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Journal of Nippon Medical School

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Blood Pressure Control in Patients with Chronic Kidney Disease

Kouichi Utsumi, Ken-ichiro Katsura, Yasuhiko Iino and Yasuo Katayama

Department of Neurological, Nephrological, and Rheumatological Science, Graduate School of Medicine, Nippon Medical School


Chronic kidney disease (CKD) is defined as either kidney damage or an estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73 m2 for more than 3 months. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies. CKD is classified as stage 1 to 5 on the basis of eGFR. Cardiovascular disease (CVD) carries a reciprocal risk of loss of kidney function in patients with chronic kidney disease (CKD) and with the development of kidney disease. CVD is a major cause of morbidity and mortality in patients with CKD. Blood pressure control in patients with CKD aims to prevent CVD and provide renoprotection. The renin-angiotensin system (RAS) is involved in every stage of the progression of CKD and is, therefore, a critical link in the pathologic relationship between hypertension and renal disease. The first-line agents for controlling blood pressure are inhibitors of the RAS: angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers. These agents have been shown to have renoprotective effects in addition to their ability to control bood pressure. In CKD, the target blood pressure is less than 130/80 mm Hg, or 125/75 mm Hg, if amount of urinary protein is more than 1 g/day. To achieve the target blood pressure, other classes of antihypertensive agents, such as diuretics and calcium channel blockers, should be administered in addition to angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers.

J Nippon Med Sch 2012; 79: 111-114

Keywords
chronic kidney disease, cardiovascular disease, renin-angiotensin system, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers

Correspondence to
Kouichi Utsumi, MD, Department of Neurological, Nephrological, and Rheumatological Science, Graduate School of Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan
utsumi@nms.ac.jp

Received, October 1, 2011
Accepted, November 30, 2011