Low high-density lipoprotein cholesterol is not responsible for decreased paraoxonase activity in chronic renal failure.

BACKGROUND/AIMS:Human paraoxonase-1 (PON1) is responsible for the antioxidant effect of high-density lipoprotein (HDL) by inhibiting low-density lipoprotein oxidation. Previous studies discovered dyslipidemia (DL) and decreased PON1 activity in chronic renal failure (CRF). We aimed to determine PON and arylesterase activity, phenotypic distribution of the PON1 enzyme, and lipid profile in low and normal HDL cholesterol (HDL-C) patients with CRF, and renal transplant (TX), compared to primary DL. METHODS:116 CRF (low or normal HDL-C), 52 TX (low or normal HDL-C), and 62 DL patients (low or normal HDL-C) were included. PON and arylesterase activities were measured spectrophotometrically. Phenotype was determined using the dual substrate method. RESULTS:Aryl/HDL-C was significantly higher in low HDL-C patients. Patients with CRF had significantly lower arylesterase activity compared to DL, independent of HDL-C. PON activity and PON/HDL-C did not differ significantly in CRF compared to TX and DL. Phenotypic distribution was similar in patient groups. Low HDL-C CRF patients had significantly lower cholesterol and triglyceride than DL. CONCLUSION:Decreased arylesterase activity, correlating with PON1 enzyme protein quantity, is not explicable by decreased HDL-C in CRF. Low HDL-C CRF patients' increased cardiovascular morbidity is not attributable to changes in PON1 activity, or phenotypic distribution.