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

Our study indicates that in renal failure elevated plasma triglyceride can first be detected when the GFR falls to 50 ml/min. Hypertriglyceridemia is the commonest abnormality found and increases further when the GFR falls below 10 ml/min. Plasma cholesterol levels remain normal even at low levels of renal function. Although plasma growth hormone, glucagon, and insulin levels become elevated when renal function diminishes, there is no definite correlation of their levels and GFR. A decreased incidence of hyperlipidemia observed in patients sustained by maintenance hemodialysis for over 5 yrs may in part be due to the triglyceride lowering effect of growth hormone and glucagon and/or the cholesterol lowering effect of insulin.
 ...
PMID:Uremic hyperlipoproteinemia: correlation with residual renal function and duration of maintenance hemodialysis. 91 Mar 86

The prevalence of coronary heart disease (58%) in 43 patients with analgesic nephropathy with moderate to severe chronic renal failure was significantly higher than in the general population of the same age and sex. Mean serum triglyceride concentration and mean diastolic blood pressure were significantly higher in the group with coronary heart disease (214 mg/dl and 102 mm Hg, respectively) than in the group without it (162 and 94). Serum triglyceride values correlated inversely with GFR, indicating that hypertriglyceridemia was largely due to associated chronic renal failure; a specific effect of analgesic abuse on prevalence of heart disease, noted by others, could not be assessed in the absence of GFR-matched controls. The prevalence of coronary heart disease was significantly higher (81%) in the group with combined hyperlipidemia (hypertriglyceridemia and hypercholesteremia) compared to the groups without it or with normal serum triglyceride concentrations (44 and 41%, respectively). Hypotryptophanemia (a possible cause of hyperlipidemia in the nephrotic syndrome) was present in 77% of patients.
 ...
PMID:Increased prevalence of coronary heart disease in analgesic nephropathy: relation to hypertension, hypertriglyceridemia and combined hyperlipidemia. 126 11

Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A inhibitor, was given to 14 patients with unremittent nephrotic syndrome (heavy proteinuria with hyperlipidaemia) for 6 months. Treatment was started at an initial dose of 20 mg/day, increasing to a maximum of 80 mg/day. Treatment was well tolerated except in two patients: one developed rhabdomyolysis and one severe hypertriglyceridaemia requiring an additional antihyperlipidaemic agent. Lovastatin was effective in reducing serum cholesterol, LDL-C and apolipoprotein B in the remaining 12 patients. Cholesterol was reduced by 31% from 8.24 +/- 0.49 mmol/l (mean +/- SEM) to 5.7 +/- 0.18 mmol/l after 6 months (P less than 0.001). LDL-C was normalized to 3.26 +/- 0.21 mmol/l from a pretreatment value of 5.76 +/- 0.48 mmol/l (P less than 0.001), a decrease of 43%. Serum apolipoprotein B was also normalized to 1.11 +/- 0.09 g/l from a basal level of 1.51 +/- 0.10 g/l (P less than 0.05). Triglyceride, HDL-C and apolipoprotein A1 concentrations were unchanged. Proteinuria as well as renal albumin clearance were unchanged. GFR by plasma radioisotope Cr-EDTA clearance for the whole group was unaltered by treatment. However, among those with relatively good pretreatment renal function (GFR greater than 70 ml/min per 1.73 m2), GFR increased at the end of 6 months' treatment (118.2 +/- 15 ml/min per 1.73 m2 versus 77.6 +/- 8.4 ml/min per 1.73 m2 in wash-out phase).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Lovastatin in glomerulonephritis patients with hyperlipidaemia and heavy proteinuria. 131 86

A number of risk factors associated with the development of diabetic nephropathy has been described, such as elevated blood pressure, poor metabolic control, hyperlipidemia, and smoking. Abnormal albuminuria also is associated with progression of renal disease, but has until recently been considered principally a marker of disease activity rather than a risk factor. This article discusses the role of elevated blood pressure versus abnormal albuminuria in a genesis and prediction of renal disease in diabetes. Controversy exists regarding parental disposition to hypertension and early blood pressure elevation in the course of diabetes, but all studies agree that elevated blood pressure--in the presence of abnormal albuminuria--constitutes a risk factor. Because abnormal albuminuria is associated with progression disease, it may itself be a risk factor because increased macromolecular traffic over the glomerular membrane may produce glomerulopathy. Problems related to blood pressure measurement are important, and 24-h recordings of blood pressure may be recommended in some situations. Regarding renal structure, preliminary results suggest that structural lesions precede blood pressure elevation. The solid end point for evaluation of renal disease progression is the fall rate of GFR, with abnormal albuminuria as an intermediate end point, also in drug trials. Abnormal albuminuria may constitute a new indication for antihypertensive treatment, being, as it is, a clear indicator of organ damage, whereas elevated blood pressure with normal AER may not increase risk substantially.
 ...
PMID:Blood pressure elevation versus abnormal albuminuria in the genesis and prediction of renal disease in diabetes. 139 16

