The most widely studied hyperlipidemies in patients affected by renal insufficiency or subsequent to kidney transplant present phenotype IIa, IIb or IV. The lipidic alteration most frequently observed in chronic renal insufficiency and/or dialytic treatment is represented by hypertrigliceridemia as a result of: 1) altered VLDL metabolism; 2) reduced activity of lecithin cholesterol acyltransferase (LCAT); 3) decrease in Apo-A1 and HDL3. Furthermore, marked anomalies in lipoprotein Lp (a) have been reported in hemodialysis. In patients undergoing peritoneal dialysis, hyperlipidemia arises from both an anomalous retrograde absorption of glucose and protein dispersion. Following kidney transplant the most frequent hyperlipidemia is hypercholesterolemia, consequent to immunosuppressive treatment (mainly steroids and cyclosporin). The documented significant increase of cardiovascular risk in the presence of hyperlipidemia points to the need for a clearer etiopathogenic definition of this anomaly, as well as the necessity to find an efficacious pharmacological treatment.
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