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      Comparison of the Antialbuminuric Effects of L-/N-type and L-type Calcium Channel Blockers in Hypertensive Patients with Diabetes and Microalbuminuria: The Study of Assessment for Kidney Function by Urinary Microalbumin in Randomized (SAKURA) Trial

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          Abstract

          Objective: To clarify whether the L-/N-type calcium channel blocker (CCB) cilnidipine is more renoprotective than the L-type CCB amlodipine in patients with early-stage diabetic nephropathy.

          Methods: In this prospective, multicenter, open-labeled, randomized trial, the antialbuminuric effects of cilnidipine and amlodipine were examined in renin-angiotensin system (RAS) inhibitor-treated patients with hypertension (blood pressure [BP]: 130-180/80-110 mmHg), type 2 diabetes, and microalbuminuria (urinary albumin to creatinine [Cr] ratio [UACR]: 30-300 mg/g).

          Results: Patients received cilnidipine ( n = 179, final dose: 10.27 ± 4.13 mg/day) or amlodipine ( n = 186, 4.87 ± 2.08 mg/day) for 12 months. Cilnidipine and amlodipine equally decreased BP. The UACR values for the cilnidipine and amlodipine groups were 111.50 ± 138.97 and 88.29 ± 63.45 mg/g, respectively, before treatment and 107.93 ± 130.23 and 89.07 ± 97.55 mg/g, respectively, after treatment. The groups showed similar changes for the natural logarithm of the UACR, serum Cr, and estimated glomerular filtration rate.

          Conclusions: Cilnidipine did not offer greater renoprotection than amlodipine in RAS inhibitor-treated hypertensive patients with type 2 diabetes and microalbuminuria.

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          Most cited references39

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          The Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2009).

          Genjiro Kimura, Jitsuo Higaki, Toshio Ogihara … (2008)
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            Antiproteinuric effect of the calcium channel blocker cilnidipine added to renin-angiotensin inhibition in hypertensive patients with chronic renal disease.

            T. Fujita, K Ando, H. Nishimura … (2007)
            Cilnidipine, a dual L-/N-type calcium channel blocker, dilates both efferent and afferent arterioles and is renoprotective. Our multi-center, open-labeled, and randomized trial compared the antiproteinuric effect of cilnidipine with that of amlodipine in hypertensive patients with kidney disease. A group of 339 patients, already receiving renin-angiotensin system inhibitor treatment, were randomly assigned to cilnidipine or amlodipine. The primary endpoint was a decrease in the urinary protein to creatinine ratio. After 1-year of treatment, systolic and diastolic blood pressures were significantly reduced in both groups which did not differ between them. The urinary protein to creatinine ratio significantly decreased in the cilnidipine compared to the amlodipine group. Cilnidipine exerted a greater antiproteinuric effect than amlodipine even in the subgroup whose blood pressure fell below the target level. This study suggests that cilnidipine is superior to amlodipine in preventing the progression of proteinuria in hypertensive patients when coupled with a renin-angiotensin system inhibitor.
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              The role of sympathetic nervous activity in renal injury and end-stage renal disease.

              Murray Esler, Kazuko Masuo, Toshio Ogihara … (2010)
              Sympathetic nervous system hyperactivity is observed in patients with renal injury, renovascular hypertension, chronic kidney disease (CKD) and end-stage renal disease (ESRD). Elevated sympathetic activity is of prognostic relevance in that plasma norepinephrine concentrations predict survival and the incidence of cardiovascular events in patients with ESRD, as well as future renal injury in normotensive healthy subjects with renal function in the normal range. Renal injury, CKD and ESRD are often associated with obesity, and its common sequelae hypertension and diabetes. In fact, hypertension and diabetes mellitus are the main causes of ESRD in western societies and together account for approximately more than 50% of ESRD incidence in the United States and Japan. Obesity also leads to increases in the incidence of cardiovascular diseases. Several clinical and epidemiological studies have clearly documented that heightened sympathetic nervous activity has an important role in the onset and maintenance of obesity and hypertension. Elevated sympathetic nervous activity may actually represent an important mechanism contributing to the onset and maintenance of renal injury at least in part through its concomitant adverse effects on obesity and hypertension. Understanding the contribution of sympathetic nervous hyperactivity to the onset and maintenance of renal injury might aid in the prevention and treatment of renal injury, CKD and ESRD. Very recently, renal sympathetic denervation was shown to be a potentially novel therapeutic strategy in resistant hypertension. In addition, renin-angiotensin system inhibitors are recommended as the initial therapy because of their renal protective effect, especially in hypertensive patients with type 2 diabetes or with proteinuria. The purpose of this review is to provide an overview of our current knowledge on the relationships between sympathetic nerve activity and renal function to further our understanding of the precise roles of sympathetic nerve activity in renal injury, particularly in the context of obesity and hypertension. These insights may be useful to improve prevention and treatment of renal injury in these patients.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Med Sci
                Journal ID (iso-abbrev): Int J Med Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Medical Sciences
                Publisher: Ivyspring International Publisher (Sydney )
                ISSN (Electronic): 1449-1907
                Publication date Collection: 2013
                Publication date (Electronic): 30 July 2013
                Volume: 10
                Issue: 9
                Pages: 1209-1216
                Affiliations
                1. Department of Nephrology and Endocrinology, University of Tokyo Graduate School of Medicine, Tokyo, Japan
                2. EBM Research Center, Kyoto University Graduate School of Medicine, Kyoto, Japan
                3. Department of Medical Ethics/Medical Genetics, Kyoto University School of Public Health, Kyoto, Japan
                4. Department of Biostatistics, Kyoto University School of Public Health, Kyoto, Japan
                5. Utsunomiya Chuoh Hospital, Tochigi, Japan
                6. Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, Japan
                7. Division of Clinical Epigenetics, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan
                Author notes
                ✉ Corresponding author: Katsuayuki Ando, MD, Department of Nephrology and Endocrinology, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655 Japan. Phone: +81-3-5800-9119, Fax: +81-3-5800-9119; E-Mail: katsua-tky@ 123456umin.ac.jp

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                Publisher ID: ijmsv10p1209
                DOI: 10.7150/ijms.5508
                PMC ID: 3739020
                PubMed ID: 23935398
                SO-VID: ad696ce5-0491-49c0-9e69-ad9a20f0bf49
                Copyright © © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.
                History
                Date received : 9 November 2012
                Date accepted : 13 May 2013
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Medicine
                Keywords: l-/n-type calcium channel blocker,urinary albumin,diabetic nephropathy,hypertension,renin-angiotensin system inhibitor
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: l-/n-type calcium channel blocker, urinary albumin, diabetic nephropathy, hypertension, renin-angiotensin system inhibitor

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