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Plasma kidney injury molecule-1 (KIM-1) is a promising biomarker for cardio-renal diseases, but its associations with vascular calcification (VC) and clinical outcomes in non-dialysis chronic kidney disease (CKD) stages G3 to G5 remain unclear. This study investigated the associations between plasma KIM-1, vascular calcification, and adverse clinical outcomes in this population. In a prospective cohort of 221 non-dialysis CKD G3 to G5 patients followed for 1.89 ± 0.96 years, associations between plasma KIM-1 and multiple VC measures-including coronary artery calcification (CAC), thoracic aortic calcification (TAC), abdominal aortic calcification (AAC), carotid artery calcification, and aortic valve calcification (AVC)-were assessed using logistic regression models and reported as odds ratios (ORs) with 95% confidence intervals (CIs). Associations with clinical endpoints, including CKD progression, cardiovascular events, and all-cause mortality, were evaluated using Cox proportional hazards regression models and reported as hazard ratios (HRs) with 95% CIs. The 221 enrolled patients had a mean age of 51 ± 14 years; 63% were male and 32% had diabetes. Median plasma KIM-1 was 266.10 pg/mL, with significantly higher levels in patients with diabetic kidney disease, glomerular disease, and VC. Elevated KIM-1 was independently associated with severe CAC (OR 32.14, 95% CI 2.36-437.21, p = 0.008) and AAC (OR 2.56, 95% CI 1.01–6.48, p = 0.047) after multivariable adjustment with confounders including estimated glomerular filtration rate (eGFR). Higher KIM-1 was also linked to faster eGFR decline (5.07 vs. 3.12 mL/min/1.73 m²/year, p = 0.046) and in associated with the composite clinical endpoint (HR 1.73, 95%CI 1.05–2.86, p = 0.031). Elevated plasma KIM-1 was associated with severe coronary artery calcification, abdominal aortic calcification, and adverse clinical outcomes in non-dialysis CKD G3 to G5 patients.
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Zhu et al. (2026) studied this question.
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