Key result
Renin-angiotensin system polymorphisms have not been consistently associated with antihypertensive response, and pharmacogenetic studies focusing on chronic kidney disease protection remain scarce.
Current evidence does not consistently support the use of RAS genetic polymorphisms to predict antihypertensive or renoprotective responses to RAS blockers in patients with hypertension and chronic kidney disease.
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Does not support RAS polymorphism-guided therapy in hypertension with CKD; leaves open targeted pharmacogenetic research on renoprotection.
About 80% of CKD (chronic kidney disease) patients are hypertensive, and kidney function and blood pressure are clearly related to both physiologic and pathologic conditions in a "vicious cycle". In this pathologic scenario, there is a renin-angiotensin system (RAS) hyperactivity associated to progression of renal damage. Current guidelines indicate as the first choice of antihypertensive intervention, the pharmacologic blockade of the RAS. Nonetheless, both response to treatment and renal protection have considerable inter-individual variability. The main aims of this review are to describe the genetic characteristics of RAS components and to identify the possible pharmacogenetic implications for RAS-blocker drugs in the hypertension-CKD scenario. To date, RAS polymorphisms have not been consistently associated to antihypertensive response and studies focusing on CKD are scarce. Nonetheless, pharmacogenetic studies for the RAS-blocker drugs could still be further explored, especially with new generation tools and focusing not only on the antihypertensive response, but also on renal protection as well.
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Santos et al. (2012) conducted a review in Hypertension and Chronic Kidney Disease. RAS-blocker drugs was evaluated. Renin-angiotensin system polymorphisms have not been consistently associated with antihypertensive response, and pharmacogenetic studies focusing on chronic kidney disease protection remain scarce.
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