Key result
The angiotensin converting enzyme II genotype was independently associated with an increased risk of acute kidney injury in critically ill patients (adjusted OR 6.5; 95% CI 2.4-17.7; p=0.0002).
Why the study?
Does the II genotype of the ACE genetic polymorphism increase the risk of acute kidney injury in critically ill white patients?
Observational (n=180)
No
Does the II genotype of the ACE genetic polymorphism increase the risk of acute kidney injury in critically ill white patients?
Odds Ratio: 6.5 (95% CI 2.4–17.7)
p-value: p=0.0002
The II genotype of the ACE genetic polymorphism is independently associated with an increased risk of acute kidney injury and subsequent mortality in critically ill white patients.
ACE II genotype was associated with higher AKI risk; hypothesis-generating and should not yet change practice in critically ill patients.
OBJECTIVE: Previous clinical studies have suggested an association between the insertion/deletion (I/D) genetic polymorphism of angiotensin converting enzyme and acute or chronic diseases. We aimed to test the prognostic value of the I-allele, which is associated with lower angiotensin converting enzyme activity, on acute kidney injury. DESIGN: Prospective 6-month noninterventional study. SETTING: Intensive care unit of a University Hospital. PATIENTS AND METHODS: One hundred eighty consecutive admitted white patients for an expected intensive care unit stay >48 hr. Angiotensin converting enzyme genetic polymorphism was screened for genotype (I/D polymorphism analysis by polymerase chain reaction amplification) and phenotype (measurement of the circulating rate of angiotensin converting enzyme by spectrophotometry). Acute kidney injury was assessed according to Risk, Injury, Failure, Loss, and End-stage Kidney classification. INTERVENTION: None. RESULTS: II, ID, and DD genotype frequencies were 25%, 48%, and 27%, respectively. II and ID genotypes were associated with lower baseline circulating rates of angiotensin converting enzyme (20 +/- 14 and 22 +/- 18 U/L, respectively, vs. 30 +/- 23 U/L for DD genotype; p = 0.04). Repartition of angiotensin converting enzyme genotypes were different in patients with and without acute kidney injury (p < 0.0001), with greater II genotype proportion in acute kidney injury patients (42% vs. 13% for those without acute kidney injury). After adjustment on the identified prognostic factors, II genotype was independently associated with increased risk of acute kidney injury (adjusted odds ratio, 6.5; 95% confidence interval, 2.4-17.7; p = 0.0002), then death among patients with acute kidney injury (adjusted odds ratio, 1.7; 95% confidence ratio, 1.1-2.6; p = 0.02). CONCLUSION: These data confirm the key role of the renin-angiotensin system to maintain glomerular filtration rate, and highlight an association between a genetic factor and susceptibility to and prognosis of acute kidney disease.
No takes yet. Share an insight, caveat, or question.
Cheyron et al. (2008) conducted an observational in Critically ill patients (n=180). Angiotensin converting enzyme II genotype vs. ID and DD genotypes was evaluated on Acute kidney injury (adjusted OR 6.5, 95% CI 2.4-17.7, p=0.0002). The angiotensin converting enzyme II genotype was independently associated with an increased risk of acute kidney injury in critically ill patients (adjusted OR 6.5; 95% CI 2.4-17.7; p=0.0002).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: