Nocturnal blood pressure is associated with sympathetic nerve activity in patients with chronic kidney disease.

Abstract

Elevated nocturnal blood pressure (BP) and nocturnal non‐dipping are frequently observed in patients with chronic kidney disease (CKD) and are stronger predictors of cardiovascular complications and CKD progression than standard office BP. The sympathetic nervous system (SNS) is thought to modulate diurnal hemodynamic changes and the vascular endothelium plays a fundamental role in BP regulation. We hypothesized that SNS overactivity and endothelial dysfunction in CKD are linked to elevated nocturnal BP and non‐dipping. In 32 CKD patients with hypertension (56 ± 7 years), office BP, 24‐hr ambulatory BP, muscle sympathetic nerve activity (MSNA) and endothelial function via flow‐mediated dilation (FMD) were measured. Participants were subsequently divided into dippers (nighttime average BP > 10% lower than the daytime average BP, n = 8) and non‐dippers (n = 24). Non‐dippers had higher nighttime BP (p < .05), but not office and daytime BP, compared to dippers. MSNA burst incidence (81 ± 13 versus 67 ± 13 bursts/100 HR, p = .019) was higher and brachial artery FMD (1.7 ± 1.5 versus 4.7 ± 1.9%, p < .001) was lower in non‐dippers compared to dippers. MSNA and FMD each predicted nighttime systolic (β = 0.48,‐0.46, p = .02, 0.07, respectively) and diastolic BP (β = 0.38,‐0.47, p = .04, 0.03, respectively) in multivariate‐adjusted analyses. Our novel findings demonstrate that unfavorable nocturnal BP profiles are associated with elevated SNS activity and endothelial dysfunction in CKD. Specifically, CKD patients with higher nighttime BP and the non‐dipping pattern have higher MSNA and lower FMD. These support our hypothesis that SNS overactivation and endothelial dysfunction are linked to the dysregulation of nighttime BP as well as the magnitude of BP lowering at nighttime in CKD.