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Diabetes mellitus is one of the major causes of end stage renal disease. After 10-15 years from the onset 30% of diabetic patients present nephropathy, and once haemodialysis is required, morbidity is particularly high and long-term survival is lower than in non-diabetic patients. Currently, it is demonstrated that simultaneous pancreas-kidney transplantation (SPK) shows beneficial effects on patient survival, on some diabetic degenerative complications and on the quality of life. Aim of the work is to report our experience in pancreas transplantation.From June 1998 to June 2005 17 type I diabetic uremic patients underwent SPK. Donor selection considered hemodynamically stable young patients without cardiac arrest or vasopressor drug excess and with a brief Intensive Care Unit hospitalization. Average donor age was 26 years (range 16-38). The cause of death was trauma for 14 donors (82.4%) and spontaneous cerebral hemorrhage for 3 donors (17.6%). Average pancreas cold ischemic time was 716 minutes (range 320-968).No patient mortality was observed. No primary or delayed graft function was observed both for pancreas and kidney. Biopsy proved the occurrence of acute rejection episode in one patient (5.8%). Five surgical (29.4%) and 2 medical (11.7%) complications developed. At a median follow-up of 36.4 months (range 4.2-88) patient survival rate was 100%. Pancreas and kidney graft survival rate was 76.5% and 94.1%, respectively. All patients referred an improvement in their quality of life.SPK represents a well-established therapy for uremic type I diabetes mellitus since it improves patient survival in selected recipients. Our experience, as reported in literature, confirm that a successful pancreas transplantation not only brings the recipient back to normal glycemic levels, but it also improves the patient's quality of life by stabilizing some of the secondary complications of diabetes.

The most frequent renal involvement in patients with chronic hepatitis C virus (HCV) infection is cryoglobulinemic glomerulonephritis, with type I membranoproliferative glomerulonephritis (MPGN) being the predominant histological pattern. The pathogenesis of HCV-related cryoglobulinemic MPGN is unknown, but the glomerular damage may be due to the deposition of immune complexes of HCV, IgG, and IgM rheumatoid factors. Clinically, cryoglobulinemic MPGN may range from isolated proteinuria to overt nephritic or nephrotic syndrome, with variable progression to chronic renal insufficiency. The management of cryoglobulinemic MPGN is difficult; the eradication of HCV by means of antiviral therapy (peginterferon plus ribavirin) leads to clinical remission in a proportion of patients, but severe renal disease may be resistant to antiviral therapy. In such cases, corticosteroids and immunosuppressive agents have been used to decrease cryoglobulin production and improve the vasculitic manifestations, but long-lasting remission of the renal disease is uncommon. Here we describe four patients with HCV-related cryoglobulinemic MPGN and the strategies used for their management. The principal message provided by these illustrative cases is that antiviral therapy alone can be the first-line treatment for patients with mild-to-moderate kidney involvement, whereas a short-term course of corticosteroids and cytotoxic agents followed by antiviral therapy may be a reasonable therapeutic strategy for patients with severe/active renal disease.

We here describe two patients with metastatic renal cell cancer (mRCC) treated with immunotherapy in whom the metastases completely regressed after a period of progressive disease. The treatment schedule was based on repeated cycles of low-dose recombinant interleukin-2 and recombinant interferon-alpha, and was never changed during the course of the disease. The first patient received immunotherapy because of multiple bilateral lung metastases. Progressive disease, with mediastinal lymph node involvement and an increased number of lung metastases, was observed after 30 months of regularly repeated therapy; complete regression was achieved after 60 months of immunotherapy (after 16 immunotherapy cycles). The second patient began immunotherapy because of three small lung metastases. Disease progression was observed after three cycles, but complete regression was obtained about 16 months after the start of immunotherapy (after 5 immunotherapy cycles). Long-term low-dose immunotherapy may bring about an effective anti-tumour response even late in the course of the disease and after an initial disease progression.