Preβ1-high-density lipoprotein metabolism is delayed in patients with chronic kidney disease not on hemodialysis

Abstract

Preβ1-high-density lipoprotein (HDL) is a lipid-poor cholesterol acceptor that is converted to lipid-rich HDL by lecithin-cholesterol acyltransferase (LCAT). In patients receiving hemodialysis, preβ1-HDL metabolism is hampered even if HDL cholesterol is normal. Hemodialysis may affect preβ1-HDL metabolism by releasing lipases from the vascular wall due to heparin. We investigated whether preβ1-HDL metabolism is delayed in patients with chronic kidney disease (CKD) who are not receiving hemodialysis. We examined 44 patients with Stage 3 or higher CKD and 22 healthy volunteers (Control group). The patients with CKD were divided into those without renal replacement therapy (CKD group, n=22) and those undergoing continuous ambulatory peritoneal dialysis (CAPD group, n=22). Plasma preβ1-HDL concentrations were determined by immunoassay. During incubation at 37°C, we used 5,5-dithio-bis (2-nitrobenzoic acid) (DTNB) to inhibit LCAT activity and defined the conversion halftime of preβ1-HDL (CHTpreβ1) as the time required for the difference in preβ1-HDL concentration in the presence and absence of 5,5-DTNB to reach half the baseline concentration. The absolute and relative preβ1-HDL concentrations were higher, and CHTpreβ1 was longer in the CKD and CAPD groups than in the Control group. Preβ1-HDL concentration was significantly correlated with CHTpreβ1 but not with LCAT activity in patients with CKD and CAPD. Preβ1-HDL metabolism is delayed in patients with CKD who are not on hemodialysis. This preβ1-HDL metabolic delay may progress as renal function declines.