Hyperaldosteronism in a Patient With Gastrointestinal Potassium Wasting

Abstract

Background: Medical conditions causing hypokalemia can be masked by a diet very rich in potassium. The following case presents a patient who developed new onset symptoms of hypokalemia after immigrating to the United States. Clinical Case: A 35 year old man, native of Mali, had a history of intermittent muscle spasms and serum potassium of 3.0 mmol/L first recognized elsewhere in 2019. He was not on any home medications. He was admitted with postprandial generalized abdominal pain, diarrhea, and bright blood in his stools. Serum potassium was 2.7 (nl 3.5–5.1mmol/L). He required at least 120 mEq of intravenous and oral potassium chloride per day while hospitalized to achieve and maintain serum potassium in the normal range. Colonoscopy found segmental colitis and it was thought that his hypokalemia was due to gastrointestinal losses. However, studies demonstrated urinary potassium wasting. A 1.9 cm nodular mass of the left adrenal gland was found on CT of the abdomen, and the differential diagnosis was expanded to include hypokalemia secondary to primary hyperaldosteronism or renal tubulopathies such as Bartter and Gitleman syndromes. The patient was normotensive and had biochemical findings that were consistent with Bartter syndrome including metabolic alkalosis, hypercalciuria, elevated urine sodium and chloride, and normal serum magnesium levels. However, he had low plasma rennin activity with an elevated serum aldosterone on three tests over two months (the last test was more than one month after normalization of bowel function). On all of these, the aldosterone to renin ratio was greater than 20 ng/mL/hour. The persistent suppression of plasma rennin with elevated aldosterone in the setting of left adrenal mass narrowed the differential diagnosis to primary hyperaldosteronism, as elevated rennin would be expected in Bartter syndrome. Since discharge, he has received 80 meq of daily oral potassium in divided doses, which has kept serum potassium at or below the lower limit of normal. Further management will consist of either pharmacologic or surgical treatment with or without adrenal venous sampling. Conclusion: The patient had hypokalemia for which an endocrine etiology could have been easily overlooked and attributed to gastrointestinal losses. This case demonstrates the very close clinical similarities between primary hyperaldosteronism and renal tubulopathies. However, there are biochemical patterns that can be relied on to help differentiate amongst these disorders. This patient with primary hyperaldosteronism may not have been hypokalemic in his native country due to consuming a diet rich in potassium.