The role of hyperlipidaemia for the outcome of renal transplantation was evaluated in a prospective study involving 151 patients. Graft losses were associated with more pronounced pre-transplant lipid abnormalities. An increased risk of graft loss during the first two post-transplant years was found in patients with marked pre-transplant hypercholesterolaemia (> or = 6.9 mmol L-1, P = 0.014; relative risk 2.2). Hypercholesterolaemia > or = 6.9 mmol L-1 at 6 months after transplantation, present in 41/115 patients, was associated with a lower GFR (P = 0.007) and more pronounced albuminuria (P = 0.009) at 2 years. In patients with graft dysfunction (serum creatinine > 160 mumol L-1) at 2 years, more pronounced lipid abnormalities before and at 6 months after transplantation were found. Between 6 months and 2 years, total and LDL cholesterol did not change significantly, but HDL cholesterol decreased (P = 0.03). In conclusion, hyperlipidaemia is also a risk factor for the long-term outcome in renal transplantation. Further investigations are needed to determine whether graft losses and late graft failure can be prevented or ameliorated by treating hyperlipidaemia in renal transplantation.
 ...
PMID:Hyperlipidaemia in renal transplantation--risk factor for long-term graft outcome. 758 13

Hyperlipidaemia of 18 male and 20 female patients following successful renal transplantation was treated with daily 20 mg fluvastatin (Lescol) for 12 weeks. The patients were several months after transplantation, and their total cholesterol levels exceeded 6.5 mmol/l following an 8-week diet. The effect of fluvastatin on the levels of total cholesterol, HDL, LDL, triglyceride, Apo A1 and Apo B, as well as of lipoprotein(a) was examined. Furthermore, changes of the renal function (GFR-urea, creatinine, uric acid) and hepatic function (bilirubin, GOT, GPT, CPK, ALP) were followed up, together with the body weight and blood pressure. The results of the examinations are summarized as follows: Fluvastatin may be administered effectively and without side effects in a daily dose of 20 mg in appropriately selected renal transplant patients. The average total cholesterol values, which were 7.91 mmol/l in men and 7.78 mmol/l in women following the diet, were reduced by 22-25% (p < 0.001) after 6 and 12 weeks, respectively, of fluvastatin treatment. The levels of LDL also decreased significantly (p < 0.001): in response to a 20 mg evening dosage, reduction of more than 25% was observed in 78% of men and 65% of women. Reductions of the Apo B levels were more pronounced in the females (18.3% men vs. 21.2% women). The ratio C/HDL-C decreased both in men (from 5.49 to 4.19) and in women (from 4.83 to 4.02). The ratio Apo B/Apo A1 also decreased (men: from 0.86 to 0.73, women: from 0.73 to 0.66). The concentrations of HDL and Apo A1 did not increase significantly, the reductions in the levels of triglyceride and lipoprotein(a) were not considerable either. An increase in the levels of hepatic enzymes and CPK was not encountered during the administration of fluvastatin. In two patients the levels of serum bilirubin increased by 2-4 micromol/l. Three patients complained about temporary myalgias of the sacroiliac or lumbar region which, however, were not accompanied by elevated CPK levels. The monitored levels of cyclosporine, urea and creatinine did not increase significantly during the 12 weeks of treatment. Two patients had temporary gastric complaints.
 ...
PMID:Fluvastatin (Lescol) treatment of hyperlipidaemia in patients with renal transplants. 920 45

Although hyperlipidemia has been associated with the progression of glomerulosclerosis, little attention has been directed toward the use of lipid-lowering agents in altering diabetic nephropathy. We tested the hypothesis that lovastatin and the combination of lovastatin and enalapril would preserve renal function in streptozotocin-induced diabetic Wistar rats. Five groups of animals were studied: group 1, nondiabetic (n = 10); group 2, diabetic, insulin only (n = 12); group 3, lovastatin, (15 mg/kg/day, n = 13); group 4, enalapril, (50 mg/L drinking water, n = 10) and group 5, lovastatin plus enalapril, (n = 14). After 8 weeks of treatment, glomerular filtration rate (GFR, insulin clearance) was measured in anesthetized animals. The diabetic group was characterized by a GFR of 0.18 +/- 0.03 ml/min/g of kidney weight (gKW), a blood glucose level of 441 +/- 36 mg/dL, plasma cholesterol and triglyceride levels of 64 +/- 6.0 and 103 +/- 26.0 mg/dL. Lovastatin preserved GFR, 0.52 +/- 0.06 ml/min/gKW compared with the diabetic control subjects (P < 0.05). Enalapril also maintained GFR (0.42 +/- 0.06 ml/min/gKW, P < 0.05). In the lovastatin plus enalapril group, GFR (0.62 +/- 0.05 ml/min/gKW) was greater than in the enalapril group (P < 0.05), but was not different from the lovastatin group. Plasma lipid levels were not altered in any of the groups. Assessment of the kidneys by histology after treatment showed that the mesangial matrix injury score was better in the lovastatin, enalapril, and lovastatin plus enalapril groups compared with the diabetic group (P < 0.05). Lovastatin, enalapril, and lovastatin plus enalapril abrogated the decline in GFR and glomerular injury in diabetic rats. Lovastatin's direct renal protective effect seems to be independent of its lipid-lowering properties.
 ...
PMID:Lovastatin preserves renal function in experimental diabetes. 1021 Mar 55

