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Abstract: FR-PO0896

Rare Presentation of Refractory Hypokalemia and Metabolic Alkalosis in a Patient with Metastatic Prostate Cancer

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Smith, Candace, The University of Vermont Medical Center, Burlington, Vermont, United States
  • Culleen, Elliot, University of Vermont The Robert Larner MD College of Medicine, Burlington, Vermont, United States
  • Agrawal, Varun, The University of Vermont Medical Center, Burlington, Vermont, United States
  • Onuigbo, Macaulay A., The University of Vermont Medical Center, Burlington, Vermont, United States
Introduction

Severe hypokalemia (serum K+<2.5 mEq/L) is a life-threatening electrolyte disorder requiring emergent evaluation. We present a patient with prostate cancer hospitalized for severe refractory hypokalemia and metabolic alkalosis in whom diagnostic workup revealed a rare etiology.

Case Description

An 86 year old male presented to the ED with lower extremity edema, muscle weakness and fatigue. History included metastatic prostate cancer treated with hormonal and radiation therapy. Finasteride and bicalutamide were discontinued two months prior due to progression. Furosemide 20mg daily was started a week prior. In the ED, he was hypertensive to 200/110. Lab testing was notable for serum K+=2.0 mEq/L, CO2=50 mEq/L, Mg2+=2.4 mg/dL, creatinine=0.95 mg/dL, CKD-EPI eGFR=78 and venous pH=7.55. Serum K+ was 4.1meq/L two months prior. K+ and Cl- repletion were started with IV KCl 20 mEq every 4 hours, oral KCl and 0.9% saline. Furosemide was held. After two days, hypokalemia (serum K+=2.6 mEq/L) and metabolic alkalosis (serum CO2=48 mEq/L) persisted. Spot urine testing showed K+ and Cl- wasting (urine K+=28 mEq/L and Cl-=50 mEq/L).

Oral Lisinopril 10mg and Spironolactone 25mg were started and workup of hypokalemia and chloride-resistant metabolic alkalosis was initiated. Hyperaldosteronism was excluded (serum aldosterone <4ng/dL, plasma renin activity =0.9ng/mL/h) and he denied licorice intake. Hypercortisolism (serum cortisol >120 ug/dL) raised suspicion for ectopic ACTH; plasma ACTH of 549 pg/mL, unremarkable pituitary, increasing PSA (from 5.1 to 45.5 ng/mL over two months) were consistent with neuroendocrine prostate cancer transformation. With his declining status, he pursued hospice care and at the time serum K+ was 3.7 mEq/L and serum CO2=46 mEq/L with lisinopril, spironolactone, and oral KCl.

Discussion

Hypercortisolism from ACTH producing prostate cancer is a rare cause of refractory hypokalemia and metabolic alkalosis. Systematic evaluation of K+ and Cl- wasting can help guide prompt diagnosis. Inappropriate renal K+ wasting is characteristic of increased mineralocorticoid-like activity, and requires evaluation beyond hyperaldosteronism.