Introduction: Posttransplant diabetes mellitus (PTDM) remains the significant clinical problem and impairs the quality of life of renal transplant recipients. Negative influence of PTDM on graft function is associated with chronic allograft nephropathy, systemic infectious complications, recurrent infections or urinary tract infections. Some earlier studies suggest that patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) are at special risk of developing PTDM. The aim of our study was to assess the influence of PTDM on graft function in recipients with ADPKD and other causes of renal failure during 12-month follow-up. Another aim of the study was to answer the question if the etiology of renal failure (ADPKD vs non-ADPKD) and the development of PTDM were independent predictors of graft function and if there was a significant interaction between them.

Material and methods: 98 pairs of kidney recipients from the same cadaveric donor were included into the study, with the ADPKD-related renal failure in one of the recipients, and different reasons for transplant in the other, with exclusion of the diabetic nephropathy. Diabetes was diagnosed according to American Diabetes Association (ADA) criteria. For statistical analysis the following parameters were included: age, sex, development ofposttransplant complications such as: PTDM, acute tubular necrosis (ATN) and early graft rejection, the presence of surgical and infectious complications (urinary tract infections excluded) and urinary tract infections as well as kidney function parameters such as serum urea, creatinine and uric acid concentrations 3, 6 and 12 months after transplantation.

Results: At the time of transplantation ADPKD patients were significantly older than non ADPKD patients (median 49.5 vs 45.3 years, p < 0.00008). There was no significant difference in incidence of PTDM between the study groups (19% in the ADPKD group and 18% in non-ADPKD group, p = 1.0). In ADPKD group no significant differences in serum urea, creatinine and uric acid following transplant were found between PTDM and non-PTDM subgroups. In non-ADPKD group, 3 and 6 months after transplantation, serum urea concentrations (77.5 mg/dL vs 54.0 mg/dL, p = 0.007 and 77.0 mg/dL vs 56.7 mg/dL, p = 0.016) and uric acid concentrations (7.7 mg/dL vs 6.8 mg/dL, p = 0.001 and 7.3 mg/dL vs 6.2 mg/dL, p = 0.034) were significantly higher in PTDM than in non-PTDM subgroup. Serum creatinine concentration was significantly higher in PTDM group 12 months following transplant (1.87 mg/dL vs 1.5 mg/dL, p = 0.035), with borderline significance 6 months following transplant (1.77 mg/dL vs 1.5 mg/dL, p = 0.057). In PTDM subgroup of ADPKD patients the percentage of infectious complications was slightly higher than in non-PTDM subgroup, but the difference was not statistically significant (37% vs 18%, p = 0.12), urinary tract infections were significantly more prevalent in PTDM subgroup (47% vs 18%, p = 0.013). In multivariate analysis no significant influence of ADPKD on any of the parameters of graft function was found. Significant interaction between ADPKD and PTDM presence for their influence on parameters of graft function was not found either what suggests that PTDM had a similar negative effect on these parameters in both ADPKD and non-ADPKD patients.

Conclusions: 1. PTDM has negative influence on graft function independently of ADPKD diagnosis. 2. PTDM presence in ADPKD group significantly predisposes to urinary tract infections.