Lipid Metabolism in 31 Chinese Patients on three 2–L Exchanges of CAPD

Abstract

The authors measured nine biochemical parameters -urea, creatinine, albumin, total cholesterol, total triglycerides, HDL- cholesterol, C3, C4 and post-heparin hepatic and lipoprotein lipase activities in 31 Chinese patients, who were carrying out three 2–L CAPD exchanges per day. Uremic plasma from 19 patients also was tested for the presence of hepatic and lipoprotein lipase inhibitors. Anthropometry included a record of height, weight and skin-fold thicknesses. The CAPD patients had mild hypertriglyceridemia -144 ± 60 vs 106 ± 55 in males, p = 0.05 and 176 ± 92 vs 100 ± 45 in females, p < 0.005. Their mean total cholesterol concentration did not differ from that of controls. Mean HDL-cholesterol concentration in CAPD patients was significantly reduced 28 ± 10 vs 42 ± 10 in males and 30 ± 15 vs 42 ± 13 in females. Both hepatic lipase -9.54 ± 4.26 in males and 30 ± 15 vs 42 ± 13 in females, and lipoprotein lipase -1.96 ± 0.93 in males and 1.91 ± 1.09 in females were reduced in CAPD patients. The correlation between serum triglycerides (TG) and lipoprotein lipase activities in CAPD patients was weak, though significant, but there was none between lipoprotein lipase activities and HDL-cholesterol concentrations. The mean albumin concentration of CAPD patients was close to the lower limit of (though still within), the normal range. Serum albumin concentrations did not correlate with total cholesterol concentrations. The mean C3 was reduced below the normal range. C3 concentrations correlated with those of serum triglyceride and with adiposity indices. C4 did not change consistently. Plasma from CAPD patients inhibited lipoprotein lipase but did not interfere with hepatic lipase activities. Hepatic lipase activities correlated with C3, serum TG concentrations and adiposity index, probably reflecting improved nutritional status. Factors other than impaired triglyceride catabolism also are responsible for the lipid abnormalities in CAPD.

Abnormalities in lipid metabolism occur in chronic renal failure and persist in patients on hemodialysis (1). Defects in catabolism of triglyceride-rich lipoproteins have been demonstrated in vivo (2–7) and in vitro (8–13) and it appears that impaired triglyceride break down by peripheral tissues is the dominant cause of hypertriglyceridemia among hemodialysis patients (3, 5, 13). Lipid abnormalities also have been reported in CAPD patients (14–16). Although glucose absorption from the dialysis solutions may play a role, the pathogenetic mechanisms are not well defined. We have been treating our end-stage renal failure patients with CAPD but, unlike those in other centres, our patients carry out three 2– L exchanges daily. This paper describes an investigation of lipid metabolism in 31 patients.