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Abstract . In agreement with recent studies showing a deleterious  effect of growth hormone treatment in critically ill patients, preliminary  data showed that insulin-like growth factor I (IGF-I) administration increased  the mortality rate of rats with ischemic acute renal failure (ARF). The  present study was designed to investigate the mechanism responsible for this  unexpected effect. Male rats with ischemic ARF were given subcutaneous IGF-I,  50 μg/100 g at 0, 8, and 16 h after reperfusion (ARF+IGF-I,  n  = 5)  or were untreated (ARF,  n  = 5). A group of 5 sham-operated rats were  used as controls. Rats were killed 48 h after declamping, and the following  studies were performed: in serum, creatinine and urea nitrogen; and in  kidneys, histologic damage score, cellular proliferation by bromodeoxyuridine  labeling, apoptosis by morphologic criteria, macrophage infiltration by  immunohistochemistry using a specific antibody against ED-1, neutrophil  infiltration by naphthol AS-D chloroacetate esterase staining, and levels of  IGF-I and IGF-I receptor mRNA by RNase protection assay. ARF and ARF+IGF-I  groups had a severe and similar degree of renal failure. Kidney damage was  histologically more evident in ARF+IGF-I (1.9 ± 0.1) than in ARF (1.3  ± 0.2) rats, and the number of neutrophils/mm 2  of tissue was  significantly greater in ARF+IGF-I than in ARF rats at the corticomedullary  junction (52.3 ± 5.2  versus  37.2 ± 4.1) as well as at  the renal medulla (172.5 ± 30.0  versus  42.1 ± 9.6). No  other differences between the groups were found. It is concluded that IGF-I  treatment enhanced the inflammatory response in rats with ischemic ARF. Cell  toxicity derived from increased neutrophil accumulation might play a key role  in the greater mortality risk of critically ill patients that are treated with  growth hormone.

Exacerbated Inflammatory Response Induced by Insulin-Like Growth Factor I Treatment in Rats with Ischemic Acute Renal Failure