Effect of Cilnidipine on Normal to Marginally Elevated Urine Albumin-Creatinine Ratio in Asymptomatic Non-Diabetic Hyper
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ORIGINAL RESEARCH ARTICLE
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Effect of Cilnidipine on Normal to Marginally Elevated Urine AlbuminCreatinine Ratio in Asymptomatic Non-Diabetic Hypertensive Patients An Exponential Decay Curve Analysis Takaaki Nakatsu,1 Shinji Toyonaga,1 Keiichi Mashima,1 Yoko Yuki,1 Aya Nishitani,1 Hiroko Ogawa,2 Toru Miyoshi,2 Satoshi Hirohata,2 Reishi Izumi1 and Shozo Kusachi2 1 Department of Cardiology, Kagawa-ken Saiseikai Hospital, Takamatsu, Japan 2 Department of Medical Technology, Okayama University Graduate School of Health Sciences, Okayama, Japan
Abstract
Background: High-normal urinary albumin excretion has been reported to have clinical significance with respect to progression of proteinuria and hypertension. Objective: We analysed the effect of cilnidipine (10 mg/day) on morning systolic blood pressure (SBP) and urine albumin-creatinine ratio (UACR) in 16 non-diabetic hypertensive patients with a normal to marginally elevated UACR (mean – SD 29.4 – 21.7; range 7.5–72.9 mg/g creatinine). Methods: Sequential home BP and UACR data were fitted to a simple exponential function as follows: y ¼ a et=b þ g, where y is SBP (mmHg) or UACR (mg/g creatinine); a is the extent of the SBP (mmHg)- or UACR (mg/g creatinine)-lowering effect; b (days) is the time-constant for SBP or UACR decrease; t is the number of days after the start of cilnidipine administration; and g is the finally stabilized SBP (mmHg) or UACR (mg/g creatinine). Results: Mean – SD morning SBP and UACR decreased by 20.4 – 11.4 mmHg and 15.2 – 13.1 mg/g creatinine, respectively, as determined by coefficient a. The mean – SD time-constant for UACR decrease was significantly longer than that for BP decrease (43.5 – 22.9 vs 15.4 – 7.1 days). UACR reduction correlated with pre-treatment UACR values (correlation coefficient [R] = 0.88, p < 0.01) but not with BP decrease. Conclusions: The present study demonstrated that cilnidipine reduced UACR in hypertensive patients with normal to marginally elevated UACR independent of its BP-lowering effect.
Nakatsu et al.
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Introduction Cilnidipine [FRC-8653; 2-methoxyethyl (E)-3phenyl-2-propen-1-yl(6)-1, 4-dihydro-2, 6-dimethyl4-(3-nitrophenyl) pyridine-3, 5-dicarboxylate] is a dihydropyridine calcium channel antagonist (calcium channel blocker [CCB]) that has been shown to have prolonged antihypertensive properties.[1] Cilnidipine has attracted attention as a blocker of N-type calcium channels distributed in sympathetic nerve endings, as well as of L-type calcium channels.[2,3] In spontaneously hypertensive rats treated with N-o-nitro-L arginine methylester, cilnidipine dilated afferent and efferent arterioles in the kidney and decreased glomerular capillary pressure, thereby reducing proteinuria and improving glomerulosclerosis and arteriolar lesions.[4] Cilnidipine has also been shown to exhibit renal protective effects in terms of urinary protein reduction in various animal models and in patients with renal dysfunction.[5-7] In addition, a study that compared cil
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