대한신장학회

Skip Navigation: Skip to contents

KOR
ENG
전체메뉴보기

간행물 검색

현재 페이지 경로

HOME
간행물
간행물 검색

논문분류	춘계학술대회 초록집
제목	Genetic and Lipoproteomic Evidence for a Non-Albuminuric Pathway to Kidney Failure Driven by LCAT Dysfunction
저자	Wencheng Jin
출판정보	2026; 2026(1):
키워드	Lecithin-cholesterol acyltransferase, HDL biology, Lipoproteomics, Non-albuminuric kidney disease, CKD progression
초록	Objectives: Many patients with chronic kidney disease (CKD) continue to experience a decline in renal function due to non-proteinuria pathways, even when using renin-angiotensin system blockers and SGLT2 inhibitors. We asked whether LCAT-related HDL dysfunction marks a distinct, non-albuminuric pathway to kidney failure. Methods: We first performed two-sample Mendelian randomization using UK Biobank HDL-C instruments and CKDGen outcomes (total N=521,088). We then profiled 112 lipoprotein measures by high-resolution NMR in 1,762 biopsy-confirmed CKD patients from the KORNERSTONE cohort, derived an LCAT Phenotype Score across five prespecified domains, and tested associations with a composite outcome (ESKD or death) and ESKD using Cox models. Results: Genetically predicted higher HDL-C was associated with lower CKD risk (IVW β=−0.133, P=0.010) but not with UACR (β=−0.032, P=0.076). In KORNERSTONE, advanced CKD showed HDL remodeling consistent with impaired esterification, including triglyceride enrichment and relative cholesteryl-ester depletion. The LCAT Phenotype Score tracked with lower eGFR (r=−0.28, P<0.001) and was unrelated to albuminuria (r=−0.01, P=0.68). Over 3.1 years median follow-up, each 1-SD increase predicted the composite outcome after full adjustment including UACR (HR 1.21, 95% CI 1.09–1.34) and showed no interaction with albuminuria. Conclusion: An LCAT-linked lipoproteomic phenotype identifies CKD risk that is largely orthogonal to albuminuria and concentrates in near-term events, supporting a metabolically defined pathway to kidney failure that may enable precision stratification.
원문(PDF)	PDF 원문보기

목록

위로가기