Postconditioning Does Not Improve Renal Function or Attenuate Tubular Damage in Ischemia/Reperfusion-Induced Acute Kidney Injury in Mice

Postconditioning (PostC), a series of brief ischemia/reperfusion (I/R) cycles at reperfusion onset, is a recently described approach to attenuate I/R injury in the heart and brain. Here, we examined its effect on acute kidney injury (AKI) induced by ischemia/reperfusion (I/R) injury in a mouse model. C57/black mice were subjected to right nephrectomy and 26-min left renal artery occlusion, and then divided into three groups: Group I, mice were only reperfused for 48 hr; Group II, mice received PostC that was initiated by three cycles of 30-s ischemia with a 30-s interval immediately after initial ischemia before reperfusion; Group III, mice were reperfused for 10 min after initial ischemia and then received the same regime of PostC prior to reperfusion. At 48 hr after reperfusion, renal function was assessed by measurement of serum creatinine and blood urea nitrogen (BUN), and tubular damage was evaluated by histology. Our results showed that I/R injury led to increased serum creatinine and BUN levels and tubular damage. However, PostC did not improve renal function, or attenuate pathological damage to tubules. These results suggest that PostC does not provide a protective effect on renal injury due to ischemia in C57/black mice with these two protocols.