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Abstract: PO1118

Prednisolone-Related Mineralocorticoid Excess: Case of Hypokalemia and Metabolic Alkalosis

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Macaraeg, Lauren Eillen, University of California San Diego, La Jolla, California, United States
  • Astashchanka, Anna, University of California San Diego, La Jolla, California, United States
  • Malhotra, Rakesh, University of California San Diego, La Jolla, California, United States
  • Miracle, Cynthia, University of California San Diego, La Jolla, California, United States
Introduction

We report a case of the mineralocorticoid effect of prednisolone resulting in hypokalemia, metabolic alkalosis and hypertension in a patient treated with checkpoint inhibitor in the setting of oropharyngeal cancer.

Case Description

A 78 year-old male with past medical history of oropharyngeal squamous cell carcinoma presented with fatigue. One week prior, he was treated with pembrolizumab. Admission vital signs were significant for fever to 39.1°C and normotensive blood pressure 130/58. Laboratory results revealed serum potassium (K) 4.1 mmol/L, bicarbonate (HCO3) 26 mmol/L and newly elevated liver enzymes. He was diagnosed with immune checkpoint inhibitor hepatitis and treated with prednisolone 70 mg via nasogastric tube (NGT). Two days later, blood pressure increased to 170/80 and laboratory studies revealed hypokalemia and metabolic alkalosis with serum K 3.0 mmol/L and HCO3 30 mmol/L. Potassium was repleted with a total of potassium chloride (KCl) 80 mEq via NGT. The next morning, blood pressure 164/78, serum K 2.7 mmol/L and HCO3 33 mmol/L. Nephrology was consulted for persistent hypokalemia and metabolic alkalosis. The triad of hypokalemia, metabolic alkalosis and hypertension lead us to suspect a hyper mineralocorticoid state. Workup revealed spot urine K of >100 mmol/L, serum aldosterone <3.0 ng/dL and serum renin <0.1 ng/dL. Findings were consistent with an exogenous source of mineralocorticoid activation. Prednisolone was thought to be the cause. He required a total of KCl 180 meq (40 mEq intravenous, 140 mEq NGT) to raise serum K to 3.4 mmol/L in 24 hours. As such, we recommended discontinuing prednisolone in favor of dexamethasone which has no mineralocorticoid effect. Two days after discontinuation of prednisolone, serum K was 5.1 mmol/L on KCl 40 mEq via NGT twice a day and serum HCO3 was 28 mmol/L. Supplemental KCl was discontinued. One week later, serum K remained in normal range at 4.1 mmol/L.

Discussion

We demonstrated clinically significant mineralocorticoid effect of prednisolone resulting in hypokalemia and metabolic alkalosis. Physicians should be aware of electrolyte disorders associated with steroid use. With increased used of checkpoint inhibitors, this scenario may be encountered more often. Treatment may require stopping prednisolone and using alternative steroids with no mineralocorticoid activity.