Cat with heart failure and kidney disease helped by bexagliflozin

Abstract

Sodium–glucose cotransporter 2 inhibitors (SGLT2i) have established cardiorenal benefits in human medicine; however, clinical reports describing their use as a decongestive strategy in cats with congestive heart failure (CHF) complicated by advanced chronic kidney disease (CKD) remain limited. This case describes an 11-year-old neutered male British Shorthair cat with advanced CKD (IRIS stage 3–4) that developed CHF manifested by pleural and pericardial effusion. Thoracic radiographs confirmed pleural effusion, and echocardiography identified pericardial effusion with a hypertrophic cardiomyopathy (HCM) phenotype and left atrial enlargement, accompanied by severe azotemia on laboratory testing. Pleural effusion was managed initially with thoracocentesis for respiratory palliation, achieving partial drainage. Because escalation of loop-diuretic therapy was considered undesirable due to concern for worsening renal function, bexagliflozin (5 mg/cat PO q24h) was initiated with pimobendan as an adjunct/bridge strategy, and subcutaneous fluids were temporarily withheld given concern for fluid overload. During follow-up, serial thoracic radiographs and echocardiography documented progressive improvement culminating in complete resolution of pleural and pericardial effusions; subcutaneous fluid therapy was reintroduced thereafter without recurrence, and the cat has remained clinically stable. Renal indices fluctuated early but subsequently showed a tendency toward stabilization rather than a progressive worsening trajectory. Structured safety monitoring—including serial assessment of urinary glucose, blood glucose, and ketones—did not reveal clinically significant adverse events. This case suggests that, in carefully selected cats with CHF and advanced CKD in which conventional diuretic escalation is high risk, SGLT2i may be considered as an adjunct/bridge option for decongestion, with particular emphasis on proactive monitoring for ketone abnormalities and euglycemic ketoacidosis.