Pseudohypoaldosteronism following Resection of Ileum and Colon

Dr. M. Sugawara, Wadsworth VA Hospital (111M), Wilshire and Sawtelle Blvds., Los Angeles, CA 90073 (USA) Dear Sir, Pseudohypoaldosteronism is a disorder of mineralo-corticoid resistance manifested by hyponatremia and/or hyperkalemia with normal or increased plasma aldosterone [1–7]. Characteristically, raising plasma mineralocorticoid level by administration of exogenous mineralocorticoid does not correct serum electrolyte imbalance in pseudohypoaldosteronism. We report a patient with a colon cancer who, after subtotal colectomy and ileal resection, developed the picture of pseudohypoaldosteronism. In contrast to the established cases of pseudohypoaldosteronism [1–7], this case was not caused by an aldosterone receptor defect [1– 3] or an abnormality of the kidney in handling sodium or potassium [4, 5]. The primary abnormality was the resection of the ileum and colon, key sites for sodium and water absorption. A marked deficit of body sodium and water caused the picture of aldosterone resistance. Case Report An 82-year-old man was admitted to the hospital because of acute onset of abdominal pain with the clinical picture of intestinal obstruction. An exploratory laparotomy revealed adenocarcinoma in the descending colon and infarction of a portion of his ileum. He underwent subtotal colectomy, resection of 40% of the small bowel including the ileum, and jejunostomy. Total parenteral nutrition was provided initially, and later he was given 0.9% sodium chloride intravenously. As oral intake increased, his intravenous fluids were gradually tapered and discontinued. Seven days later he developed hyponatremia and hyperkalemia without clinical evidence of Ad-dison’s disease. Serum electrolytes showed Na of 125 mEq/1, K of 6.1 mEq/1, Cl of 90 mEq/1, and C02 of 25.5 mEq/1. BUN and serum creatinine were 51 mg/dl and 2.2 mg/dl, respectively. Plasma corti-sol level obtained at 2:00 PM was 25 μg/dl. Plasma renin activity was 28.9 ng/ml/h (upper limit: 27 under dehydrated condition) and serum aldosterone level was 120 ng/ml (normal: 3–31). He responded to intravenous administration of 5% glucose/0.9% sodium chloride with normalization of serum electrolytes, BUN, creatinine, plasma renin activity, and serum aldosterone levels. Hyponatremia and hyperkalemia were reproducible 6–7 days after discontinuation of intravenous fluid therapy. A balance study was carried out with oral ingestion of 5–10 g salt and 40 mmol potassium daily without intravenous fluid. Before the study, he received 9 g sodium chloride daily by intravenous infusion and oral salt ad libitum. Figure 1 shows the results of the balance study. Fecal volume and fecal sodium excretion exceeded his oral intake of water and sodium, indicating loss of water