Impact of graft infection on long-term survival after kidney transplant.

BACKGROUND: Patients undergoing transplantation procedures are at a high risk of developing infections because of the need for immunosuppression. Infections presenting directly after renal transplantation greatly influence the overall success of the procedure. The aim of this study was to evaluate the influence of postoperative infection on the length of survival after renal transplant. METHODS: In 2009 a multicenter prospective trial evaluating the factors that influence the occurrence of postoperative infective complications was published by the authors. That study reported that 25 out of 232 recipients of a renal transplant were diagnosed with an infection. The present study shows the effect of postoperative infection on the length of survival after renal transplantation during a 15-year observation period. Statistical methods involved monofactorial and multifactorial Kaplan-Meier analysis for the length of survival and the Cox proportional hazards model for mortality prediction. A P value of <.05 was considered to indicate statistical significance. RESULTS: The analysis demonstrated that the lifespan of renal transplant recipients was decreased in those with postoperative infection, at both year 10 of the observation period (P = .013) and 15 years after transplantation (P = .012). Moreover, it was ascertained that an infection in the postoperative period was an independent risk factor increasing the mortality after renal transplantation: P = .026; hazard ratio 2.90 (95% confidence interval, 1.13-7.41). CONCLUSIONS: The occurrence of an infection in the postoperative period significantly decreases the lifespan of a renal transplantation recipient.

The impact of interleukin 12B (1188A>C), interleukin 16 (-295T>C), and interleukin 18 (607C>A, 137G>C) gene polymorphisms on long-term renal transplant function and recipient outcomes.

BACKGROUND: Inflammatory mediators play an important role in kidney graft outcome. The cytokine and chemokine gene polymorphisms are associated with variable production, activity, expression, or ligand-receptor affinity. Genetic variation in the DNA sequence of the interleukin 12B (IL12B), interleukin 16 (IL16), and interleukin 18 (IL18) genes may lead to altered cytokine production and activity. These variations can lead to changes in individual patient outcomes after kidney transplantation. It is known that polymorphisms of interleukins have an influence on inflammatory diseases, eg, Crohn's disease, diabetes, and asthma. AIM: The aim of this study was to evaluate the correlation between IL12B, IL16, and IL18 gene polymorphisms with delayed graft function (DGF), acute rejection episodes (AR), and chronic rejection episodes (CR). MATERIALS AND METHODS: A total of 267 (38.6% women, 61.4% men) recipients were included in the study. Cadaveric kidney transplantations were performed at the Department of General Surgery and Transplantation. Polymerase chain reaction was used to determine gene polymorphisms of IL12B (rs3212227), IL16 (4778889), and IL18 (rs1946518, rs187238) in 2 mL of serum. Statistical significance (P < .05) was analyzed by logit regression, ANOVA and odds ratio (OR) of χ(2) with Yates correction (95% confidence interval). RESULTS: Regression analysis revealed no significance between AR/DGF/CR and IL-2B, IL16, IL18rs1946518, and IL18-rs187238 (P > .05). The CR group, AA vs CC genotype of IL18 (rs1946518), had an OR = 2.35 (P = .04). AR and DGF groups had no significance in OR. CONCLUSIONS: There was no statistical significance between IL12B, IL16, and IL18 (rs187238) gene polymorphisms and kidney graft outcome after transplantation. Presence of AA genotype (IL18-rs1946518) is connected with a 2.35 times higher risk of CR occurrence.

Serum myeloperoxidase levels and platelet activation parameters as diagnostic and prognostic markers in the course of coronary disease.

Early prediction of coronary artery disease complications is vital for the prevention and effective treatment of patients with coronary cardiac disease. It has been reported that inflammatory markers play a key role in the progression of cardiovascular diseases. Platelet count and platelet morphological parameters were analyzed on a fully-automated hematological analyzer ADVIA 2120 (Siemens). Serum myeloperoxidase (MPO) level was determined with an enzyme immunoassay (BioCheck). The measuring range of this assay is between 0 and 40 ng/ml. We demonstrate that serum MPO concentration and platelet activation increase systematically with the advancement of coronary artery disease. Moreover, MPO level is significantly higher in patients with unstable coronary artery disease and myocardial infarction compared with healthy subjects and patients with stable angina. The diagnostic sensitivity of these parameters was higher than of TnI (cardiac troponin I), CK-MB (creatine kinase-heart type), CRP (C-reactive protein), and fibrinogen and DD (D-dimers). MPO, L-PLT (large platelet), MPV (mean platelet volume), and MPC (mean platelet component concentration) may serve as attractive diagnostic and prognostic markers in the assessment of the risk for unstable atheroma in the course of coronary artery disease.