Pathological triad of perioperative acute kidney injury: renal microcirculatory hypoxia, mitochondrial damage, and immuno-metabolic reprogramming.

In these patients, initial hemodynamic disturbances may not be significant or have been quickly corrected, but factors such as drug accumulation in renal tubular cells and reperfusion stress lead to particularly prominent ETC inhibition, mtROS burst, and mPTP opening, with ATP depletion and cell death becoming decisive events ( 150 , 151 ).

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