Nephrotoxin

Nephrotoxin refers to any substance capable of causing damage to the kidneys. Nephrotoxicity may manifest as acute kidney injury (AKI) or contribute to chronic kidney disease with chronic exposure. Mechanisms include direct injury to tubular epithelial cells, glomerular injury, interstitial inflammation, and ischemia from reduced renal perfusion. Proximal tubule cells are particularly susceptible; injury can lead to cellular necrosis and tubular obstruction, while glomerular and interstitial processes may disrupt filtration and reabsorption. Oxidative stress, inflammation, and altered renal hemodynamics commonly participate in these injuries.

Common nephrotoxins include certain medications—aminoglycoside antibiotics (for example, gentamicin), platinum-based chemotherapeutics (such as cisplatin), nonsteroidal anti-inflammatory drugs, amphotericin B, and calcineurin inhibitors—radiographic contrast agents, heavy metals (lead, cadmium, mercury), organic solvents such as ethylene glycol, and plant-derived toxins including aristolochic acid.

Clinical features depend on exposure and dose and may appear days to weeks after exposure. AKI is characterized by rising serum creatinine and reduced urine output; urinalysis can show tubular casts or eosinophils in interstitial nephritis. Diagnosis relies on history of exposure, laboratory testing, and exclusion of other causes.

Prevention focuses on avoiding nephrotoxins when possible, ensuring adequate hydration, and adjusting drug doses in impaired kidney function. Management consists of stopping the offending agent, providing supportive care, correcting electrolyte disturbances, and, if necessary, renal replacement therapy. Risk factors include preexisting kidney disease, advanced age, dehydration, and concomitant nephrotoxins.