Journal of Clinical Oncology, Vol 8, 1839-1846, Copyright © 1990 by American Society of Clinical Oncology
Acute renal dysfunction during interleukin-2 treatment: suggestion of an intrinsic renal lesion
CL Shalmi, JP Dutcher, DA Feinfeld, KJ Chun, KR Saleemi, LM Freeman, RI Lynn and PH Wiernik
Department of Oncology, Albert Einstein Cancer Center/Montefiore Medical Center, Bronx, NY 10467-2490.
Adoptive immunotherapy with interleukin-2 (IL-2) and lymphokine- activated
killer (LAK) cells has been effective in treating some advanced
malignancies in animals and humans. One complication of this treatment is a
reversible, oliguric, acute renal failure, which has been ascribed to renal
hypoperfusion and resultant prerenal azotemia. We serially studied renal
function in 10 patients receiving high-dose regimens of recombinant
interleukin-2 (rIL-2) to attempt to delineate further the nature of the
renal dysfunction caused by IL-2 treatment. Renal plasma flow was computed
from iodine 131 (I-131 Hippuran; Mediphysics, Paramus, NJ)
orthoiodohippurate, excretion curves, and glomerular filtration rate (GFR)
was determined by creatinine clearance. Studies done prior to and on day 4
of treatment showed that GFR fell in nine of 10 patients, with a mean
decrease of 43% +/- 8%, and renal plasma flow fell in five of the 10
patients with a mean decrease of 5% +/- 10%. The average pretherapy
filtration fraction was calculated to be 23% +/- 1% and after 4 days of
treatment, decreased to a mean value of 15 +/- 2%. The BUN to creatinine
ratio also declined in all patients. These findings collectively suggest
that IL-2 nephrotoxicity may result from an intrarenal defect in addition
to the previously described prerenal azotemia. Additionally, radionuclide
studies of renal function are a reliable and reproducible noninvasive
method of assessing these changes in renal function.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Facebook 
Reddit 
Technorati 
Twitter What's this?
