Author(s): Cruzado JM, Rico J, Griny JM
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Abstract Besides the immunological mediated damage on the graft, the intrarenal renin-angiotensin system (RAS) is viewed as an additional mechanism in the development and progression of chronic allograft injury. RAS blocking agents efficiently control post-transplant hypertension and are useful to reduce proteinuria and for treating post-transplant erythrocytosis. However, RAS blockade is associated with some potentially relevant adverse events as hyperkalemia, anemia, and even to a decline in renal function. There are consistent experimental data showing that RAS blockade has a therapeutic effect on chronic allograft injury. Some clinical studies have shown that RAS blockade reduces transforming growth factor-beta1 and other markers of fibrosis but, up to now, there is not convincing evidence supporting that RAS blockade has further benefit on the progression of chronic allograft injury in comparison with other antihypertensive interventions. Theoretically, RAS blockade may also improve cardiovascular disease, which constitutes the main cause of mortality and morbidity in renal allograft recipients. Nevertheless, to date there is lack of evidence for supporting that RAS blockade improves neither graft nor patient survival in comparison with other antihypertensive drugs. Randomized, prospective, double blind, placebo-controlled trials with enough sample size and follow-up are needed to address the potential role of RAS blockade to improve graft and patient outcome. Meanwhile, we should empirically balance case to case the pros and cons of RAS blockade in renal transplantation.
This article was published in Transpl Int
and referenced in Journal of Nephrology & Therapeutics