Insufficiency of the zona glomerulosa of the adrenal cortex and progressive kidney insufficiency following unilateral adrenalectomy - case report and discussion

• Published in: Blood pressure 2018-09, Vol.27 (5), p.304-312
• Main Authors: Kanarek-Kucner, Joanna, Stefański, Adrian, Barraclough, Rufus, Gorycki, Tomasz, Wolf, Jacek, Narkiewicz, Krzysztof, Hoffmann, Michał
• Format: Article
• Language: English
• Subjects: Adrenal Cortex - physiopathology; adrenal cortex insufficiency; Adrenalectomy - adverse effects; Aged; Anti-Inflammatory Agents; chronic kidney failure; Fludrocortisone - therapeutic use; Humans; Hyperaldosteronism - complications; hyperkalemia; Hyperkalemia - etiology; Hypertension - complications; Male; primary aldosteronism; Renal Insufficiency - etiology; Zona Glomerulosa - physiopathology
• ISSN: 0803-7051; 1651-1999
• DOI: 10.1080/08037051.2018.1470460

Primary aldosteronism (PA) is the most common cause of secondary hypertension and bilateral adrenal hyperplasia (BAH) and aldosterone-producing adenoma (APA) seem to be the most common causes of PA. Unilateral adrenalectomy (UA) is the preferred treatment for APA, although the benefits are still difficult to assess. We present a case report of a 69-year old man with a 30 year history of hypertension and probably long-standing PA due to APA, with typical organ complications. Since repeated abdominal CT scans were equivocal, not showing radiological changes characteristic for PA, the diagnosis of APA was delayed and was only finally confirmed by adrenal venous sampling which demonstrated unilateral aldosteronism. The patient underwent UA, complicated by mineralocorticoid deficiency syndrome and increased creatinine and potassium levels. At 12 months follow-up the patient still had hyperkalemia and was fludrocortisone dependent. Older patients and patients with long-lasting PA who are treated with UA may demonstrate deterioration of renal function and develop transient or persistent insufficiency of the zona glomerulosa of the remaining adrenal gland necessitating fludrocortisone supplementation. Transient hyperkalemia may be observed following UA as a result of the prolonged effects of aldosterone antagonists and/or transient mineralocorticoid/glucocorticoid insufficiency. Additionally, the level of progression of chronic kidney disease after UA is difficult to predict. There likely exists a group of patients who might paradoxically have higher cardiovascular risk due to significant deterioration in kidney function not only resulting from the removal of the aldosterone induced glomerular hyperfiltration phenomenon. Identification of such a group requires further detailed investigation.