Advanced lipoprotein parameters could better explain atheromatosis in non-diabetic chronic kidney disease patients

Abstract

Background: Chronic kidney disease (CKD) patients have a high burden of atheromatous cardiovascular disease (ASCVD) not fully explained by traditional lipid parameters. Lipoprotein composition and subclass particle number information could improve ASCVD risk assessment. The objective of this study is to investigate the association of advanced lipoprotein parameters with the risk of atheromatosis in a subpopulation of the NEFRONA study.

Methods: This was a cross-sectional study in 395 non-diabetic individuals (209 CKD and 186 non-diabetic and non-CKD) without statin therapy. Vascular ultrasound examination assessing 10 territories was combined with advanced lipoprotein testing performed by nuclear magnetic resonance spectroscopy. Logistic regression was used to estimate adjusted odds ratios (ORs) per 1 standard deviation increment.

Results: Atheromatosis was more prevalent in CKD patients (33.9% versus 64.6%). After adjusting for age, gender, smoking habit and CKD stage, the amount of triglycerides (TGs) within low-density lipoprotein (LDL) lipoproteins was independently and positively associated with atheromatosis [OR 1.33; 95% confidence interval (CI) 1.03-1.74; P = 0.03]. Similarly, total and medium LDL particles (LDL-Ps) showed a positive association (OR 1.29; 95% CI 1.00-1.68; P = 0.05 and OR 1.34; 95% CI 1.04-1.75; P = 0.03, respectively). TG-loaded medium LDL-Ps were higher in CKD patients compared with controls and showed an adjusted OR of 1.40 (95% CI 1.09-1.82; P = 0.01) in non-diabetic patients (CKD and non-CKD individuals). In contrast, non-diabetic CKD patients showed a similar coefficient but the significance was lost (OR 1.2; 95% CI 0.8-1.7; P = 0.359).

Conclusions: Non-diabetic CKD patients showed a higher amount of TG-loaded medium LDL-Ps compared with controls. These particles were independently associated with atheromatosis in non-diabetic patients.

Keywords: LDL cholesterol; atherosclerosis; chronic kidney disease; dyslipidemia; lipoprotein subfractions; triglycerides.

FIGURE 1:

Association of lipoprotein composition with atheromatosis. Multivariate logistic regression model adjusted for age, gender, smoking habit and CKD stage. Estimates were ORs per 1 SD increment. SD was expressed in mg/dL (VLDL-C, 8.95; VLDL-TG, 31.65; LDL-C, 19.98; LDL-TG, 4.01; IDL-C, 3.76; IDL-TG, 2.95; HDL-C, 11.61; and HDL-TG, 5.13).

FIGURE 2:

Association of lipoprotein particle number with atheromatosis. Multivariate logistic regression model adjusted for age, gender, smoking habit and CKD stage. Estimates were ORs per 1 SD increment. SD was expressed in nmol/L (total VLDL-P, 22.83; large VLDL-P, 0.57; medium VLDL-P, 3.31; small VLDL-P, 19.05; total LDL-P, 137.33; large LDL-P, 21.40; medium LDL-P, 53.52; small LDL-P, 71.54; total HDL-P, 5.35; large HDL-P, 0.15; medium HDL-P, 2.19; and small LDL-P, 3.60).

FIGURE 3:

Atheroma plaque presence and levels of LDL-TG–medium LDL-P in non-CKD and CKD patients. Prevalence of atheromatous plaques (P < 0.01) and the levels of LDL-TG–medium LDL-P (P = 0.05) were expressed as percentage and mg/dL × nmol/L, respectively.

FIGURE 4:

Multivariate logistic regression model adjusted for age, gender, smoking habit and CKD stage. LDL-TG–medium LDL-P estimate was ORs per 1 SD increment. SD: 1674.45 mg/dL × nmol/L. Multivariate logistic regression to model presence of atheromatosis in non-diabetic CKD patients.