Calcium Channel Blocker versus Angiotensin II Receptor Blocker in Autosomal Dominant Polycystic Kidney DiseaseNutahara K. · Higashihara E. · Horie S. · Kamura K. · Tsuchiya K. · Mochizuki T. · Hosoya T. · Nakayama T. · Yamamoto N. · Higaki Y. · Shimizu T.
aDepartment of Urology, Kyorin University School of Medicine, Tokyo; bDepartment of Urology, Teikyo University School of Medicine, Tokyo; cDepartment of Urology, Sakura National Hospital, Sakura; dDepartment of Medicine, Kidney Center, Tokyo Women’s Medical University, Tokyo; eDepartment of Internal Medicine, Hokkaido University Graduate School of Medicine, Sapporo; fDepartment of Kidney and Hypertension, Jikei University School of Medicine, Tokyo; gDepartment of Internal Medicine, Nihon University School of Medicine, Tokyo; hDepartment of Urology, Hikari City General Hospital, Hikari; iDepartment of Urology, National Hospital, Tokyo Disaster Medical Center, Tokyo, and jDepartment of Clinical Genetics, Kyorin University School of Health Sciences, Tokyo, Japan
Background: Although hypertension is commonly found in patients with autosomal dominant polycystic kidney disease (ADPKD), there is no consensus about which antihypertensive agents are most appropriate. The effects of calcium channel blockers (CCB) and angiotensin II receptor blockers (ARB) on blood pressure and renoprotection were compared in hypertensive patients with ADPKD. Methods: We randomly assigned 49 participants to CCB amlodipine-based (2.5–10 mg/day) or ARB candesartan-based (2–8 mg/day) regimens. Twenty-five patients (13 males and 12 females) received amlodipine, and 24 patients (13 males and 11 females) received candesartan. This was followed up for 36 months. Results: Baseline characteristics were similar, and blood pressure was well controlled in both groups throughout the study period. Six out of 25 (24.0%) amlodipine and 1 out of 24 (4.2%) candesartan patients were terminated from the protocol due to a twofold increase in serum creatinine and/or decrease in creatinine clearance (Ccr) to half of the baseline. The renal event-free survival rate was significant (p < 0.05, Breslow-Gehan-Wilcoxon test). Serum creatinine was higher in the amlodipine group than in the candesartan group at 24 and 36 months (p < 0.05). The decrease in Ccr at 36 months was larger in the amlodipine group than in the candesartan group (ΔCcr: –20.9 ± 13.1 vs. –4.8 ± 13.8 ml/min, p < 0.01). Urinary protein excretion was significantly lower in the candesartan group than in the amlodipine group at 36 months. Urinary albumin excretion was significantly lower in the candesartan group than in the amlodipine group at 12, 24 and 36 months. Conclusions: The renoprotective effect of candesartan is considered more favorable than amlodipine in the treatment of ADPKD. This is independent of the antihypertensive effect per se.
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