RAS blockade provides much smaller BP-independent renoprotection in chronic kidney disease than what is due to its antihypertensive effects, suggesting its specific benefits are overemphasized.
Does renin-angiotensin system (RAS) blockade provide significant blood pressure-independent renoprotection in patients with chronic kidney disease?
This review suggests that the specific, blood pressure-independent renoprotective benefits of RAS blockade in chronic kidney disease have been greatly overemphasized compared to its primary antihypertensive effects.
Recent guidelines for management of patients with chronic kidney disease recommend both lower optimal BP targets and agents that block the renin-angiotensin system (RAS) for specific additional BP-independent renoprotection. Although there are other compelling rationales to use RAS blockade in patients with chronic kidney disease, including its antihypertensive effectiveness and ability to counteract the adverse effects of diuretics, a critical review of the available scientific evidence suggests that the specificity of renoprotection that is provided by RAS blockade has been greatly overemphasized. Little evidence of truly BP-independent renoprotection is observed in experimental animal models when ambient BP is assessed adequately by chronic continuous BP radiotelemetry. Although the clinical trial evidence is somewhat stronger, nevertheless, even when interpreted favorably, the absolute magnitude of the BP-independent component of the renoprotection that is observed with RAS blockade is much smaller than what is due to its antihypertensive effects.
Griffin et al. (Thu,) conducted a review in Chronic kidney disease. Renin-angiotensin system (RAS) blockade was evaluated on BP-independent renoprotection. RAS blockade provides much smaller BP-independent renoprotection in chronic kidney disease than what is due to its antihypertensive effects, suggesting its specific benefits are overemphasized.
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