RENOVASCULAR ARTERIOVENOUS DIFFERENCES IN LP[A] PLASMA-CONCENTRATIONSSUGGEST REMOVAL OF LP[A] FROM THE RENAL CIRCULATION

High plasma concentrations of lipoprotein[a] (Lp[a]) are considered a genetically determined risk factor for atherosclerosis. Lp[a] is produ ced by the liver. The site(s) and mechanism(s) of catabolism are prese ntly unclear. Lp [a] is elevated secondary to end-stage renal disease which suggests a direct or indirect role of the kidney in the metaboli sm of Lp[a]. We therefore investigated, by a simple in vivo approach, whether Lp[a] is removed by the human kidney. Lp[a] plasma concentrati ons were measured simultaneously by various methods in the ascending a orta and renal vein of 100 patients undergoing coronary angiography or coronary angioplasty. Lp[a] levels differed significantly between the two vessels even after correcting for hemoconcentration (20.1 +/- 21. 6 mg/dL versus 18.7 +/- 20.3 mg/dL, P < 0.001). This corresponds to a mean arteriovenous difference of -1.4 mg/dL or -9% of the arterial con centration. No Lp[a] or intact apo[a] could be detected in urine from healthy probands. Although we cannot assign the kidney a regulatory ro le for Lp[a] plasma levels in humans with normal renal function, we co nclude from our data that substantial amounts of this atherogenic lipo protein are taken up by the kidney. The underlying mechanisms are unkn own at the moment. This study therefore demonstrates for the first tim e that the human kidney plays an active role in the catabolism of Lp[a ]. This may explain the elevated Lp[a] concentrations found in patient s with chronic renal insufficiency.