[Replacing calcineurin inhibitors with proliferation signal inhibitors after kidney transplantation: indications, results, and disadvantages]

Abstract

In the kidney transplant patient, calcineurin inhibitor (CNI) treatment is a major risk factor for chronic allograft nephropathy (CAN). Immunosuppressive strategies based on non-nephrotoxic drugs such as proliferation signal inhibitors (PSIs) have been conceived to reduce or even interrupt CNIs. CNI conversion, with progressive cessation over 3 months with a PSI can significantly improve renal function, notably if the patient presents proteinuria less than 0.8 g/day and if conversion is undertaken early, when the glomerular filtration rate (GFR) is 40 ml/min or greater. In these conditions GRF improvement is associated with a histological CADI score and chronic lesion markers. Nevertheless, replacing CNIs with a PSI can occasionally induce proteinuria that is potentially related to direct toxicity of the PSI on the podocytes, which must be monitored to prevent recurrence of nephrotoxicity lesions.