Lipoprotein (a) and the kidney

Abstract

Summary: Cardiovascular disease is the main cause of death in chronic renal failure patients. Lipoprotein (a) [Lp(a)] is an independent risk factor for development of vascular disease in non‐renal and renal populations. the atherogenicity of Lp(a) is thought to relate to the structural homology between its apolipoprotein moiety [apo(a)] and plasminogen. Raised low‐density‐lipoprotein (LDL) cholesterol concentrations increase the atherogenic potential of Lp(a). Normally Lp(a) level is genetically determined but in renal disease positive correlations with urinary protein loss and peritoneal dialysate protein loss have been found. Levels are highest in nephrotic patients and chronic renal failure patients treated with peritoneal dialysis but are also increased in pre‐dialysis and haemodialysis patients. Lipoprotein (a) falls following renal transplantation but cyclosporine therapy may adversely affect post transplant cardiovascular risk profile. Treatment with antiproteinuric drugs (converting enzyme inhibitors or non‐steroidal anti‐inflammatory agents) has been shown to reduce Lp(a) (and total cholesterol) concentrations. Most lipid‐lowering drugs do not affect Lp(a) concentration but lowering LDL‐cholesterol alone may significantly reduce the atherogenic effect of Lp(a). Routine measurement of Lp(a) concentration is not recommended but antiproteinuric therapy should have favourable effects on cardiovascular risk profile.