J Clin Lipidol. 2026 Jul 10:S1933-2874(26)00441-1. doi: 10.1016/j.jacl.2026.07.013. Online ahead of print.
ABSTRACT
BACKGROUND: Dyslipidemia has been identified as a crucial factor for atherosclerotic disease. Recently, evidence for involvement of non-high-density lipoprotein cholesterol (nHDL-C) in atherosclerotic cardiovascular disease has been accumulating, and an association with the development of chronic kidney disease (CKD) has been reported. However, few studies have investigated the relationships between nHDL-C levels and renal pathological changes.
OBJECTIVE: To investigate the associations between nHDL-C levels and renal pathological changes in living kidney donors with apparently normal kidney function.
METHODS: In this cross-sectional study, we examined time-zero biopsy specimens from 345 living kidney donors and evaluated the relationships between serum nHDL-C levels and renal pathological changes, including arteriolar hyalinization, luminal stenosis of small-to-medium arteries, global glomerulosclerosis, and glomerular hypertrophy. We also evaluated the predictive performance of nHDL-C by calculating the net reclassification improvement (NRI) vs low-density lipoprotein cholesterol (LDL-C).
RESULTS: The distribution of nHDL-C levels was as follows: <100 mg/dL in 15 patients (4%), 100 to 129 mg/dL in 84 patients (24%), 130 to 169 mg/dL in 160 patients (46%), and ≥170 mg/dL in 86 patients (25%). High nHDL-C was significantly associated with the prevalence of severe luminal stenosis (multivariable-adjusted odds ratio [OR] for nHDL-C ≥170 mg/dL vs nHDL-C 100 to 129 mg/dL: 3.62 [95% CI: 1.09-12.0]). Higher nHDL-C level was also associated with glomerular hypertrophy (OR per 10 nHDL-C increase: 1.19 [1.00-1.41]). In the NRI analyses, the model with nHDL-C added to the basic atherosclerotic factors exhibited better predictive performance for severe luminal stenosis than the model with LDL-C added to these factors (continuous NRI: 0.45 [0.13-0.78]).
CONCLUSION: High nHDL-C levels are potentially associated with renal pathological injury in subjects without CKD.
PMID:42509094 | DOI:10.1016/j.jacl.2026.07.013