A lack of serum bicarbonate frequently occurs in people suffering from acute (AKI) or chronic (CKD) kidney disease as a result of disrupted renal synthesis and reabsorption processes. Although alkali therapy is commonly used in both human and animal CKD treatment, information about how often such imbalances appear in canine AKI and CKD remains limited. This study aimed to determine how prevalent and how severe bicarbonate depletion is among dogs diagnosed with AKI, acute-on-chronic kidney disease (ACKD), or CKD, and to explore possible links with IRIS classification and calcium–phosphate metabolism changes. Medical records from dogs evaluated at the Nephrology and Urology Service of the Veterinary Teaching Hospital, University of Pisa, between January 2014 and January 2022 were retrospectively reviewed. Serum bicarbonate levels below 22 mmol/L were considered deficient, with moderate cases defined as 18–22 mmol/L and severe ones as <18 mmol/L. Among 521 dogs, 397 (76%) had reduced bicarbonate, including 142 (36%) with moderate and 255 (64%) with severe deficiency. The AKI and ACKD groups showed significantly greater occurrence (p = 0.004) and severity (p = 0.02) compared with CKD dogs. In these groups, serum bicarbonate had an inverse relationship with creatinine, urea, and phosphate levels. The frequency of deficiency rose in advanced stages in AKI (p = 0.01), ACKD (p = 0.0003), and CKD (p = 0.009). Dogs with calcium–phosphate product (CaxP) ≥70 mg²/dL² were more often and more severely affected (p = 0.01 for both) than those with lower CaxP values. These results suggest that bicarbonate shortage is highly common in AKI, ACKD, and CKD, worsening with disease progression. The stronger impact seen in AKI and ACKD may stem from rapid renal decline or non-renal factors. The observed association with CaxP disturbances indicates a likely link between metabolic acidosis and mineral–bone imbalance.
