Acute changes in renal function associated with deferoxamine therapy
G. Koren, Y. Bentur, D. Strong, E. Harvey, J. Klein, R. Baumal, S. P. Spielberg and M. H. Freedman
Division of Clinical Pharmacology, Hospital for Sick Children, Toronto, Ontario, Canada.
In three patients who received intravenous deferoxamine there was a twofold
to eightfold increase in plasma creatinine level and a parallel decrease in
creatinine clearance that resolved when treatment with the drug was
discontinued. In two thalassemic patients, diuresis was evident by urine
output exceeding fluid intake. The mechanism was studied in dogs that
exhibited an acute and significant decrease in inulin and
para-aminohippuric acid clearances induced by intravenous deferoxamine.
Saline diuresis could prevent the decrease in the glomerular filtration
rate but not the decrease in renal blood flow caused by deferoxamine.
Deferoxamine induced an acute increase in the fractional excretion of
sodium, potassium, chloride, phosphate, and urate, which may explain the
relative diuresis observed in two of the patients. In a subsequent
experiment, ferrioxamine induced an increase in the fractional excretion of
sodium and chloride but did not affect the glomerular filtration rate and
renal blood flow. Our studies suggest that adequate hydration may be needed
to preserve renal hemodynamics during intravenous deferoxamine therapy.
Repeated measurements of renal function should accompany treatment with
this agent.
