A single 2-hour serum TIMP-2 measurement offered limited standalone discrimination for 90-day chronic kidney disease (AUC 0.528) in STEMI patients undergoing emergent percutaneous coronary intervention.
Cohort (n=88)
No
Does early serum TIMP-2 predict 90-day chronic kidney disease in STEMI patients undergoing emergent angiography/PCI?
Early serum TIMP-2 measured 2 hours post-procedure in STEMI patients has limited standalone discrimination for 90-day CKD, indicating it may be better suited for multivariable risk panels rather than as an isolated biomarker.
Estimación del efecto: AUC 0.528 (95% CI 0.39-0.65)
valor p: p=0.668
Abstract Background Contrast-induced acute kidney injury (CI-AKI) remains a concern in patients with ST-elevation myocardial infarction (STEMI) undergoing emergent percutaneous coronary intervention (PCI), but creatinine-based CI-AKI definitions incompletely capture longer-term renal trajectories. Early tubular stress biomarkers such as tissue inhibitor of metalloproteinases-2 (TIMP-2) may provide incremental risk information beyond conventional functional markers. Methods In this prospective single-centre cohort, we enrolled 88 consecutive STEMI patients undergoing urgent coronary angiography with or without PCI. Routine laboratory parameters were obtained at admission and 48 h. Serum TIMP-2 was measured 2 h after the procedure using a standardized sandwich ELISA. Early CI-AKI was defined by conventional creatinine-based criteria within 48 h, whereas 90-day chronic kidney disease (CKD) was defined as an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m² or persistent creatinine elevation at 90 days. We evaluated paired changes, between-group differences by 90-day CKD status, correlations, multivariable linear and logistic regression, and receiver operating characteristic (ROC) discrimination. Results Early CI-AKI occurred in 6/88 patients (6.8%), whereas 90-day CKD was diagnosed in 15/88 (17%), indicating substantial delayed renal dysfunction beyond the 48-h window. The median 2-h serum TIMP-2 concentration was 1.20 ± 0.38 ng/mL. TIMP-2 showed modest correlations with creatinine and urea and remained independently associated with higher 90-day creatinine in multivariable linear regression (B = + 12.0 µmol/L per 1-ng/mL increase; p = 0.016) after adjustment for baseline creatinine and clinical covariates. In parsimonious logistic models, TIMP-2 demonstrated a borderline association with 90-day CKD (odds ratio ≈ 6.38; p = 0.056), while older age was a significant predictor. Standalone ROC discrimination for 90-day CKD was limited (AUC 0.528; 95% confidence interval 0.39–0.65; p = 0.668). Conclusions In STEMI patients undergoing emergent angiography/PCI, 90-day CKD was considerably more frequent than early creatinine-defined CI-AKI, underscoring the need for extended renal follow-up. A single 2-hour serum TIMP-2 measurement reflects early tubular stress and independently associates with 90-day creatinine, but offers only modest standalone discrimination for 90-day CKD. TIMP-2 is therefore more likely to have a role within multivariable or biomarker panel-based risk stratification pathways rather than as an isolated classifier.
Mugazov et al. (Wed,) conducted a cohort in ST-elevation myocardial infarction (STEMI) (n=88). Serum TIMP-2 measurement was evaluated on 90-day chronic kidney disease (CKD) (AUC 0.528, 95% CI 0.39-0.65, p=0.668). A single 2-hour serum TIMP-2 measurement offered limited standalone discrimination for 90-day chronic kidney disease (AUC 0.528) in STEMI patients undergoing emergent percutaneous coronary intervention.