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Abstract: FR-PO571

Hypokalemia: A Diagnostic Challenge

Session Information

  • Trainee Case Reports - III
    October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 902 Fluid and Electrolytes: Clinical

Authors

  • Anam, Smitha Reddy, VA Loma Linda Healthcare system, Loma Linda, California, United States
  • McMillan, James I., VA Loma Linda Healthcare system, Loma Linda, California, United States
  • Zhang, Zhiwei, VA Loma Linda Healthcare system, Loma Linda, California, United States
Introduction

Hypokalemia, a very common clinical problem is generally due to decreased oral intake, urinary loss, gastrointestinal loss or transcellular shifts. Here we present a challenging case of refractory hypokalemia.

Case Description

A 72-year-old man with new diagnosis of prostate adenocarcinoma not yet on treatment presented with hematuria, new hypertension and hypokalemia. He denied poor oral intake, vomiting or diarrhea. He denied medications or herbal, dietary supplements. There was no family history of hypokalemia or hypertension. Laboratory: Serum Na 145mmol/L, K 2.0mmol/L, HCO3 34mmol/L, Plasma Renin 0.62ng/ml/hr, Aldosterone< 1ng/dl, Cortisol 38.8mcg/dl, ACTH 81pg/ml, Urine K 88.5mmol/L. Cystoscopy: large friable prostate, likely the cause of hematuria so palliative TURP was performed. Androgen deprivation therapy (Bicalutamide) was begun. Refractory hypokalemia persisted despite aggressive potassium replacement.

Discussion

In our patient, inappropriately high urine K, Hypokalemia and Chloride-resistant metabolic alkalosis and Hypertension suggested mineralocorticoid excess. However low plasma renin and aldosterone indicated pseudohyperaldosteronism. Differential diagnosis included Liddle's, Gellers syndromes, Syndrome of apparent mineralocorticoid excess or chronic licorice use, Cushing syndrome and Congenital adrenal hyperplasia. Patient’s age and pertinent history excluded several of these leading us to a diagnosis of ACTH-dependent Cushing’s syndrome. This was further confirmed by overnight dexamethasone suppression test.

ACTH-dependent Cushing’s syndrome could be due to Cushing's disease but MRI of brain was negative, making this unlikely. Ectopic ACTH producing tumor was felt more likely. A high grade prostatic adenocarcinoma with a neuroendocrine component was found in prostate tissue.

The basic mechanism for hypokalemia is mineralocorticoid receptor (MR) activation by excess cortisol, leading to sodium reabsorption via ENaC. Treatment strategies focus on decreasing tumor burden and inhibition of MR or ENaC. Since some reports indicated spironolactone may potentially promote prostate cancer, we instead recommended ENaC inhibitor triamterene. Chemotherapy (Etoposide/Carboplatin) was then initiated with resolution of hypokalemia after 5 days of treatment. He was off triamterene and potassium replacement by the end of 3rd cycle of chemotherapy.