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

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 (u_normTIMP-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 u_normTIMP-2 at T0, were potential predictors of survival.