Assessment of Bicarbonate Deficiency in Feline Acute and Chronic Kidney Disease

Abstract

Bicarbonate deficiency is a common complication of acute kidney injury (AKI) and chronic kidney disease (CKD), resulting from impaired renal bicarbonate handling. It promotes bone demineralization and calcium–phosphate (CaxP) imbalance. In dogs, elevated CaxP has been linked to increased frequency and severity of bicarbonate deficiency. This 10-year study evaluated the prevalence and degree of bicarbonate deficiency in 618 cats diagnosed with AKI, acute-on-chronic kidney disease (ACKD), and CKD, and its association with azotemia and mineral imbalance. A retrospective analysis was conducted on serum biochemical profiles, including creatinine, urea, ionized and total calcium, phosphate, CaxP, and bicarbonate. Cats with incomplete datasets or receiving sodium bicarbonate therapy were excluded. According to IRIS guidelines, bicarbonate deficiency was defined as <16 mmol/L and categorized as moderate (12–16 mmol/L) or severe (<12 mmol/L). Deficiency was found in 45% of cats, of which 63% were moderate and 37% severe. Prevalence was higher in AKI (58%) and ACKD (60%) compared to CKD (38%) (<i>p</i> = 0.002). Negative correlations between bicarbonate and creatinine, phosphate, and CaxP were detected in AKI and CKD, while in ACKD, only creatinine and phosphate correlated. Deficiency increased with disease severity in AKI (<i>p</i> = 0.0145) and CKD (<i>p</i> < 0.0001). Cats with CaxP > 70 mg²/dL² had higher deficiency rates (<i>p</i> < 0.0001). However, 21% with elevated CaxP had normal bicarbonate, suggesting mineral imbalance may occur independently of acidosis.