Objective: To investigate the associations of hypertriglyceridemia, small low-density lipoproteins (sdLDL) and the endothelial nitric oxide synthase (eNOS) G894T (rs 1799983) polymorphism with residual cardiorenal risk in patients with diabetic kidney disease (DKD) and hypertension beyond low-density lipoprotein cholesterol (LDL-C) Design and method: A total of 126 patients were examined (mean age 62,6±1,2 years; 62,7% women). Lipid parameters were assessed, including sdLDL-C and triglyceride-rich LDL particles (TG-LDL) calculated using the Sampson and Wolska-Sampson formulas. Insulin resistance (IR) indices (HOMA-IR, TyG, and METS-IR) were analyzed. Albuminuria and estimated glomerular filtration rate (eGFR) were determined using the CKD-EPI equation. Genotyping of the eNOS G897T (rs 1799983) polymorphism was performed using TaqMan polymerase chain reaction/ Genotype frequencies were in Hardy-Weinberg equilibrium (p=0,59). A dominant T-allele model was applied for comparative analysis. Results: Visceral obesity was present in 96,8% of patients and dyslipidemia in 60,3%. Genotype distribution was GG 63,5%, GT 33,3%, and TT 3,2%. Patients with triglyceride (TG) levels >1,7 mmol/L exhibited higher sdLDL-C and TG-LDL (50,5±2,6 and 57,1±2,0 mg/dL) compared with those with TG 1,7 mmol/L (69,6% vs 52,5%; relative risk RR ∼2,3; p<0,001) and showed higher TG, very low-density lipoprotein cholesterol (VLDL-C), TG-LDL, sdLDL-C, and METS-IR values. Conclusions: In patients with DKD and hypertension, hypertriglyceridemia is associated with unfavorable cardiometabolic phenotype characterised increased sdLDL-C, TG-rich lipoproteins, and albuminuria, consistent with residual cardiorenal risk beyond LDL-C. The eNOS G894T (rs 1799983) polymorphism acts as a genetic modulator of residual risk, where T-allele carriage doubles the likelihood of hypertriglyceridemia and promotes a pro-atherogenic lipid phenotype characterized by elevated sdLDL-C and IR.
Zlatkina et al. (2026) studied this question.