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Colistin-induced nephrotoxicity has widely been identified through the elevation of serum creatinine level or a reduction of glomerular filtration rate, but tubulopathy associated with colistin use is poorly understood. Herein, the authors describe a unique case of a 32-year-old quadriplegic male who developed persistent hypomagnesaemia, hypokalaemia, and metabolic alkalosis >4 weeks into therapy with intravenous colistimethate sodium for the treatment of decubitus sacral osteomyelitis by extensively drug-resistant Klebsiella pneumoniae. This required daily aggressive intravenous repletion of electrolytes and fluids while on the treatment, but it was only after 6 days of finishing the treatment with the antibiotic that metabolic changes resembling acquired Bartter-like syndrome started resolving.