Urinary KIM-1 at a threshold of 3.38 ng/mL achieved 90% sensitivity and 91% specificity for AKI detection in ACS patients, with ridge logistic regression AUC of 0.98 in a synthetic reconstructed cohort.
Observational (n=90)
No
Does urinary KIM-1 predict acute kidney injury in patients with acute coronary syndrome?
In a synthetic dataset of ACS patients, urinary KIM-1 showed strong discriminative performance for predicting acute kidney injury, supporting its potential as an early biomarker.
Effect estimate: At KIM-1 cutoff 3.38 ng/mL: sensitivity 0.90, specificity 0.91; Ridge logistic regression AUC=0.98 (95% CI 0.95–1.00) (95% CI 0.95-1.00)
Absolute Event Rate: 0.222% vs 0.778%
Acute Kidney Injury (AKI) is a serious complication of Acute Coronary Syndrome (ACS) that increases morbidity and mortality. Traditional markers such as serum creatinine are delayed indicators of renal injury. Kidney Injury Molecule-1 (KIM-1) has been reported as an early biomarker of proximal tubular injury. In the reference ACS cohort used in this work, original patient-level data were not available for secondary analysis, motivating reconstruction of a synthetic dataset to enable additional modeling. A synthetic dataset of 90 ACS patients was reconstructed using published summary statistics from the reference cohort. Demographic, clinical, and biomarker variables were simulated to preserve reported distributions. AKI status was assigned probabilistically based on established clinical risk factors, independent of KIM-1. Urinary KIM-1 was modeled as a continuous variable and generated conditionally to reflect reported separation between AKI and non-AKI groups. Multivariable modeling was performed using ridge logistic regression, Random Forest, and Extreme Gradient Boosting (XGBoost), with performance evaluated using five-fold stratified cross-validation and 1,000-iteration bootstrapping. Urinary KIM-1 levels were higher in simulated AKI patients (4.19 ± 0.50 ng/mL) than in non-AKI patients (2.75 ± 0.43 ng/mL), consistent with the reference cohort summaries. Within the reconstructed dataset, a KIM-1 threshold of 3.38 ng/mL yielded sensitivity of 0.900 and specificity of 0.914. Ridge logistic regression demonstrated high discrimination (AUC = 0.984 ± 0.030), followed by XGBoost (AUC = 0.968 ± 0.024) and Random Forest (AUC = 0.904 ± 0.103). Bootstrap analysis showed stable ridge performance (AUC = 0.983; 95% CI: 0.953–1.000). Under assumptions consistent with the reference cohort summaries, urinary KIM-1 showed strong discriminative performance in multivariable models within a reconstructed synthetic dataset. These results should be interpreted as scenario-based and hypothesis-generating rather than as estimates of real-world diagnostic accuracy. External validation using patient-level data is required before clinical application.
Qasem et al. (2026) conducted an observational in Adults aged 18-70 with Acute Coronary Syndrome (STEMI, NSTEMI, or unstable angina) without chronic kidney disease or baseline creatinine ≥1.5 mg/dL (n=90). Urinary Kidney Injury Molecule-1 (KIM-1) Measurement vs. No KIM-1 elevation (non-AKI patients) was evaluated on Acute Kidney Injury (AKI) defined by AKIN criteria: increase in serum creatinine of ≥0.3 mg/dL or ≥50% from baseline within 48h (At KIM-1 cutoff 3.38 ng/mL: sensitivity 0.90, specificity 0.91; Ridge logistic regression AUC=0.98 (95% CI 0.95–1.00), 95% CI 0.95-1.00). Urinary KIM-1 at a threshold of 3.38 ng/mL achieved 90% sensitivity and 91% specificity for AKI detection in ACS patients, with ridge logistic regression AUC of 0.98 in a synthetic reconstructed cohort.