Sympathetic activity in chronic kidney disease patients is related to left ventricular mass despite antihypertensive

Laima Siddiqi1, Niek H Prakken, Birgitta K Velthuis

  • 1Department of Nephrology and Hypertension, University Medical Center Utrecht, The Netherlands.

Insights

Chronic kidney disease patients show increased left ventricular mass despite controlled blood pressure. Muscle sympathetic nerve activity predicts this cardiac damage, suggesting additional sympatholytic therapy may be beneficial.

Area of Science:

  • Nephrology
  • Cardiology
  • Hypertension

Background:

  • Chronic kidney disease (CKD) is associated with sympathetic hyperactivity, contributing to hypertension and cardiovascular damage.
  • Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) can reduce sympathetic activity.
  • The relationship between sympathetic activity and organ damage in CKD requires further investigation.

Purpose of the Study:

  • To compare left ventricular mass (LVM) in CKD patients treated with ACEi or ARBs versus controls.
  • To determine if muscle sympathetic nerve activity (MSNA) and blood pressure predict increased LVM in CKD patients.

Main Methods:

  • Restudied 20 CKD patients and 30 age-matched healthy controls.
  • Quantified MSNA using microneurography.
  • Measured LVM using contrast-free magnetic resonance imaging (MRI).

Main Results:

  • CKD patients exhibited significantly greater LVM, LVM index, and mean wall thickness than controls (P < 0.01).
  • MSNA was positively correlated with LVM (r=0.65), LVM index (r=0.46), and LV mean wall thickness (r=0.84) (P < 0.03).
  • These associations persisted despite guideline-adherent ACEi/ARB treatment and controlled blood pressure.

Conclusions:

  • CKD patients have increased LVM compared to controls, even with controlled blood pressure.
  • Pre-existing MSNA predicts increased LVM in CKD patients, independent of standard antihypertensive treatment.
  • Additional sympatholytic therapy may be beneficial for managing cardiovascular organ damage in CKD.
Abstract

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