Open AccessEffects of the N/L‐Type Calcium Channel Blocker Cilnidipine on Nephropathy and Uric Acid Metabolism in Hypertensive Patients With Chronic Kidney Disease (J‐ CIRCLE Study)
Author(s) -
Uchida Shunya,
Takahashi Masato,
Sugawara Masahiro,
Saito Tomoaki,
Nakai Kazuhiko,
Fujita Masami,
Mochizuki Koichi,
Shin Isu,
Morita Takashi,
Hikita Tomoyuki,
Itakura Hironao,
Takahashi Yuko,
Mizuno Shigeki,
Ohno Yasumi,
Ito Kageki,
Ito Takafumi,
Soma Masayoshi
Publication year - 2014
Publication title -
the journal of clinical hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 67
eISSN - 1751-7176
pISSN - 1524-6175
DOI - 10.1111/jch.12412
Subject(s) - medicine , uric acid , amlodipine , albuminuria , endocrinology , creatinine , kidney disease , urinary system , urology , blood pressure
This study assessed the urinary albumin/creatinine ratio ( ACR ) and uric acid metabolism in 70 hypertensive patients with chronic kidney disease in whom urinary ACR had remained ≥30 mg/g under the treatment of the L‐type calcium channel blocker amlodipine. Three months after switching to the N/L‐type calcium channel blocker cilnidipine, blood pressure ( BP ) did not change; however, urinary ACR significantly decreased with cilnidipine. Serum uric acid levels showed no significant change. In cases where uric acid production had been high (urinary uric acid/creatinine ratio ≥0.5), the urinary uric acid/creatinine ratio decreased significantly after cilnidipine treatment, suggesting that cilnidipine can suppress excessive uric acid formation. These results suggest that switching from amlodipine to cilnidipine results in a significant reduction in urinary ACR as well as significant reduction in uric acid production. Thus, cilnidipine is more useful than amlodipine in improving albuminuria and uric acid metabolism in hypertensive patients with chronic kidney disease.