We propose that MRB, administered 24 h after the ischemic injury that leads to AKI, reduces inflammation and promotes efficient tissue repair that avoids the AKI to CKD transition. These data highlight a therapeutic window to preclude CKD development after AKI.

No abstract

Recently, we showed that CKD induced by an AKI episode in the rat is associated with podocyte injury and aberrant tubular epithelium proliferation. This study was designed to evaluate the temporal influence of oxidative stress in this model of renal injury. Forty‐seven Wistar male rats that were divided into two groups: sham operated (S) and rats underwent to renal bilateral ischemia for 45 minutes (I). The animals were followed since 1 to 4 months after ischemia and at least six rats were studied and sacrificed each 30 days. At the end of each experimental period, mean arterial pressure (MAP), renal blood flow (RBF) and creatinine clearance (CCr), as well as, urinary protein (UProt) and peroxide excretion (UH2O2) were measured. Rats underwent to ischemia exhibited a significant increase in UProt that returned to normal values after 1 month, then, a progressive increment was observed, reaching a significant difference after 4 months. In spite of the absence in MAP or renal function alterations a significant increase in UH2O2 was observed since 24‐h after ischemia and the values did not return to basal level along the study. Our results suggest that oxidative stress contributes to renal progression injury since a very early stage and pointed out the importance of studying the effect of anti‐oxidants just when ischemic insult has happened and determining their impact in the progression to CKD. Grant Funding Source: National council of science and technology of Mexico. grant to NAB 181267