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Immune checkpoint inhibitors (ICIs), pembrolizumab, are known to induce renal immune-related adverse events (irAEs), most frequently presenting as acute interstitial nephritis (AIN). However, Type 4 renal tubular acidosis (RTA) resulting from immune-mediated hypoaldosteronism is a less commonly reported complication.
This report details a case of acute tubulointerstitial nephritis concurrent with Type 4 RTA that arose following pembrolizumab-integrated chemotherapy.
Case: A 64-year-old woman with a history of hypertension, Type 2 diabetes, dyslipidemia, gout, iron-deficiency anemia, and advanced intrahepatic cholangiocarcinoma initiated treatment with cisplatin-gemcitabine plus pembrolizumab in February 2025. Approximately three weeks later, she developed significant hyperkalemia and normal-anion-gap metabolic acidosis without evidence of sepsis or hemodynamic compromise.
Key Findings: Laboratory analysis demonstrated severe hyperkalemia (K 7.3 mmol/L) and normal gap metabolic acidosis (Na+138, Cl-111, HCO3− 13 mmol/L), despite near-normal renal function (creatinine 1.06 mg/dL). Arterial blood gas analysis confirmed pH 7.40, pCO2 20.5 mmHg, and HCO3− 12.9 mmol/L. Urinalysis showed an acidic pH 5.0 and specific gravity 1.006, with no proteinuria or glucosuria. Renin was markedly elevated with low aldosterone, indicating hypoaldosteronism. Kidney biopsy confirmed mild, patchy lymphoplasmacytic tubulointerstitial nephritis with focal lymphocytic tubulitis and early chronic changes.
Management and Outcomes: Both pembrolizumab and cytotoxic chemotherapy were immediately withheld. The patient received supportive management, which included oral sodium bicarbonate and calcium polystyrene sulfonate. Notably, no systemic corticosteroids (e.g., methylprednisolone) were administered. Both serum potassium and bicarbonate levels were nearly normalized with supportive therapy alone. Her renal function remained stable, and she was subsequently able to resume the cisplatin-gemcitabine regimen (Figure 2).
Pembrolizumab may precipitate AIN concurrent with Type 4 RTA, likely mediated by immune-induced hypoaldosteronism. In selected patients with mild AIN and no significant AKI, a conservative approach without corticosteroids is appropriate if renal parameters are stable.
