LIPOPROTEIN (A) AND THE KIDNEY

Cardiovascular disease is the main cause of death in chronic renal fai lure patients. Lipoprotein (a) [Lp(a)] is an independent risk factor f or development of vascular disease in non-renal and renal populations. The atherogenicity of Lp(a) is thought to relate to the structural ho mology between its apolipoprotein moiety [apo(a)] and plasminogen. Rai sed low-density-lipoprotein (LDL) cholesterol concentrations increase the atherogenic potential of Lp(a). Normally Lp(a) level is geneticall y determined but in renal disease positive correlations with urinary p rotein loss and peritoneal dialysate protein loss have been found. Lev els are highest in nephrotic patients and chronic renal failure patien ts treated with peritoneal dialysis but are also increased in pre dial ysis and haemodialysis patients. Lipoprotein (a) falls following renal transplantation but cyclosporine therapy may adversely affect post tr ansplant cardiovascular risk profile. Treatment with antiproteinuric d rugs (converting enzyme inhibitors or non-steroidal anti-inflammatory agents) has been shown to reduce Lp(a) (and total cholesterol) concent rations. Most lipid-lowering drugs do not affect Lp(a) concentration b ut lowering LDL-cholesterol alone may significantly reduce the atherog enic effect of Lp(a). Routine measurement of Lp(a) concentration is no t recommended but antiproteinuric therapy should have favourable effec ts on cardiovascular risk profile.