We used the qualitative Hanssen technique in albino rats to seek morphologic demonstration of tubular obstruction in two types of acute renal failure: one induced by folic acid and another by methemoglobin.
Solution hybridization RNAase protection assays showed that renal IGF-1 mRNA, IGF-1 receptor (IGF-1R) mRNA, and IGF-binding protein-1 (IGFBP-1) mRNA were unaffected by exogenous IGF-1, but this treatment significantly increased renal IGF-1 in ARF rats compared with normal rats and ARF rats not receiving IGF-1.
Thus, (1) IGF-1 enhances recovery from nephrotoxic ARF both functionally and histologically; (2) in nephrotoxic ARF, there is (a) a reduction in IGF-1 mRNA expression that is not prevented by IGF-1 infusion, and (b) an increase in renal IGFBP-1 mRNA.
Further studies to determine the role of IGF-I as a therapeutic agent for acute renal failure and its utility as a medical therapy for chronic renal insufficiency are required.
These findings indicate that ET-1 participates in the pathogenesis of acute tubular injury in glycerol-induced ARF and that ETA antagonist may be useful in the treatment of some types of human ARF.
Exogenous administration of some growth factors, such as IGF-I, EGF and HGF, accelerates recovery of renal function in experimental acute renal failure (ARF).
Altered expression of endothelin-1 and endothelial nitric oxide synthase in the juxtaglomerular apparatus of rats with HgCl2-induced acute renal failure.