Hypoalbuminemia and Hyperalbuminuria as Major Factors Regulating Circadian Blood Pressure Rhythm in Normal Subjects and Non-diabetic Patients with Early Stages of Chronic Kidney DiseaseDaisaku Ando, Nobuhito Hirawa and Gen Yasuda*
Division of Nephrology and Hypertension, Yokohama City University Center Hospital, Kanagawa, Japan
- *Corresponding Author:
- Gen Yasuda
Division of Nephrology and Hypertension
Yokohama City University Center Hospital
4-57, Urafune, Minami, Yokohama 232-0024, Kanagawa, Japan
Tel: +81 45 261 5656
E-mail: [email protected]
Received Date: January 21, 2014; Accepted Date: February 21, 2014; Published Date: February 24, 2014
Citation: Ando D, Hirawa N, Yasuda G (2014) Hypoalbuminemia and Hyperalbuminuria as Major Factors Regulating Circadian Blood Pressure Rhythm in Normal Subjects and Non-diabetic Patients with Early Stages of Chronic Kidney Disease. J Hypertens 3:142. doi:10.4172/2167-1095.1000142
Copyright: © 2014 Ando D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Study background: Albuminuria and nighttime blood pressure (BP) elevation are notable risk markers of chronic kidney disease (CKD). In non-diabetic patients with albuminuria, the effect of albuminuria on nocturnal BP and other risk factors that may disrupt circadian BP rhythm remain unclear. The aim of this study was to evaluate the relationship among albuminuria, serum albumin level and 24-hour BP rhythm in non-diabetic subjects.
Methods: This prospective study enrolled 778 subjects (aged 20-80 years, estimated glomerular filtration rate ≥ 60 mL/min/1.73 m2). Main outcome measure was sleeping/waking mean BP (MBP) ratio as an indicator of circadian BP rhythm. First, a cross-sectional study was performed in all individuals showing no proteinuria. Second, a study was done in subjects never treated for hypertension (hypertensive-naïve) stratified by urinary albumin excretion. Third, an intervention study was conducted in patients with massive albuminuria and hypoalbuminemia to examine circadian BP changes induced by treatment.
Results: In 441 subjects without proteinuria, multivariate regression analyses identified serum albumin, cholesterol level and circadian sympathovagal rhythm as independent predictors of sleeping/waking MBP ratio. Among hypertensivenaïve non-diabetic subjects (n=231), sleeping/waking MBP ratio increased with increasing albuminuria and decreasing serum albumin. Of 37 non-diabetic nephrotic patients who underwent treatment, 25 with serum albumin level increased to >3 g/dL showed a significant decrease (P=0.026) in sleeping/waking MBP ratio after treatment, whereas 13 with urinary albumin/creatinine lowered to <300 mg/g showed no significant difference (P=0.191).
Conclusions: This study identified low serum albumin as an independent predictor of loss of nocturnal BP decline, which was also associated with massive albuminuria. Furthermore, sleeping/waking MBP ratio was improved after hyperalbuminuria and hypoalbuminemia were reversed by treatment. These findings suggest that low serum albumin level and massive albuminuria are risk markers of disrupted circadian BP rhythm in non-diabetic early stage CKD.