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Background <p>Metabolic acidosis is common in chronic kidney disease (CKD). However, when the severity of acidosis is disproportionate to renal dysfunction, exogenous causes must be excluded. Topical carbonic anhydrase inhibitors (CAIs) used for glaucoma are commonly perceived as locally acting; in patients with normal renal function their plasma free-drug concentrations are far below those required for systemic effects. In CKD, however, reduced clearance and reduced renal acid-excretory reserve can unmask systemic toxicity. Individual recognition of the syndrome remains uncommon at the bedside, particularly when it presents in the context of acute-on-chronic kidney injury, where its laboratory features can be obscured by acute kidney injury(AKI)-related acidosis.</p> Case presentation <p>A 73-year-old Asian male with stage 3 CKD and glaucoma presented with progressive dyspnea, anorexia, and a 3-kg weight loss one month after starting fixed-combination brinzolamide 1% / timolol 0.5% eye drops. Laboratory evaluation revealed severe metabolic acidosis (pH 7.29; serum bicarbonate 8.9 mmol/L, from a pre-exposure baseline of 20.3 mmol/L) and acute-on-chronic kidney injury (creatinine 3.9&#xa0;mg/dL versus baseline ~ 2.0&#xa0;mg/dL). The disturbance was mixed: a delta-delta ratio of 0.42 (calculated using a reference normal serum bicarbonate of 24 mmol/L) indicated a substantial non-anion-gap (hyperchloremic) component superimposed on a smaller high-anion-gap component, with hypokalemia (K<sup>+</sup> 3.3 mmol/L), hyperchloremia (Cl<sup>-</sup> 107 mmol/L), positive urine anion gap (+ 33.4 mmol/L), and a fractional excretion of bicarbonate of 4.3% measured during established acidosis (without bicarbonate loading). Other causes of metabolic acidosis were systematically excluded. Causality assessment by the Naranjo Adverse Drug Reaction Probability Scale yielded a score of 7 (probable). Discontinuation of the ophthalmic solution and alkali therapy resulted in the resolution of acidosis and recovery of renal function to baseline within one week, sustained at one-year follow-up.</p> Conclusions <p>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.</p>

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Severe metabolic acidosis with renal tubular acidosis features attributed to topical brinzolamide in a patient with stage 3 chronic kidney disease: a case report

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  • 发表日期：

    2026年7月7日

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  • Ming-Yuan Victor Chao,
  • Yi-chun Wang

摘要

Background

Metabolic acidosis is common in chronic kidney disease (CKD). However, when the severity of acidosis is disproportionate to renal dysfunction, exogenous causes must be excluded. Topical carbonic anhydrase inhibitors (CAIs) used for glaucoma are commonly perceived as locally acting; in patients with normal renal function their plasma free-drug concentrations are far below those required for systemic effects. In CKD, however, reduced clearance and reduced renal acid-excretory reserve can unmask systemic toxicity. Individual recognition of the syndrome remains uncommon at the bedside, particularly when it presents in the context of acute-on-chronic kidney injury, where its laboratory features can be obscured by acute kidney injury(AKI)-related acidosis.

Case presentation

A 73-year-old Asian male with stage 3 CKD and glaucoma presented with progressive dyspnea, anorexia, and a 3-kg weight loss one month after starting fixed-combination brinzolamide 1% / timolol 0.5% eye drops. Laboratory evaluation revealed severe metabolic acidosis (pH 7.29; serum bicarbonate 8.9 mmol/L, from a pre-exposure baseline of 20.3 mmol/L) and acute-on-chronic kidney injury (creatinine 3.9 mg/dL versus baseline ~ 2.0 mg/dL). The disturbance was mixed: a delta-delta ratio of 0.42 (calculated using a reference normal serum bicarbonate of 24 mmol/L) indicated a substantial non-anion-gap (hyperchloremic) component superimposed on a smaller high-anion-gap component, with hypokalemia (K+ 3.3 mmol/L), hyperchloremia (Cl- 107 mmol/L), positive urine anion gap (+ 33.4 mmol/L), and a fractional excretion of bicarbonate of 4.3% measured during established acidosis (without bicarbonate loading). Other causes of metabolic acidosis were systematically excluded. Causality assessment by the Naranjo Adverse Drug Reaction Probability Scale yielded a score of 7 (probable). Discontinuation of the ophthalmic solution and alkali therapy resulted in the resolution of acidosis and recovery of renal function to baseline within one week, sustained at one-year follow-up.

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.