[Kidney transplant failure and retransplantation.]. / Fallimento di trapianto renale, rientro in dialisi e retrapianto.

Transplant failure is a more and more frequent cause of end stage renal failure and dialysis. Patient survival rate after graft failure is very varied according to different reports. Better survival is mainly a consequence of good continuum of care thanks to improved interaction between dialysis and transplant center. Diabetic and elderly patients, as well as patients affected by cardiovascular disease are the subjects at higher risk: if judged clinically adequate to enter the waiting list, they should be retransplanted as soon as possible. Dialysis survival of patients with failed kidney transplant is strictly linked to adequate dialysis dose. Second transplant survival rate is higher in the case of a living donor and if the first transplant survived longer. Good immunologic match is also a condition linked to higher graft and patient survival rate. High body mass index, smoking and severe cardiovascular comorbidity should be avoided. Whether to keep low immunosuppression levels after first graft failure and whether to excise the failed kidney, even though it shows no clinical problems, are issues still under debate. Low-dose immunosuppression is not recommended since it may result in higher rate of infectious and neoplastic diseases. The failed kidney should be removed not only in the case of clinical disease, but also when the retained failed kidney is associated with chronic inflammation, as shown by high C-reactive protein levels and erythropoietin resistance.

Immunosuppression in renal transplantation: viral diseases and chronic allograft nephropathy.

Chronic allograft dysfunction after renal transplantation can be ascribed to different causes, among which are viral infections. The aim of this work was to show the various ways by which different kinds of viruses affect transplant structure and function. Polyoma virus is an example of viruses directly affecting the kidney because of a specific tropism to the uroepitelial cells. Cytomegalovirus (CMV) has been chosen both because of the frequency of this infection and because CMV (as other viruses) can produce transplant vascular sclerosis. Finally, we describe hepatitis C virus (HCV) because of its capacity to induce renal lesions independently from chronic allograft nephropathy. Indeed HCV is likely to determine immunologically mediated nephritis in the transplanted kidney as well in the native one.