COMPARISON OF LP(A) CONCENTRATIONS AND SOME POTENTIAL EFFECTS IN HEMODIALYSIS, CAPD, TRANSPLANTATION, AND CONTROL-GROUPS, AND REVIEW OF THELITERATURE

Apolipoprotein (a)- Lp(a)- is reported to be an independent risk facto r for coronary artery disease and for hemodialysis (HD) access occlusi on. Homology with plasminogen may predispose to thrombosis. High conce ntrations usually have been reported in patients on HD and on continuo us ambulatory peritoneal dialysis (CAPD), but near-normal values in ma ny kidney transplants (TP). We used Pharmacia immunoradiometric assay in 52 patients on HD, 58 on CAPD, 94 after TP, and 56 controls. The Lp (a) mean levels for CAPD, HD, TP, and control groups were 738, 647, 34 8, and 368 U/l and the medians were 542, 537, 96 and 143 U/l, respecti vely. The means and medians for CAPD and HD were significantly greater than those for TP and controls (p <0.003 for means and <0.005 for med ians). We found no significant difference between: (1) Lp(a) means or medians comparing HD and CAPD or TP and controls; (2) Lp(a) means for the 33 patients with insulin-dependent diabetes mellitus and the 171 w ithout; (3) number of occlusions of HD fistulae or grafts in patients with high Lp(a) values and without; (4) mean Lp(a) for CAPD patients o n gemfibrozil and also for TP patients on 3-hydroxy-methylglutaryl coe nzyme 1 reductase inhibitors, or diet alone, before and after treatmen t, and (5) mean Lp(a) values for HD and CAPD patients with and without myocardial infarction. Lp(a) did not correlate significantly with fra ctional shortening or left ventricular end systolic or diastolic diame ter by echocardiogram or with ejection fraction. For TP patients, Lp(a ) and serum creatinine correlated (p = 0.004), and mean Lp(a) for 71 T P on ciclosporin A exceeded that for the other 23 patients (p < 0.03). Lp(a) fell in 13 of 14 patients after TP (mean fall 77%). The dominan t Apo(a) isoform in 10 of 13 patients on CAPD or KD with high Lp(a) va lues was the equivalent of S2 (Utermann). Lp(a) in HD or CAPD is often elevated and regulated by both genetic and renal failure factors, but falls after TP with return of renal function and mainly genetic regul ation. Lp(a) was not a risk factor for coronary artery disease in HD o r CAPD patients and did not fall significantly with two drugs or diet.