The present study investigated the effect of curcumin on adriamycin (ADR) nephrosis in rats. The results indicate that ADR-induced kidney injury was remarkably prevented by treatment with curcumin. Treatment with curcumin markedly protected against ADR-induced proteinuria, albuminuria, hypoalbuminaemia and hyperlipidaemia. Similarly, curcumin inhibited ADR-induced increase in urinary excretion of N-acetyl-beta-D-glucosaminidase (a marker of renal tubular injury), fibronectin and glycosaminoglycan and plasma cholesterol. Curcumin restored renal function in ADR rats, as judged by the increase in GFR. The data also demonstrated that curcumin protected against ADR-induced renal injury by suppressing oxidative stress and increasing kidney glutathione content and glutathione peroxidase activity. In like manner, curcumin abolished ADR-stimulated kidney microsomal and mitochondrial lipid peroxidation. These data suggest that administration of curcumin is a promising approach in the treatment of nephrosis caused by ADR.
 ...
PMID:Curcumin prevents adriamycin nephrotoxicity in rats. 1069 26

Chronic renal failure (CRF) is the irreversible deterioration of renal function that gradually progresses to end stage renal disease (ESRD). The chief causes of CRF include obstructive uropathy, primary glomerular diseases, reflux nephropathy and hypoplastic or dysplastic kidneys. Progressive hyperperfusion and hyperfiltration causes increasing glomerular injury and further renal damage. Symptoms of CRF are usually seen when GFR is between 10-25% of normal. Children with severe CRF often suffer from failure to thrive, growth retardation, acidosis, anemia and renal osteodystrophy. Management of CRF aims at retarding progression of renal damage and treatment of complications related to renal dysfunction. Measures suggested to retard progression include protein restriction, strict control of hypertension, use of angiotensin converting enzyme inhibitors and control of hyperlipidemia. Appropriate amounts of protein and calories are recommended to prevent growth failure. Nutritional supplements are often required. The availability of recombinant erythropoietin, calcitriol and human growth hormone has significantly improved the management of these patients. Once ESRD supervenes, renal replacement therapy in the form of chronic peritoneal or hemodialysis and transplantation is necessary.
 ...
PMID:Evaluation and treatment of chronic renal failure. 1079 66

This study correlated the dynamic effects of sirolimus (rapamycin; RAPA) and cyclosporine (CsA) alone versus in combination to produce renal dysfunction, myelosuppression, or hyperlipidemia, with their corresponding blood and tissue concentrations. After salt-depleted rats were treated with RAPA (0.4 to 6.4 mg/kg per d) and/or CsA (2.5 to 20.0 mg/kg per d) for 14 d, the GFR, lipid levels, bone marrow cellularity, and CsA/RAPA concentrations in whole blood versus liver or renal tissues were measured, and the median effect model was used to discern the type of drug interactions. Compared with vehicle controls (1.98 +/- 0.34 ml/min), GFR values were reduced only by large doses of drug monotherapy, namely RAPA (3.2 mg/kg per d = 1.2 +/- 0.02 ml/min or 6.4 mg/kg per d = 1.3 +/- 0.2 ml/min; both P < 0.01) or CsA (10.0 mg/kg per d = 1.2 +/- 0.1 ml/min or 20.0 mg/kg per d = 0.8 +/- 0.4 ml/min; both P < 0.01). In contrast, hosts that were treated with smaller doses of CsA/RAPA combinations showed more pronounced effects in reduction of GFR values: 2.5/0.4 mg/kg per d, modestly (1.5 +/- 0.5 ml/min; P < 0.01); 5.0/0.8 mg/kg per d, moderately (0.23 +/- 0.01 ml/min; P < 0.001); and higher-dose groups, markedly. The exacerbation of renal dysfunction seemed to be due to a pharmacokinetic interaction of RAPA to greatly increase CsA concentrations in whole blood and, particularly, in kidney tissue. In contrast, the pharmacodynamic effects of CsA to potentiate two RAPA-mediated toxicities-myelosuppression and increased serum cholesterol/low-density lipoprotein cholesterol-occurred independently of pharmacokinetic interactions. RAPA aggravates CsA-induced renal dysfunction owing to a pharmacokinetic interaction, whereas CsA produces a pharmacodynamic effect that augments RAPA-induced myelosuppression and hyperlipidemia.
 ...
PMID:Pharmacokinetic interactions augment toxicities of sirolimus/cyclosporine combinations. 1131 66


1 2 3 Next >>