High Plasma Renin Activities in Primary Aldosteronism with Malignant Hypertension A Case Report

• Published in: Japanese Heart Journal Vol. 21; no. 3; pp. 423 - 428
• Main Authors: IWAOKA, Taisuke, UMEDA, Teruhisa, SATO, Tatsuo, KATSURAGI, Shoichi, TAKEUCHI, Tadao
• Format: Journal Article
• Language: English
• Published: Japan International Heart Journal Association 01.01.1980
• Subjects: Adenoma - complications; Adrenal Cortex Neoplasms - complications; Adrenocortical tumor; Adult; Aldosterone - analysis; Aldosterone contents of the tumor; Humans; Hyperaldosteronism - blood; Hyperaldosteronism - complications; Hyperaldosteronism - diagnosis; Hypertension, Malignant - blood; Hypertension, Malignant - etiology; Male; Plasma aldosterone concentration; Renal insufficiency; Renin - blood
• ISSN: 0021-4868; 1348-673X
• DOI: 10.1536/ihj.21.423

Primary aldosteronism usually shows mild hypertension and is characterized by suppression of plasma renin activity (PRA) and elevation of plasma aldosterone concentration (PAC). Almost all previously reported cases of malignant hypertension associated with primary aldosteronism showed low PRA.3)-6) However, only I case which showed high PRA was reported by Baglin et al in 1973.2) The patient reported below is the second case of primary aldosteronism with high PRA. A 34-year-old man was admitted to our clinic because of severe hypertension, renal insufficiency, and papilledema. Both PRA and PAC were abnormally high, 4.6ng/ml/hr and 23.0ng/100ml, respectively. Serum cortisol levels and urinary catecholamine excretion were within normal ranges. Serum K was normal ranging from 3.6 to 4.9mEq/L. In spite of strong anti-hypertensive drugs, peritoneal, and hemodialysis, the patient died of pulmonaly infection about 3 months later. Postmortem examination revealed a right adrenocortical tumor of 8mm in diameter. Histologically, the tumor consisted of large clear cells; that was adenomatous hyperplasia characteristic in primary aldosteronism. Neither juxtaglomerular tumor nor renal artery stenosis was found. We thought that PRA in primary aldosteronism could rise with progress of renal involvement as secondary changes due to long-standing and untreated hypertension. Normal serum K could be explained by the fact that retention of potassium due to severely disturbed renal function exceeded its loss through aldosterone action. It must be kept in mind that normokalemia and elevated PRA can be encountered under these circumstances.