Background: Posttransplant complications especially “new-onset diabetes after transplantation” (NODAT) have shown to increase the risk of morbidity and mortality in kideny transplant recipients. NODAT is now considered to be determinant of loss of renal allograft, development of infections, and increased risk of cardiovascular mortality. Prevalence of NODAT may vary from 2% to 53%.
Methods: We examined the characteristics and risk factors for NODAT in kidney transplant recipients who are monitored in our center.
Results: At the Clinical Center of Montenegro, 147 kidney transplant recipients are currently being monitored.  13 have confirmed NODAT, which is 8.84%. The distribution by gender is 8 men (61.5%) and 5 women (38.5%). 8 patients, ie 61.5%, had obesity. The average age of patients with NODAT at the time of transplantation was 40.6 years. The average time from transplantation to the development of NODAT was 5 years. There were 7 (53.8%) patients on CIN inhibitor therapy (tacrolimus) and 6 patients (46.2%) on cyclosporin therapy. In the immunosuppressive protocol, all patients had corticosteroid (methylprednisolone), the dose of which was successively reduced after transplantation, while the maintenance dose was 5 mg every second day. There were 13 patients (100%) on mycophenolate mofetil (MMF) therapy. Two (15.4%) patients are being treated with m TOR inhibitor (everolimus), because in the post-transplantation period they developed tumors (breast cancer), both patients were additionally on hormone therapy with tamoxifen. Two of the 13 patients were on methylprednisolone therapy before transplantation due to the underlying diagnosis (SLE, sarcoidosis). One of the patients had proven BK nephropathy in the follow-up, for which the immunosuppressive therapy was corrected by reducing the dose of tacrolimus and corticosteroids, but he still developed NODAT. One patient had chronic hepatitis C infection before transplantation, and developed NODAT after retransplantation with standard doses of immunosuppressants. One patient with primary diagnosis of ADPKD and biopsy-proven FSGS with nephrotic syndrome developed NODAT after a second kidney transplant with standard doses of tacrolimus and steroids, another day after rituximab administration due to proven recurrence of FSGS in the transplanted kidney. One patient developed NODAT in the context of proven CMV reactivation after kidney transplantation and in addition to steroid dose reduction in therapy, and it is interesting that he developed an acute myocardial infarction within the same episode of CMV reactivation. NODAT was the earliest to develop after transplantation in patients who had previously received steroid therapy, elderly patients, and patients who had received cyclosporin therapy.
Conclusion: The main risk factors for the development of NODAT in our kidney transplant recipients were obesity, therapy with CIN inhibitors,  long-term usage of corticosteroids before kidney transplantation.