Acute kidney injury (AKI), formerly called acute renal failure (ARF), is commonly defined as decline and damage of renal function, with a reversible acute increase in nitrogen waste products—measured by blood urea nitrogen (BUN) and serum creatinine levels over hours to weeks. It’s generally characterized by the risk, injury, failure, loss, and end-stage kidney disease (RIFLE). In last decay, reducing or protecting against its nephrotoxicity has become the most concerning one. This article reviews some of the literature published during the last decade on the effects of agents that ameliorate or augment GM nephrotoxicity. Notable among the ameliorating agents are antioxidant agents. During the last decade, ameliorating nephrotoxicity has gained much effort and attention throughout the world. Most of the ameliorating agents are antioxidant agents, hormones (melatonin), β-blockers (metoprolol), vitamins (Vit. C and E), Superoxide dismutase, Iron chelators (fereptossin), and some medicinal plants (garlic). Other ameliorating agents include antibiotics (e.g. ceftriaxone), antiplatelet drugs (e.g. trapidil), and Ca++. Some agents that may augment nephrotoxicity include cyclosporin and the Ca++-channel blocker (verapamil), antibiotics (Gentamicin), chemotherapeutics (Doxorubicin), PPIs, and NSAIDs. Although these augmenting agents are vital agents for life threatening conditions, so we have to find out the ameliorating agents which may reduce and protect against nephrotoxicity. Various drugs (i.e., cobicistat, trimethoprim, and cimetidine) are potent inhibitors of these transporters, affecting the tubular secretion component of Cr clearance and can increase SCr levels by 0.2–0.4 mg/dL and decrease Cr clearance by 15–34 mL/min. Some antibiotics (piperacillin, tazobactam, and vancomycin) could significantly diminish the number and activity of organic anion transporters (OAT) on the basolateral membranes of proximal tubular cells and cause impaired Cr secretion and increased SCr, with apparent AKI. The risk factors that are included in AKI are prolonged duration of therapy, concomitant nephron-toxin exposure, and a variety of comorbidities.

Abbreviations: AKI (Acute kidney injury), OAT (Organic anion transporter), SCr (Serum Creatinine)