title: Effects 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).
abstract: 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.
authors.affiliation: Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.
authors.forename: Shunya
authors.initials: S
authors.lastname: Uchida
authors.forename: Masato
authors.initials: M
authors.lastname: Takahashi
authors.forename: Masahiro
authors.initials: M
authors.lastname: Sugawara
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Saito
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Nakai
authors.forename: Masami
authors.initials: M
authors.lastname: Fujita
authors.forename: Koichi
authors.initials: K
authors.lastname: Mochizuki
authors.forename: Isu
authors.initials: I
authors.lastname: Shin
authors.forename: Takashi
authors.initials: T
authors.lastname: Morita
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Hikita
authors.forename: Hironao
authors.initials: H
authors.lastname: Itakura
authors.forename: Yuko
authors.initials: Y
authors.lastname: Takahashi
authors.forename: Shigeki
authors.initials: S
authors.lastname: Mizuno
authors.forename: Yasumi
authors.initials: Y
authors.lastname: Ohno
authors.forename: Kageki
authors.initials: K
authors.lastname: Ito
authors.forename: Takafumi
authors.initials: T
authors.lastname: Ito
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Soma
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000419:Albuminuria / Q000097:blood / Q000188:drug therapy; D017311:Amlodipine / Q000009:adverse effects / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000009:adverse effects / Q000627:therapeutic use*; D003404:Creatinine / Q000097:blood; D018592:Cross-Over Studies; D003928:Diabetic Nephropathies / Q000097:blood / Q000188:drug therapy; D004095:Dihydropyridines / Q000009:adverse effects / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D057915:Drug Substitution; D005260:Female; D006801:Humans; D006977:Hypertension, Renal / Q000097:blood / Q000188:drug therapy*; D007564:Japan; D007676:Kidney Failure, Chronic / Q000097:blood / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D009400:Nephrosclerosis / Q000097:blood / Q000188:drug therapy; D014527:Uric Acid / Q000097:blood*
chemical_list: D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D017311:Amlodipine; D014527:Uric Acid; C065927:cilnidipine; D003404:Creatinine