Hypertension and chronic kidney disease progression: why the suboptimal outcomes?

Abstract

Current therapeutic interventions to retard the progression of chronic kidney disease have yielded disappointing outcomes despite adequate renin-angiotensin system blockade. The parameters to gauge the adequacy of blood pressure control need to be reassessed because clinic blood pressure constitutes a poor gauge of such control. The biologically relevant parameter for hypertensive target organ damage is total blood pressure burden, and reliance on isolated clinic blood pressure measurements per se does not accurately reflect the total blood pressure burden. This is particularly relevant to the population with chronic kidney disease in whom masked daytime or nocturnal hypertension and blood pressure lability are both widely prevalent and more difficult to control. Consequently, it is possible that the limited success currently being achieved in preventing or attenuating chronic kidney disease progression may be attributable in part to suboptimal 24-hour blood pressure control. Recent data and analyses also indicate that blood pressure variability, instability, episodic and nocturnal blood pressure elevations, and maximum systolic blood pressure may constitute additional strong predictors of the risk of target organ damage independently of mean systolic blood pressure. Accordingly, we suggest that future research should include the development of safe and effective strategies to achieve around-the-clock blood pressure control in addition to targeting mechanisms that reduce intrarenal blood pressure transmission or interrupt subsequent downstream pathways. Meanwhile, more aggressive use of patient education and home blood pressure monitoring with selection of longer-acting antihypertensive agents or nocturnal dosing should be considered to improve the current suboptimal results.