Tohoku J. Exp. Med., 1998, 186 (3)

Case Report

A Case of Aldosterone-Producing Adenoma with Severe Postoperative Hyperkalemia

RYOJI TANIGUCHI, HIROYUKI KOSHIYAMA, MIKA YAMAUCHI, SATSUKI TANAKA, DAISUKE INOUE, YUKIHITO SATO,1 AKIRA SUGAWA,2 YASUNARI MURAMATSU3 and HIRONOBU SASANO3

Division of Endocrinology and Metabolism and 1Division of Cardiovascular Medicine, Department of Internal Medicine, Hyogo Prefectural Amagasaki Hospital, Amagasaki 660-0828, 2Division of Nephrology, Department of Internal Medicine, Saiseikai Nakatsu Hospital, Osaka 530-0012, and 3The Second Department of Pathology, Tohoku University, Sendai 980-8575

  • It is known that some patients with primary aldosteronism show postoperative hyperkalemia, which is due to inability of the adrenal gland to secrete sufficient amounts of aldosterone. However, hyperkalemia is generally neither severe nor prolonged, in which replacement therapy with mineralocorticoid is seldom necessary. We report a case of a 46-year-old woman with an aldosterone-producing adenoma associated with severe postoperative hyperkalemia. After unilateral adrenalectomy, the patient showed episodes of severe hyperkalemia for four months, which required not only cation-exchange resin, but also mineralocorticoid replacement. Plasma aldosterone concentration (PAC) was low, although PAC was increased after rapid ACTH test. Histological examination indicated the presence of adrenocortical tumor and paradoxical hyperplasia of zona glomerulosa in the adjacent adrenal. Immunohistochemistry demonstrated that the enzymes involved in aldosterone synthesis, such as cholesterol side chain cleavage (P-450scc), 3b-hydroxysteroid dehydrogenase (3b-HSD), and 21-hydroxylase (P-450c21), or the enzyme involved in glucocorticoid synthesis, 11b-hydroxylase (P-450c11b), were expressed in the tumor, but they were completely absent in zona glomerulosa of the adjacent adrenal. These findings were consistent with the patterns of primary aldosteronism. Serum potassium level was gradually decreased with concomitant increase in PAC. These results suggest that severe postoperative hyperkalemia of the present case was attributable to severe suppression of aldosterone synthesis in the adjacent and contralateral adrenal, which resulted in slow recovery of aldosterone secretion. It is plausible that aldosterone synthesis of adjacent and contralateral adrenal glands is severely impaired in some cases with primary aldosteronism, as glucocorticoid synthesis in Cushing syndrome.
    Key words--- aldosteronism; hyperkalemia; postoperative; hypoaldosteronism; paradoxical hyperplasia
    © 1998 Tohoku University Medical Press

    Tohoku J. Exp. Med., 1998, 186, 215-223
    Address for reprints: Hiroyuki Koshiyama, M.D., Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo Prefectural Amagasaki Hospital, Amagasaki 660-0828, Japan.
    e-mail: ime@amahosp.amagasaki.hyogo.jp

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