Amikacin-induced nephrotoxicity is primarily due to its accumulation in the renal proximal tubular cells. Once inside the cells, amikacin can induce oxidative stress and mitochondrial damage, leading to cellular apoptosis or necrosis. This cytotoxicity disrupts the normal functioning of the kidneys and may result in acute kidney injury. Monitoring kidney function through serum creatinine levels and urine output is essential during therapy.
