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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

16.9K

Nitric oxide status in patients with chronic kidney disease

Y S Reddy1, V S Kiranmayi2, A R Bitla2

  • 1Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India.

Indian Journal of Nephrology
|December 3, 2015
PubMed

Insights

Chronic kidney disease (CKD) patients exhibit reduced nitric oxide (NO) production and elevated asymmetric dimethyl arginine (ADMA) levels, contributing to endothelial dysfunction. Interventions to boost NO may aid cardiovascular disease management in CKD.

Area of Science:

  • Nephrology
  • Cardiovascular Medicine
  • Biochemistry

Background:

  • Patients with chronic kidney disease (CKD) face elevated risks of cardiovascular disease (CVD) morbidity and mortality, primarily linked to atherosclerosis.
  • Endothelial dysfunction (ED), characterized by reduced nitric oxide (NO) bioavailability, is a key factor in CKD-related CVD.
  • Several mechanisms contribute to a state of NO deficiency in CKD patients.

Purpose of the Study:

  • To investigate the levels of NO precursors and inhibitors in patients across different stages of CKD.
  • To assess the relationship between CKD progression and alterations in NO metabolism.
  • To identify potential therapeutic targets for managing CVD risk in CKD.

Main Methods:

  • Plasma concentrations of nitrites (as a marker of NO), L-arginine, asymmetric dimethyl arginine (ADMA), and citrulline were measured.
  • Subjects were categorized into four groups: healthy controls, CKD stage 1-2 (group-1), CKD stage 3-4 (group-2), and CKD stage 5 (group-3), with 25 subjects per group.
  • Statistical analysis was performed to compare biochemical parameters between groups.

Main Results:

  • All CKD patient groups demonstrated significantly lower NO levels and higher ADMA levels compared to healthy controls.
  • Progressive CKD stages (group-2 and group-3) showed further reductions in NO and increases in ADMA compared to early stages (group-1).
  • While L-arginine levels did not differ between CKD patients and controls, they were lower in stage 5 CKD patients. Citrulline levels were decreased in stage 5 CKD patients.

Conclusions:

  • NO production is impaired across all stages of CKD, potentially due to reduced L-arginine availability or increased inhibition by ADMA.
  • These findings highlight the critical role of NO deficiency and ED in the heightened CVD risk observed in CKD patients.
  • Therapeutic strategies aimed at enhancing NO production, alongside conventional CVD risk factor management, are crucial for improving outcomes in CKD patients.

Keywords:
Asymmetric dimethyl argininechronic kidney diseasecitrullineendothelial dysfunctionnitric oxide

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