Acute kidney injury (AKI) accelerates CKD progression that leads to end-stage renal disease (ESRD) through cell death, endothelial dysfunction, inflammation, and fibrosis [1]
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These findings, along with the fact that the lung can normally maintain GSH for long periods even with the oxidant burden of CS, lend credence to the theory that disease symptoms could arise when adaptive responses fail or are dysfunctional
