Key result
Modulating opposing renin-angiotensin axes protects against renal ischemia-reperfusion injury.
Why the study?
Renal ischemia-reperfusion injury is the leading cause of acute kidney injury, and the renin-angiotensin system plays an important role through alterations in its conventional and nonconventional axes.
This review summarizes the complex interactions and effects of the renin-angiotensin system axes in the pathogenesis of acute kidney injury following renal ischemia-reperfusion.
May support RAS modulation for renoprotection in renal IRI; hypothesis-generating and requires clinical trials before practice change.
Renal ischemia-reperfusion injury (RIRI) is a sequence of complicated events that is defined as a reduction of the blood supply followed by reperfusion. RIRI is the leading cause of acute kidney injury (AKI). Among the diverse mediators that take part in RIRI-induced AKI, the renin-angiotensin system (RAS) plays an important role via conventional (angiotensinogen, renin, angiotensin-converting enzyme (ACE), angiotensin (Ang) II, and Ang II type 1 receptor (AT 1 R)) and nonconventional (ACE2, Ang 1-7, Ang 1-9, AT 2 receptor (AT 2 R), and Mas receptor (MasR)) axes. RIRI alters the balance of both axes so that RAS can affect RIRI-induced AKI. In overall, the alteration of Ang II/AT 1 R and AKI by RIRI is important to consider. This review has looked for the effects and interactions of RAS activities during RIRI conditions.
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Karimi et al. (2022) conducted a review in Acute Kidney Injury (AKI) induced by Renal Ischemia-Reperfusion Injury (RIRI). Renin-Angiotensin System (RAS) modulators was evaluated. Modulation of the renin-angiotensin system plays a critical role in renal ischemia-reperfusion injury, where inhibiting the conventional axis and activating the nonconventional axis offer renoprotection.
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