Abstract
Acute kidney injury (AKI) is characterized by a sudden rise in serum creatinine levels, a reduction in urine output, or both. Despite its frequent occurrence in clinical settings, AKI remains poorly understood from a pathophysiological standpoint. As a result, management primarily relies on supportive care rather than targeted treatments. Emerging evidence underscores the pivotal role of oxidative stress in both the initiation and progression of AKI, thereby identifying it as a potential therapeutic target. This review aims to comprehensively examine the pharmacological effects and underlying mechanisms of apocynin (APO) in the context of AKI, with a particular focus on ischemia-reperfusion injury (IRI) and nephrotoxic-induced AKI. Experimental preclinical studies have consistently demonstrated that APO offers protective effects primarily through its inhibition of NADPH oxidase-mediated oxidative stress. In renal IRI and drug-induced nephrotoxicity models, APO has been shown to attenuate oxidative damage, reduce inflammatory responses, and preserve renal structure and function. These results suggest that it may serve as an effective treatment for reducing kidney damage caused by acute ischemia or exposure to nephrotoxic agents. Although the results are encouraging, further investigation is required to establish the optimal dosing strategy and treatment protocol, as well as to confirm the translational relevance of these findings in human clinical settings.