Outcome in Critically Ill Dogs and Dogs With Acute Kidney Injury Based on Neutrophil Gelatinase‐Associated Lipocalin and Tissue Inhibitor of Metalloproteinase‐2

ABSTRACT Background Neutrophil gelatinase‐associated lipocalin (NGAL) and tissue inhibitor of metalloproteinase‐2 (TIMP‐2) have potential as early biomarkers for acute kidney injury (AKI) in dogs. Objectives Assess whether NGAL and TIMP‐2 at admission (T0) and 24 h later (T1) identify survival in critically ill (CI) and AKI dogs, development of hospital‐acquired AKI in CI dogs, and development of chronic kidney disease (CKD) in AKI dogs after 3 months. Animals Sixty‐two client‐owned dogs: 10 healthy, 24 with AKI, and 28 CI. Methods Prospective study with blood and urine samples collected at T0, T1, and up to 1 week in CI dogs, 1 month in healthy dogs, and 3 months in AKI dogs. Serum and urinary NGAL (sNGAL; uNGAL) and urinary TIMP‐2 (uTIMP‐2) were measured using validated ELISA kits. Results Dogs with AKI that did not survive had significantly higher uNGAL concentrations and u/sNGAL ratios at T0 compared with survivors (p = 0.05, n = 23; and p = 0.03, n = 21, respectively). In CI dogs, sNGAL was significantly higher in non‐survivors at T0 and T1 compared with survivors (p = 0.02, n = 26; and p = 0.003, n = 26, respectively). At T0, normalized urinary tissue inhibitor of metalloproteinase‐2 (unormTIMP‐2) was significantly higher in non‐survivor CI dogs compared with survivors (p = 0.04, n = 25). No significant differences were found for the other variables. Conclusions and Clinical Relevance In AKI dogs, uNGAL and u/sNGAL at T0, and in CI dogs, sNGAL at T0 and T1 and unormTIMP‐2 at T0, were potential predictors of survival.