title: Antiproteinuric effect of cilnidipine in hypertensive Japanese treated with renin-angiotensin-system inhibitors - a multicenter, open, randomized trial using 24-hour urine collection.
abstract: Sustained proteinuria is an important risk factor for not only renal but also cardiovascular morbidity and mortality. Although inhibitors of the renin-angiotensin system (RAS) have been shown to reduce proteinuria. Monotherapy with those drugs is often insufficient for optimal blood pressure (BP)-lowering and therefore, combined therapy is needed. Recent reports suggested that cilnidipine, a dual L-/N-type calcium channel blocker, has renoprotective effect by dilating both efferent and afferent arterioles. In this study, a multicenter, open, randomized trial was designed to compare the antiproteinuric effect between cilnidipine and amlodipine when coupled with RAS inhibitors in hypertensive patients with significant proteinuria. Proteinuria was evaluated by 24-h home urine collection for all patients. A total of 35 proteinuric (>0.1 g/day) patients with uncontrolled BP (>135/85 mmHg) were randomized to receive either cilnidipine (n = 18) or amlodipine (n = 17) after a 6-month treatment with RAS inhibitors and were followed for 48 weeks. At baseline, the cilnidipine group was older and had lower body mass index (BMI) compared to the amlodipine group. After 32 weeks of treatment, diastolic blood pressure (DBP) was slightly, but significantly reduced, in the cilnidipine group, although systolic blood pressure (SBP) and mean BP did not differ. The urinary protein did not differ at baseline (cilnidipine group 0.48 g/day, amlodipine group 0.52 g/day); however, it significantly decreased in the cilnidipine group (0.22 g/day) compared to the amlodipine group (0.50 g/day) after 48 weeks of treatment. Our findings suggest that cilnidipine is superior to amlodipine in preventing the progression of proteinuria in hypertensive patients even undergoing treatment with RAS inhibitors.
authors.affiliation: Department of Internal Medicine, Sasaguri Hospital, Flukuoka, Japan. nctmf039@yahoo.co.jp
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Miwa
authors.forename: Takuya
authors.initials: T
authors.lastname: Tsuchihashi
authors.forename: Yuko
authors.initials: Y
authors.lastname: Ohta
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Tominaga
authors.forename: Yuhei
authors.initials: Y
authors.lastname: Kawano
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Sasaguri
authors.forename: Michio
authors.initials: M
authors.lastname: Ueno
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Matsuoka
mesh_terms: D017311:Amlodipine / Q000008:administration & dosage* / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002121:Calcium Channel Blockers / Q000008:administration & dosage* / Q000627:therapeutic use; D004095:Dihydropyridines / Q000008:administration & dosage* / Q000627:therapeutic use; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000652:urine; D007564:Japan; D008297:Male; D011507:Proteinuria / Q000517:prevention & control* / Q000652:urine; D016896:Treatment Outcome
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D017311:Amlodipine; C065927:cilnidipine