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Primary aldosteronism: changes in cystatin C-based kidney filtration, proteinuria, and renal duplex indices with treatment

Wu, Vin-Centa; Kuo, Chin-Chib; Wang, Shuo-Mengc; Liu, Kao-Langd; Huang, Kuo-Howc; Lin, Yen-Hunga; Chu, Tzong-Shinna; Chang, Hung-Weia; Lin, Chien-Yue; Tsai, Chia-Tia; Lin, Lian-Yua; Chueh, Shih-Chiehc,f; Kao, Tze-Waha; Chen, Yung-Minga; Chiang, Wen-Chiha; Tsai, Tun-Juna; Ho, Yi-Luwna; Lin, Shuei-Lionga; Wang, Wei-Jeig; Wu, Kwan-Dunathe TAIPAI Study Group

doi: 10.1097/HJH.0b013e3283495cbb
Original papers: Aldosteronism

Objectives To obtain information about the effect of prolonged aldosterone excess on kidney function.

Methods We determined kidney function changes defined by cystatin C-based estimations of glomerular filtration rate (CysC-GFR). Pretreatment proteinuria and intrarenal Doppler velocimetric indices in primary aldosteronism were examined and followed after adrenalectomy or spironolactone treatment.

Results This prospective, multicenter study included 130 primary aldosteronism patients (56 men; age, 49.9 ± 13.4 years: 100 with adenoma and 30 with idiopathic hyperaldosteronism) and 73 essential hypertension patients (36 men; age, 51.4 ± 14.8 years) as controls. Patients with primary aldosteronism had higher CysC-GFR (P < 0.05) and heavier proteinuria (0.042) than those with essential hypertension. With primary aldosteronism, a higher aldosterone–renin ratio (odds ratio, OR = 7.85, P = 0.008) was independently related to pretreatment CysC-GFR. The factors related to pretreatment proteinuria included CysC-GFR (OR, −0.006, P = 0.001), plasma aldosterone concentration (OR, 0.004, P = 0.002), and duration of hypertension (OR, 0.016, P = 0.032). Duration of hypertension was also independently correlated with the pretreatment resistive index among primary aldosteronism patients (OR, 0.004, P = 0.035). CysC-GFR (all, P < 0.05), proteinuria (P < 0.001), and resistive index (P < 0.001) decreased 1 year after adrenalectomy but not with spironolactone treatment.

Conclusion Our data suggest that prolonged hyperaldosteronism will cause relative kidney hyperfiltration and reversible intrarenal vascular structural changes, which disguise the consequent renal injury, including declining GFR and proteinuria. Adrenalectomy and spironolactone treatment exert different clinical impacts toward kidney damage even with a similar blood pressure-lowering effect.

aDepartment of Internal Medicine

bDepartment of Yun-Lin Branch

cDepartment of Urology

dDepartment of Medical Image, National Taiwan University Hospital

eDepartment of Internal Medicine, En- Chu- Kong Hospital, Taipei County, Taipei , Taiwan

fCleveland Clinic Glickman Urological and Kidney Institute, Cleveland, Ohio, USA

gDepartment of Internal Medicine, Tao-Yuan General Hospital, Tao-Yuan, Taiwan

Correspondence to Kwan-Dun Wu, MD, Department of Internal Medicine, National Taiwan University Hospital, Room 1419, Clinical Research Building, 7 Chung-Shan South Road, Taipei 100, Taiwan Tel: +886 2 23562082; fax: +886 2 23934176; e-mail: q91421028@ntu.edu.tw

Abbreviations: APA, aldosterone–renin ratio adenoma; ARR, aldosterone–renin ratio; CKD, chronic kidney disease; CVD, cardiovascular disease; CysC, cystain-C; eGFR, estimated glomerular filtration rate; IHA, idiopathic hyperaldosteronism; PAC, plasma aldosterone concentration; PRA, plasma renin activity

Received 10 March, 2011

Revised 26 May, 2011

Accepted 31 May, 2011

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© 2011 Lippincott Williams & Wilkins, Inc.