Acute renal dysfunction during interleukin-2 treatment: Suggestion of an intrinsic renal lesion

Craig L. Shalmi, Janice P. Dutcher, Donald A. Feinfeld, K. J. Chun, Khalid R. Saleemi, Leonard M. Freeman, Robert I. Lynn, Peter H. Wiernik

Research output: Contribution to journalArticlepeer-review

39 Scopus citations


Adoptive immunotherapy with interleukin-2 (IL-2) and lymphokine-acrivared 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.

Original languageEnglish (US)
Pages (from-to)1839-1846
Number of pages8
JournalJournal of Clinical Oncology
Issue number11
StatePublished - Nov 1990
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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