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however, this response was blunted compared to normal subjects, despite higher plasma IGF-1 concentrations, indicating partial resistance in advanced CKD.67 This reduced response is likely due to a decrease in the distribution and shortened half-life of the IGF-1 in dialysis patients.68 Furthermore, resistance to the GH-mediated bioactive IGF-1 stimulation has been demonstrated in non-diabetic hemodialysis patients, suggesting the presence of additional inhibitory mechanisms.69 In predialysis patients, increased production of IGFBPs has been observed, which may bind free IGF-1 and contribute to the attenuation of its renal effects.70 Therefore, as previously mentioned, elevated levels of renal IGFBPs in conditions of renal insufficiency may act as inhibitors of IGF-1 contributing to resistance in the proximal tubular cells.4 On the other hand, the renal anabolic actions of IGF-1 can be detrimental in the context of polycystic kidney disease (PKD), as it promotes renal cell proliferation and kidney enlargement
To measure the cytotoxicity, CellTox Green assay (#G8741, Promega) was used
Rarely, rashes or skin reactions have been reported
Journal of Thoracic Diseases 16(9):6339-6341, 2024
