Role of Antibiotics and Heavy Metals on Kidney Failure

Abstract

Kidney failure is one of the biggest concerns in terms of worldwide healthcare problems, caused by a wide range of clinical and environmental factors. Among the most important factors involving major contributors to renal damage are nephrotoxic antibiotics and exposure to heavy metals. The kidneys are very sensitive to causing toxic damage due to their rich blood supply, aggressive transport systems, and the ability to concentrate xenobiotics in renal tubular cells. Several commonly used antibiotics, like aminoglycosides and vancomycin, have been documented to cause renal impairment by mechanisms involving oxidative stress, mitochondrial dysfunction, inflammation, and tubular cells undergo apoptosis. Like antibiotics, heavy metals, including cadmium and lead, accumulate in renal tissue and impair antioxidant mechanisms, lipid peroxidation, enzyme inhibition, and loss of kidney function. This study aims to examine the biochemical mechanisms of kidney failure caused by both antibiotics & heavy metals individually and combined.  Great emphasis is placed upon analyzing the important biomarkers for renal function, including Serum Creatinine, Urea, and Blood Urea Nitrogen (BUN), and markers of oxidative stress, which include malondialdehyde, glutathione, superoxide dismutase, and catalase. Moreover, the potential protective effects of antioxidant drugs are investigated as a way to lower nephrotoxicity. Understanding the biochemical pathways involved in drug and metal-induced kidney failure may contribute to improving clinical management, using antibiotics in safer ways, and the development of preventive strategies against environmental nephrotoxins.