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This paper provides a review of the significant problem of humoral, or antibody-mediated rejection, in kidney transplantation. The main cause of antibody-mediated rejection is donor-specific anti-HLA antibodies. Patients with anti-HLA antibodies are called sensitised patients. The outcome of humoral rejection is unfavourable: graft dysfunction and failure have been frequent from the early post-transplant period and are continuing. International laboratories and clinics offer sensitive and accurate methods to determine antibodies before and after kidney transplantation, but the methods are not always successful in recognition of sensitised patients. For diagnostics of humoral rejection the important issue is detecting complement breakdown deposition (C4d) in peritubular capillaries during immunohistological examination. On the one hand, their presence is characteristic for humoral rejection, but on the other hand, they can occur without any clinical changes or can remain undetected during severe humoral rejection. Current methods of prevention, diagnostics and treatment of humoral rejection are discussed. Difficulties of evaluation of chronic antibody-mediated injury are particularly highlighted.

BK virus (BKV) infection was studied prospectively in 50 unselected consecutive patients who had undergone kidney transplantation. Infection was monitored for one year after transplantation. Viral DNA in urine (viruria) and plasma (viremia) samples was detected by nested, qualitative polymerase chain reaction. BKV screening data was available for 92% (n = 46) of patients enrolled in the study. Four groups of patients were distinguished: uninfected patients (group 1, n = 30), patients with viruria (group 2, n = 3), patients with viremia (group 3, n = 6) and patients with developed BKV nephropathy (group 4, n = 7). Infection was observed starting form the first month, and the maximum number of patients with active BKV infection occurred at six months after transplantation. Five-year graft survival was 69% for patients with any evidence of BKV infection, compared with 80.0% (P = NS) for patients without BKV infection. The best graft function was observed in group one patient (mean serum creatinine 130 mkmol/l and glomerular filtration rate (GFR) 60.9 ml/min) and the worst in group 4 (mean serum creatinine 180 mkmol/l and GFR 52.31 ml/min) at five years after transplantation. Five-year patient survival was 82.6% and was not affected by presence of BKV infection.

Abstract
Kidney transplant recipients have higher incidence of human papillomavirus (HPV)-related malignancies, but studies on the natural history of HPV infection are insufficient, especially regarding in male recipients. The aim of this study was to evaluate the course of high-risk HPV (HR-HPV) infection after kidney allograft transplantation in male recipients: to estimate frequency and activity of HR-HPV infection under immune system suppression. Twenty male renal recipients (age 20 - 68) were enrolled in this investigation and examined in dynamics. Peripheral EDTA-blood samples and urine samples were collected from each patient 2 weeks, 6 months and 12 months after transplantation. Polymerase chain reaction (PCR) with consensus primers was used for initial detection of high range HPV types, a commercial qPCR kit for detection of HR-HPV load in urine samples and ELISA for detection of serum IgG class antibodies to HR-HPV L1-capsid protein. Overall, combining molecular (HR-HPV genomic sequences detected by real-time PCR) and serological studies (IgG class antibodies to HR-HPV L1-capsids' protein), high frequency of HRHPV infection among male kidney transplant recipients (9/20; 45%) was showed. However, the majority of HR-HPV positive recipients (7/9; 78%) showed signs of infection clearance. It means that, despite the applied immune suppressive therapy, the host's immune system is capable of dealing with HR-HPV infection up to the 12th month after transplantation. However, the sample size should be increased to enable through statistical analysis before final conclusions are made.

Abstract
Our study was focused on identification and correction of early hyperglycaemia, with the aim to reduce the risk of developing post-transplant diabetes mellitus (PTDM) and its associated complications. In a single centre, the prospective study included adult kidney transplant recipients without diabetes mellitus whose pre-transplant glucometabolic data did not show signs of diabetes mellitus. Starting from the first day after kidney transplantation, patients were closely monitored for hyperglycaemia; glucose level measurements were started to obtain pre-prandial levels. If the blood glucose level exceeded 11.1 mmol/l, hyperglycaemia was corrected with short-acting insulin. A total of 14 patients completed a three-month follow-up. During the first post-transplant week, the blood glucose level exceeded 11.1 mmol/l in nine patients (63.9%). From those patients five (55.5%) did not develop PTDM. None of the patients who did not need insulin treatment developed PTDM. Higher pre-lunch glucose levels increased the risk of developing PTDM (p = 0.006). Patients with diabetes required a two times higher insulin dosage than other patients during the first post-transplantation week. We found that hyperglycaemia is a common problem in the early post-transplant period. Early recognition and correction of inpatient hyperglycaemia was associated with reduction of the prevalence of PTDM in more than a half of the patients in the studied group at three months post transplant.