Abstract: TH-PO355
Wasting K, the Ampicillin Way: An Uncommon Cause of Hypokalemia
Session Information
- Sodium, Potassium, and Volume Disorders: Clinical
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Swartzman, Isaac, University of California Davis, Davis, California, United States
- Luo, Jack, University of California Davis, Davis, California, United States
- Beck, Natalie M., University of California Davis, Davis, California, United States
Introduction
Hypokalemia arises from transcellular shift, reduced intake or increased loss of potassium (K). Elevated urinary K in a hypokalemic individual prompts further workup for renal K loss. We describe a case of renal K-wasting secondary to high dose intravenous (IV) ampicillin use.
Case Description
A 49-year-old male with a history of multidrug resistant disseminated tuberculosis (TB) was hospitalized with abdominal pain and nausea and found to have a small bowel obstruction secondary to an ileal stricture. His home TB regimen was converted to IV linezolid and moxifloxacin. Initial labs revealed normal electrolytes and renal function. On hospital day (HD) 6, he resumed a liquid diet. The following day, he was initiated on ampicillin/sulbactam 3 g TID and meropenem 2 g TID to replace long-acting bedaquiline from his home regimen. On HD 8, he became hypokalemic to 2.8 mmol/L and hypophosphatemic to nadir of 1.2 mg/dL with normal serum magnesium and bicarbonate. Blood pressures were low-normal range. Refeeding syndrome was considered but thought less likely given the persistence of hypokalemia several days after the patient resumed eating, prompting quantification of urinary K. On HD 15, urine studies revealed a spot K:Cr ratio of 155 mEq/g (normal < 13) and a 24-hour K excretion of 143 mmol with a urine anion gap of 110. These findings supported renal K wasting due to nonreabsorbable anions, most likely ampicillin and/or meropenem. He continued on antibiotic therapy and was able to maintain a normal serum K on oral repletion for the remainder of the hospitalization. He resumed his home oral antibiotics upon discharge on HD 22.
Discussion
Workup for renal K loss includes assessing mineralocorticoid activity, acid-base status, and the presence of a urine anion gap if concerned for renal tubular acidosis (RTA). This patient had a low-normal blood pressure and no metabolic alkalosis or acidosis to suggest increased mineralocorticoid activity or RTA, respectively. Hypokalemia associated with antibiotics is a known risk factor, with few cases associated with high dose ampicillin described in the literature. In our case, the high urine anion gap suggests the presence of nonreabsorbable anions. The proposed mechanism is the inability to reabsorb the anion along the nephron, preserving a negative luminal charge and resulting in K secretion at the distal tubule.