Which drugs cause crystalline induced nephropathy?
Acute Kidney Injury from drug-induced crystalline nephropathy requires the presence of a significant amount of drug crystal within tubular lumens that favor crystal insolubility in a low urinary flow state.
This is accomplished by supersaturation of constituent molecules, low or high urine pH (depending on the drug), volume depletion, and the absence of urinary inhibitors of crystallization.
Sulfadiazine causes crystalline nephropathy or nephroliths in the setting of hypoalbuminemia, volume depletion, acid urine, and high drug doses. Prevention and/or treatment are directed at correcting hypovolemia and alkalizing the urine.
Acyclovir can precipitate in the setting of hypovolemia, rapid IV bolus administration, and with excessive dosing. IV fluids and slower IV administration are employed to prevent/reduce the occurrence.
IV methotrexate and its metabolites can precipitate within the tubules when given in high doses, with acid urine, and in the setting of hypovolemia.
Prevention includes aggressive alkaline IV fluids and induction of high urine flow rates.
When Acute Kidney Injury develops, in addition to leucovorin rescue, drug removal can be achieved with prolonged high-flux hemodialysis (HD) or drug metabolism with carboxypeptidase G.
