What is the Ideal Blood Pressure Goal for Patients with Stage III or Higher Chronic Kidney Disease?

Abstract

Hypertension and chronic kidney disease (CKD) are public health problems well known to the national and international medical communities. Blood pressure (BP) control in patients with CKD stage III and IV plays a key factor in reducing cardiovascular risk and renal disease progression. We conducted a literature review of recent studies addressing BP targets and cardiorenal outcomes in patients with CKD. Multiple studies demonstrated cardiovascular benefits associated with greater BP reduction. Nevertheless, a U-shaped relationship between BP, cardiovascular events, and renal function was present. In patients with CKD stage III and IV, a BP less than 140/90 mm Hg appeared to be a reasonable target. Moreover, in patients with CKD and proteinuria of more than 1 g/day, a target systolic BP of 120 to 130 mm Hg and diastolic BP of 70 to 80 mm Hg yielded the greatest benefit while avoiding most of the adverse cardiovascular outcomes associated with lower levels of BP.

Treatment of Hypertension in Patients With Coronary Artery Disease

“…57 In this patient population, hypertension itself is a leading cause of renal failure. BP goals in patients with CKD and microalbuminuria are lower than in the general population, 22,58 with a target the same as that in patients with established CAD. Recent investigations have demonstrated that standard treatments for cardiovascular risk factors, including statin therapy, ACE inhibitors, ARBs, and antiplatelet agents, are equally effective at risk reduction in patients with CKD (who are not on dialysis) as in those without CKD and should be offered to this patient population.…”

A Call to Action to Develop Integrated Curricula in Cardiorenal Medicine

“…Every CKD and end-stage renal disease (ESRD) patient is almost inevitably a cardiac patient with several issues to be considered [36]. From the point of view of the kidneys, the main task is the reduction of CKD progression through the control of intraglomerular hemodynamics and hyperfiltration, the limitation of protein and salt intake, neurohormonal modulation, and control of blood pressure [37]. Recent evidence has pointed out that chronic inflammation, anemia, and metabolic alterations typical of uremia (e.g., hyperuricemia) [38,39] even at its early stages may influence the rate of vascular calcification, myocardial fibrosis, aortic and mitral calcification, and the propensity for atrial and ventricular arrhythmias [40,41].…”