Polymyxin B–Induced Bartter‑Like Tubulopathy: A Case Report of Severe Potassium and Magnesium Wasting

Abstract

Bartter syndrome is a rare inherited salt‑wasting tubulopathy characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, and hypercalciuria. Although typically genetic, Bartter‑like phenotypes can occur secondary to nephrotoxic medications such as polymyxins, which induce tubular dysfunction through oxidative and mitochondrial injury. These acquired presentations are underrecognized in critically ill adults receiving salvage antimicrobial therapy.

We report a 77‑year‑old woman who developed acute electrolyte wasting consistent with a Bartter‑like phenotype shortly after initiation of polymyxin B for multidrug‑resistant Acinetobacter pneumonia. She developed progressive hypokalemia (2.3–2.9 mmol/L by day 5), hypomagnesemia (1.11 mg/dL by day 6), metabolic alkalosis (bicarbonate 35 mmol/L; chloride 90 mmol/L), and polyuria (4–5.8 L/day). A spot urine sample during hypokalemia (serum potassium 2.6 mmol/L) showed urine potassium 48.9 mmol/L, urine creatinine 31.8 mg/dL, and urine chloride 23 mmol/L, yielding a K/Cr ratio of 154 mmol/g—confirming inappropriate renal potassium wasting. No osmotic diuresis or increased urinary calcium excretion was present. Competing causes, including diuretics, beta‑agonists, gastrointestinal losses, aminoglycosides, amphotericin, and refeeding, were absent. Kidney function remained stable (creatinine 0.76–0.98 mg/dL). Despite aggressive electrolyte replacement, abnormalities persisted until polymyxin B was discontinued on day 14, after which potassium and magnesium normalized within 48 hours and polyuria resolved.

Polymyxin-associated nephrotoxicity is well described, but Bartter-like electrolyte-wasting phenotypes are less frequently recognized. The earlier‑than‑typical onset in this patient may reflect advanced age, critical illness, and reduced renal reserve. This case highlights the importance of routine electrolyte surveillance during polymyxin therapy and prompt evaluation for renal wasting when new hypokalemia, hypomagnesemia, or polyuria develops.