The Role of Systemic Blood Pressure in the Progression of Chronic Kidney Disease

Abstract

Chronic kidney disease (CKD) regardless of etiology tends to progress. Substantial evidence indicates that even modest coexistent hypertension (HTN) plays a major role in such progression due to an increased transmission of systemic HTN to the renal microvasculature in CKD states. This is due to preglomerular vasodilation and an impairment of the renal autoregulatory responses that normally protect against such transmission. Accordingly, effective BP control that also includes renin-angiotensin system (RAS) blockade is recommended as a primary management strategy for slowing CKD progression. It is widely believed that RAS blockade provides additional renoprotection beyond BP lowering. While the BP-independence of such renoprotective effects remains a matter of some controversy, there is nevertheless other compelling rationale for the use of RAS blockade in CKD patients. Hypertension in CKD states is usually volume dependent and requires effective diuretic therapy for adequate and sustained BP control. Not only is RAS blockade a very effective antihypertensive regimen in adequately diuresed patients, it counteracts the negative effects of diuretics on potassium and magnesium balance. Although definitive clinical trial evidence in favor of lower BP goals in proteinuric CKD is not yet available, some guidelines also recommend a lower systolic BP target of <130 mmHg for proteinuric CKD vs. <140 mmHg that is recommended for most individuals including those with non-proteinuric CKD. Finally, given that ambulatory blood pressure monitoring (ABPM) has shown that masked and nocturnal HTN may be both more frequent and more difficult to control in CKD patients, it may be as important to focus on achieving 24-h BP control as on the clinic BP targets.