Nephrotoxicity

Nephrotoxicity is kidney injury caused by exposure to a drug or other harmful substance. It can impair filtration, tubular function, or blood flow within the kidneys.

Acute tubular injury: Kidney damage involving tubular epithelial cells, often caused by ischemia or toxic exposure. Many nephrotoxic substances directly injure tubular cells, disrupting reabsorption and filtration.
Nephrotoxic drug: A medication capable of causing kidney injury under particular conditions or doses. Medication exposure is a major, potentially preventable source of nephrotoxicity.
Glomerular filtration rate: The volume of fluid filtered by kidney glomeruli per unit time. A fall in filtration is a central functional consequence of many nephrotoxic injuries.
Drug-induced kidney disease: Kidney disorders caused by medications through toxic, immune, or altered-hemodynamic effects. This clinical category includes nephrotoxicity alongside medication-related kidney effects.
Acute interstitial nephritis: Inflammation of kidney interstitial tissue and tubules, commonly triggered by medications. Some drugs provoke immune-mediated inflammation rather than direct tubular toxicity.
Aminoglycoside: An antibiotic class that includes gentamicin and can injure renal tubules. Aminoglycosides accumulate in tubular cells, making exposure duration and dose relevant.
Serum creatinine: A blood measurement of creatinine used to estimate kidney filtration. Creatinine trends help detect and stage functional decline after a toxic exposure.
Electrolyte disorder: An abnormal concentration of electrically charged minerals in body fluids. Tubular injury can disrupt electrolyte reabsorption and secretion.
Glomerular disease: A group of disorders that damage the kidney's filtering units, the glomeruli. Toxic exposures can injure glomeruli and alter the selective filtration of blood.
Cisplatin: A platinum-based chemotherapy drug that can cause dose-related kidney injury. Its tubular toxicity is a major limit on treatment dosing.

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