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Assessment of Vascular Function in Patients With Chronic Kidney Disease
08:50

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

Renal microvascular dysfunction, hypertension and CKD progression

Anil K Bidani1, Aaron J Polichnowski, Rodger Loutzenhiser

  • 1Loyola University and Hines VA Hospital, Maywood, Illinois 60153, USA. abidani@lumc.edu

Current Opinion in Nephrology and Hypertension
|November 8, 2012
PubMed

Insights

Optimal 24-hour blood pressure (BP) control is crucial for improving chronic kidney disease (CKD) outcomes by reducing glomerular BP transmission. Further research into autoregulation and nitric oxide pathways may offer additional therapeutic targets for kidney disease.

Area of Science:

  • Nephrology
  • Cardiovascular Medicine
  • Renal Physiology

Background:

  • Suboptimal chronic kidney disease (CKD) outcomes persist despite apparent blood pressure (BP) control and renin-angiotensin system (RAS) blockade.
  • Renal microvascular and autoregulatory impairments contribute to enhanced dynamic glomerular BP transmission in CKD progression.

Purpose of the Study:

  • To review the role of renal microvascular and autoregulatory impairments in CKD progression.
  • To highlight the importance of adequate 24-hour BP control for improving CKD outcomes.

Main Methods:

  • Review of clinical data and accumulated evidence on BP control, autoregulation, and renal injury mechanisms in CKD.
  • Analysis of the role of nitric oxide and angiotensin II in mitigating glomerular hypertension and barotrauma.

Main Results:

  • Inadequate 24-hour BP control is a significant factor in suboptimal CKD outcomes.
  • Preglomerular autoregulatory impairment impacts dynamic glomerular BP transmission, while nitric oxide-mediated efferent vasodilation may mitigate glomerular hypertension.
  • RAS blockade's renoprotection is largely linked to its antihypertensive effectiveness.

Conclusions:

  • Achieving adequate 24-hour BP control is the most practical intervention to reduce glomerular BP transmission and improve CKD outcomes.
  • Future therapeutic strategies may involve enhancing myogenic autoregulation and nitric oxide-mediated efferent dilation.
Abstract

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