[Alterations of fat metabolism in renal disease - pathogenetic mechanisms (author's transl)].
Hypertriglyceridaemia is often observed in patients (1) with chronic renal insufficiency, (2) on haemodialysis and (3) after successful renal transplantation. HDL cholesterol is reduced in all three groups of patients and plasma cholesterol is elevated after renal transplantation. In these three patient groups type IV hyperlipoproteinaemia is found most frequently and after renal transplantation there is a relative increase in the incidence of type II hyperlipoproteinaemia. The role of glucagon resistance and carnitine deficiency in the alteration of fat metabolism seen in patients with chronic renal failure and patients on haemodialysis is discussed. Other factors which may influence fat metabolism in uraemia include calcium and vitamin D status as well as beta adrenergic receptor blocking agents and diuretics. Steroid therapy may be one cause of the hypercholesterolaemia and hypertriglyceridaemia seen after renal transplantation. PHLP lipase activity is reduced in all three groups of patients. In nephrotic syndrome, if hypercholesterolaemia occurs, the HDL cholesterol fraction is increased and thus the cardiovascular risk may be lower than in the three patient group mentioned above.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D002331:Carnitine / Q000097:blood; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL; D004232:Diuretics / Q000494:pharmacology; D006801:Humans; D006951:Hyperlipoproteinemias / Q000209:etiology*; D007676:Kidney Failure, Chronic / Q000150:complications*; D016030:Kidney Transplantation; D050356:Lipid Metabolism; D008075:Lipoproteins, HDL / Q000097:blood; D009404:Nephrotic Syndrome / Q000378:metabolism; D006435:Renal Dialysis; D014280:Triglycerides / Q000097:blood
D000319:Adrenergic beta-Antagonists; D008076:Cholesterol, HDL; D004232:Diuretics; D008075:Lipoproteins, HDL; D014280:Triglycerides; D002784:Cholesterol; D002331:Carnitine
Fettstoffwechselstörungen bei Nierenkrankheiten - Pathogenetische Mechanismen.