statin therapy was well tolerated without clinical or laboratory adverse effects. In spite of a significant hypolipidemic response to statin therapy there were no changes observed in the degree of proteinuria, hypoalbuminemia, or in the rate of progression to chronic renal failure. Long-term controlled studies with statin therapy are needed to further document or negate their renoprotective role in refractory nephrotic syndrome.
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PMID:Management of hyperlipidemia in children with refractory nephrotic syndrome: the effect of statin therapy. 906 27

Abnormal renal diseases including nephrotic syndrome and chronic renal failure are associated with hyperlipidemia, significance of abnormal lipid metabolism has been thought to be limited in some inherited renal diseases. However, recent studies have postulated that glomerulosclerosis is induced by hyperlipidemia and is in common with atherosclerosis. This involvement is found in the progressive renal disorders, e.g., focal glomerular sclerosis, diabetic nephropathy and glycogen storage disease. Interaction between macrophages and mesangial cells may play an important role in such conditions. This evidence is supported by experimental models with hyperlipidemia. On the other hand, discovery and new hereditary metabolic disorders, such as type III hyperlipoproteinemia and lipoprotein glomerulopathy, shows that apolipoprotein (apo) E abnormalities are responsible for the glomerular lesions. Especially, lipoprotein glomerulopathy has specific features different from those of lipid-induced renal diseases. In this disease, apo E Sendai which results from new substitution (Arginine 145-->Proline) may induce intraglomerular lipoprotein thrombi characteristic of lipoprotein glomerulopathy.
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PMID:Abnormal lipid metabolism and renal disorders. 916 48


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