Topical Brinzolamide-induced renal tubular acidosis in a patient with chronic kidney disease: a case report and review of the diagnostic blind spot

Background Metabolic acidosis is a common complication of advanced chronic kidney disease (CKD). However, when the severity of acidosis outweighs the degree of renal dysfunction, exogenous causes must be excluded. Carbonic anhydrase inhibitors (CAIs) are known to cause hyperchloremic metabolic acidosis, but the systemic toxicity of topical ophthalmic formulations is frequently overlooked. We report a case of severe distal renal tubular acidosis (RTA) precipitating acute-on-chronic kidney injury, caused by the systemic absorption of topical brinzolamide. Case presentation: A 73-year-old Asian male with stage 3 CKD and glaucoma presented with progressive dyspnea, anorexia, and weight loss one month after initiating brinzolamide/timolol eye drops. Laboratory evaluation revealed severe metabolic acidosis (pH 7.29, HCO3 ^- 8.9 mEq/L) and acute kidney injury. While the serum anion gap was elevated, the delta-delta ratio of 0.55 and a positive urine anion gap (+ 33.4 mEq/L) indicated a concomitant normal anion gap metabolic acidosis consistent with RTA. Discontinuation of the ophthalmic solution and alkali therapy resulted in the resolution of acidosis and recovery of renal function to baseline. Conclusions Topical CAIs can undergo significant systemic absorption, bypassing first-pass metabolism, and precipitate life-threatening acidosis in patients with reduced renal reserve. Clinicians must maintain a high index of suspicion for ophthalmic medications as hidden causes of mixed acid-base disorders in patients with CKD.