Key result
The use of ACE inhibitors was protective against genetically-mediated creatinine variations independent of blood pressure changes in older patients with Alzheimer disease.
Why the study?
Does the use of ACEis and specific ACE genotypes affect yearly variations in urea and creatinine in older patients with Alzheimer disease?
Cohort (n=190)
Does the use of ACEis and specific ACE genotypes affect yearly variations in urea and creatinine in older patients with Alzheimer disease?
The effects of ACE inhibitors on creatinine variations in older patients with Alzheimer disease are genetically mediated and independent of blood pressure variations.
ACEi use may protect against genetically mediated creatinine changes in AD; leaves open outcome impact and need for prospective validation.
BACKGROUND: Renal function declines according to age and vascular risk factors, whereas few data are available regarding genetically-mediated effects of anti-hypertensives over renal function. OBJECTIVE: To estimate urea and creatinine variations in dementia due to Alzheimer disease (AD) by way of a pharmacogenetic analysis of the anti-hypertensive effects of angiotensin-converting enzyme inhibitors (ACEis). METHODS: Consecutive outpatients older than 60 years-old with AD and no history of kidney transplant or dialytic therapy were recruited for prospective correlations regarding variations in fasting blood levels of urea and creatinine in one year, considering ACE genotypes of rs1800764 and rs4291 and their respective haplotypes, and treatment with ACEis along with blood pressure variations. RESULTS: For 190 patients, 152 had arterial hypertension, and 122 used ACEis. Minor allele frequencies were 0.492 for rs1800764-C and 0.337 for rs4291-T, both in Hardy-Weinberg equilibrium. There were no overall significant yearly variations in levels of urea and creatinine, but their concurrent variations were positively correlated (ρ <0.0001). Each A allele of rs4291 led to an yearly urea increase of 3,074 mg/dL, and an yearly creatinine increase of 0.044 mg/dL, while the use of ACEis was protective regarding creatinine variations. The use of ACEis was also protective for carriers of rs1800764-CT/rs4291-AA, while carriers of rs1800764-CT/rs4291-AT had steeper reductions in creatinine levels, particularly when they were treated with ACEis. CONCLUSIONS: Effects of ACEis over creatinine variations are genetically mediated and independent of blood pressure variations in older people with AD.
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Oliveira et al. (2016) conducted a cohort in Dementia due to Alzheimer disease (AD) (n=190). Angiotensin-converting enzyme inhibitors (ACEis) vs. No ACEis was evaluated on Yearly variations in fasting blood levels of urea and creatinine. The use of ACE inhibitors was protective against genetically-mediated creatinine variations independent of blood pressure changes in older patients with Alzheimer disease.
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