Urinary diversion after cystectomy using autologous intestinal segments has been the gold standard treatment in several urinary tract diseases. The most frequent metabolic consequence is hyperchloremic metabolic acidosis, due to ammonium hydrogen and chloride ions absorption in exchange for the excretion of bicarbonate and sodium ions in the bowel conduit.

Sodium-glucose co-transporter-2 (SGLT2) inhibitors are a class of antihyperglycemic agents that block the reabsorption of filtered glucose in the renal proximal convoluted tubules, promoting greater urinary glucose and sodium excretion.

The authors describe two cases of patients with bowel conduit and mild/severe hyperchloremic metabolic acidosis, after starting SGLT2 inhibitors. Both were presented with mild acute kidney injury, moderate hyperglycemia, normal ketoacids, normal lactate and normal anion gap. Clinical and laboratory normalization were reached after this drug was withdrawn and fluid support therapy was applied.

We hypothesize that SGLT2 inhibitors could exacerbate chronic hyperchloremic metabolic acidosis in these patients, by enhance sodium loss and volume depletion, subsequent acute kidney injury (AKI), increase renal chloride elimination due to sodium loss and subsequent chloride/bicarbonate bowel exchange. Rebound hyperglycemia due to bowel absorption and bicarbonate renal elimination through Na+-H+exchanger 3 (NHE3) suppression, could also contribute. This association needs further investigation.