The Role of N-Acetylcysteine (NAC) in Renal Ischemia-Reperfusion Injury
Abstract
Background: Ischemia-reperfusion (IR) injury is a pathological process that exacerbates tissue damage upon the restoration of blood flow after ischemia. In the kidneys, IR injury can lead to acute tubular necrosis, endothelial dysfunction, and progressive renal impairment. N-acetylcysteine (NAC), a thiol-containing compound and precursor to glutathione, has shown promise as a nephroprotective agent due to its antioxidant and anti-inflammatory properties.
Methods: This review synthesizes findings from experimental studies and clinical trials investigating the effects of NAC in renal IR injury. A literature search was conducted across databases such as PubMed and ScienceDirect, focusing on studies that evaluated renal function markers, oxidative stress parameters, histopathological changes, and clinical outcomes following NAC administration.
Results: Animal studies demonstrate that NAC improves renal perfusion, reduces oxidative stress (e.g., lower MDA, MPO), and enhances antioxidant defenses (e.g., GSH, SOD, CAT). Histopathological evaluation revealed less tubular necrosis and interstitial damage in NAC-treated groups. Clinical trials in renal transplant recipients indicate a potential benefit in reducing early graft dysfunction and biomarkers of tubular injury, although findings remain inconsistent. Notably, prolonged use of NAC in chronic ischemic settings may alter redox homeostasis unfavorably, potentially worsening outcomes.
Conclusion: NAC exhibits beneficial effects in mitigating renal damage from acute ischemia-reperfusion injury via its antioxidant and anti-inflammatory actions. However, its long-term use in chronic or prolonged ischemia remains controversial and requires further investigation to clarify its therapeutic window and clinical applicability.
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