The renin-angiotensin system: a potential therapeutic target in ARDS? | Thorax

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The renin-angiotensin system: a potential therapeutic target in ARDS?

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ARDS risk and ACE polymorphism
Prasanta Padhan
Published on: 29 April 2016

Published on: 29 April 2016
ARDS risk and ACE polymorphism
- Prasanta Padhan, MD, Sr in Internal Medicine
Dear Editor,
ARDS remains a major cause of death, yet factors contributing to the syndrome have not yet been clearly identified. During its early stages, ARDS may include high-permeability pulmonary edema, loss of alveolar epithelial cells and neutrophil infiltration which may lead to remodelling of the alveoli and interstitium. Experimental findings suggested that activation of a renin-angiotensin system in the l...
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Dear Editor,
ARDS remains a major cause of death, yet factors contributing to the syndrome have not yet been clearly identified. During its early stages, ARDS may include high-permeability pulmonary edema, loss of alveolar epithelial cells and neutrophil infiltration which may lead to remodelling of the alveoli and interstitium. Experimental findings suggested that activation of a renin-angiotensin system in the lung could mediate changes in vascular tone and permeability, fibroblast activity, and epithelial cell survival.
Thus, variations in the renin-angiotensin system could be crucial in ARDS aetiology. Furthermore, ARDS patients show increased pulmonary ACE activity. Because genotypic differences can account for 45% of the variance in plasma ACE activity, Richard P. Marshall et al. from the Centre for Respiratory Research at Rayne Institute in London sought to relate ACE genotype with ARDS incidence and outcome. Frequencies of the D allele and of the DD genotype were significantly higher among ARDS patients than among non-ARDS patients. In comparison, the II genotype was markedly rare among ARDS patients; all patients had similar frequencies of the ID genotype. Mortality was also increased among patients within the ARDS group who had two D alleles i.e. with DD genotype.[1]
ACE’s putative role in ARDS aetiology supports the notion that inhibitors of ACE activity might effectively reduce the propensity of individuals with a DD genotype to develop ARDS. Thus, genotyping could reveal a subpopulation who might particularly benefit from therapy with ACE inhibitors—either as prophylaxis in healthy individuals who are homozygous for the D allele or to improve outcome in a genetic subpopulation of patients with lung disease.
References
1. Marshall RP, Webb S, Bellingan GJ, et al.Angiotensin converting enzyme insertion/deletion polymorphism is associated with susceptibility and outcome in acute respiratory distress syndrome.Am J Respir Crit Care Med. 2002;166:646-650.
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Conflict of Interest:
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