Abstract: TH-PO1163
Cisplatin-Associated Isolated Persistent Type 1 (Distal) Renal Tubular Acidosis: A Rare Manifestation of Tubular Toxicity
Session Information
- Onconephrology: Emerging Biomarkers, Preclinical Models, Clinical Challenges, and Therapeutic Strategies
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Author
- Nawaz, Iqra, SUNY Upstate Medical University, Syracuse, New York, United States
Introduction
Cisplatin-induced nephrotoxicity is a well-recognized dose-limiting complication of platinum-based chemotherapy and commonly presents with acute kidney injury, electrolyte abnormalities, and tubular dysfunction. Distal (type 1) renal tubular acidosis is a rare manifestation of cisplatin-associated tubular toxicity and may rarely persist despite limited exposure and treatment discontinuation.
Case Description
We present a case of a 55-year-old female with tonsillar squamous cell carcinoma who received cisplatin chemotherapy on 10/25/2023, 40 mg/m2. Baseline renal function prior to chemotherapy was normal, with creatinine 0.9 mg/dL, bicarbonate 25 mmol/L, and potassium 3.6 mmol/L. Following chemotherapy initiation, the patient developed persistent metabolic acidosis with hypokalemia, requiring ongoing potassium and alkali supplementation, with abnormalities persisting from 2023 to the present. Urine studies demonstrated renal potassium wasting, positive urine anion gap, and inappropriately elevated urine pH of 7.0 despite systemic metabolic acidosis, consistent with a distal tubular acidification defect. Serum glucose, phosphorus, and magnesium remained normal, with no glucosuria or proteinuria to suggest Fanconi syndrome. Renal ultrasound showed no nephrolithiasis or obstructive uropathy, and there was no history of diarrhea, chronic kidney disease, or alternative nephrotoxic exposures. Overall, findings were most consistent with persistent isolated distal (type 1) renal tubular acidosis temporally associated with limited cisplatin exposure.
Discussion
Persistent distal tubular dysfunction following limited cisplatin exposure appears uncommon and may reflect ongoing tubular injury requiring prolonged alkali and electrolyte supplementation. Recognition of this entity is important, as delayed or persistent tubular dysfunction may continue despite discontinuation of therapy.
Biochemical evaluation
| Serum Potassium Serum Magnesium Serum Phosphorus Serum Glucose Serum Bicarbonate Serum Creatinine Anion Gap Lactic acid Urine potassium Urine Magnesium Urine Glucose Urine Creatinine Urine pH Fractional excretion of potassium (FEK) Urine K/Cr | 3.8 mmol/L 1.8 mg/dL 3.4 mg/dL 112 mg/dL 20 mmol/L 0.9 mg/dL 10 mmol/l 0.9 mmol/L 21.4 mmol/L <2.0 mg/dL Negative 12.0 mg/dL 7.0 42.2% 20 mEq/g |
Figure 1. Serum Potassium and Bicarbonate Trends Following Cisplatin Exposure.