L/N-type calcium channel blocker cilnidipine reduces plasma aldosterone, albuminuria, and urinary liver-type fatty acid binding protein in patients with chronic kidney disease.
Cilnidipine inhibits both L- and N-type calcium channels and has been shown to dilate efferent arterioles as effectively as afferent arterioles. We conducted an open-label, randomized trial to compare the effects of cilnidipine against those of amlodipine on blood pressure (BP), albuminuria, and plasma aldosterone concentration in hypertensive patients with mild- to moderate-stage chronic kidney disease. Patients with BP ≥130/80 mmHg, an estimated glomerular filtration rate of 90-30 ml/min/1.73 m(2), and albuminuria ≥30 mg/g, despite treatment with the maximum recommended dose of angiotensin II receptor blockers, were randomly assigned to two groups. Patients received either 10 mg/day cilnidipine (increased to 20 mg/day; n = 35) or 2.5 mg/day amlodipine (increased to 5 mg/day; n = 35). After 48 weeks of treatment, a significant and comparable reduction in systolic and diastolic BP was observed in both groups. The percent reduction in the urinary albumin to creatinine ratio and liver-type fatty acid binding protein (L-FABP) in the cilnidipine group was significantly greater than in the amlodipine group. Although plasma renin activity did not differ between the two groups, the plasma aldosterone level was significantly decreased in the cilnidipine group. Cilnidipine therefore appears to reduce albuminuria, urinary L-FABP, and plasma aldosterone levels more than amlodipine, and these effects are independent of BP reduction.
Division of Nephrology, Hypertension and Endocrinology, Department of Internal Medicine, Nihon University School of Medicine, 30-1, Oyaguchi Kami-chou, Itabashi-ku, Tokyo, 173-8610, Japan. abe.masanori@nihon-u.ac.jp
Masanori
M
Abe
Noriaki
N
Maruyama
Hiroko
H
Suzuki
Atsushi
A
Inoshita
Yoshinori
Y
Yoshida
Kazuyoshi
K
Okada
Masayoshi
M
Soma
D000368:Aged; D000419:Albuminuria / Q000175:diagnosis / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D000450:Aldosterone / Q000097:blood*; D017311:Amlodipine / Q000627:therapeutic use; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D020746:Calcium Channels, L-Type / Q000187:drug effects* / Q000378:metabolism; D020864:Calcium Channels, N-Type / Q000187:drug effects* / Q000378:metabolism; D003404:Creatinine / Q000652:urine; D004095:Dihydropyridines / Q000627:therapeutic use*; D015536:Down-Regulation; D050556:Fatty Acid-Binding Proteins / Q000652:urine*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D007564:Japan; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011446:Prospective Studies; D051436:Renal Insufficiency, Chronic / Q000175:diagnosis / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D013997:Time Factors; D016896:Treatment Outcome
D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D015415:Biomarkers; D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D020864:Calcium Channels, N-Type; D004095:Dihydropyridines; C493319:FABP1 protein, human; D050556:Fatty Acid-Binding Proteins; D017311:Amlodipine; D000450:Aldosterone; C065927:cilnidipine; D003404:Creatinine