Primary Aldosteronism With Mild Autonomous Cortisol Secretion Increases Renal Complication Risk


In primary aldosteronism (PA), renal impairment has been identified as an important comorbidity. Excess cortisol production also may lead to renal damage; thus, concomitant mild autonomous cortisol secretion (MACS) may predispose PA patients to renal disorders. However, there is limited evidence to support this claim. Therefore, this study aimed to determine whether the concurrence of MACS and PA increases the risk of renal complications. This study is a retrospective cross-sectional study. A total of 1310 patients with PA were stratified into two groups according to 1 mg dexamethasone suppression test (DST) results (cut-off post-DST serum cortisol 1.8 µg/dL): MACS (n = 340) and non-MACS (n = 970). The prevalence of renal complications was compared between the group. We also performed multiple logistic regression analysis to determine factors that increase the risk for renal complications. The prevalence of lowered estimated glomerular filtration rate (eGFR) and proteinuria was nearly twice higher in the MACS group than in the non-MACS group. Not only plasma aldosterone concentration (PAC) but also the presence of MACS was selected as independent factors that were associated with the two renal outcomes. The risk of lower eGFR or proteinuria in patients who had MACS and higher levels PAC was several folds higher than in those who had an absence of MACS and lower levels of PAC. MACS is an independent risk factor for renal complications in patients with PA, and MACS concomitant with higher aldosterone secretion in PA patients causes an increase in the risk of developing renal complications.

Authors: Takuyuki Katabami, Ren Matsuba, Hiroki Kobayashi, Tomoko Nakagawa, Isao Kurihara, Takamasa Ichijo, Mika Tsuiki, Norio Wada, Yoshihiro Ogawa, Masakatsu Sone, Nobuya Inagaki, Takanobu Yoshimoto, Katsutoshi Takahashi, Koichi Yamamoto, Shoichiro Izawa, Miki Kakutani, Akiyo Tanabe, Mitsuhide Naruse
Keywords: cortisol, autonomous secretion
DOI Number: 10.1530/EJE-21-1131      Publication Year: 2022

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