Acute kidney injury (AKI) is caused by sudden kidney damage. In studies using mouse model of AKI, the blood concentrations of fibroblast growth factor-23 (FGF-23) increased persistently in AKI. In addition, higher FGF-23 concentrations were associated with the progression of AKI to chronic kidney disease (CKD), and AKI disrupted magnesium homeostasis. However, no study has evaluated these factors in dogs and cats with AKI. This study aimed to measure serum FGF-23 and magnesium concentrations in dogs and cats with AKI. This cross-sectional study used data available in medical records. The AKI group included six dogs and six cats, while the control group consisted of eight dogs and six cats, all of which were client-owned animals. Results showed that in dogs, the AKI group had significantly higher serum FGF-23 (median control, 278.5 pg/mL; AKI, 2104.0 pg/mL; P = 0.02), and magnesium (median control, 2.0 mg/dL; AKI, 2.65 mg/dL; P = 0.043) concentrations than the control group. In cats, the AKI group had significantly higher FGF-23 (median control, 138 pg/mL; AKI, 1195 pg/mL; P = 0.015) concentrations than the control group. In addition, serum FGF-23 concentrations were a significant positive correlation with serum creatinine (r = 0.67, P = 0.018) and phosphate concentrations (r = 0.893, P < 0.001) in dogs.To the best of knowledge, the current study first reported that dogs and cats with AKI had increased serum FGF-23 concentrations. Moreover, dogs with AKI exhibited high serum magnesium concentrations.
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