Prevalence of diabetes and impaired fasting glucose in Poland--the NATPOL 2011 Study.

AIMS: The aim of the analysis was to assess the prevalence of diabetes and impaired fasting glucose in Poland. METHODS: A questionnaire survey on a representative sample of 2411 Polish adults, complemented by blood pressure, anthropometric and fasting plasma glucose measurements. The research was part of the national cross-sectional NATPOL 2011 Study. Diabetes was assessed as self-reported (diagnosed) or screened (fasting plasma glucose level ≥ 7 mmol/l, based on one blood draw). RESULTS: Total prevalence of diabetes in 2011 was 6.7% (95% CI 5.6-7.9); 6.4% (95% CI 5.0-8.0) in women and 7.0% (95% CI 5.4-8.8) in men and did not change from 2002 (6.8%, 95% CI 95% CI 5.8-7.9). Over one quarter of individuals with diabetes were not aware of having the condition. Obesity, arterial hypertension and male gender were strong predictors of screened diabetes. Total prevalence of impaired fasting glucose in the surveyed population was 15.6% (95% CI 14.0-17.2). CONCLUSIONS: The prevalence of diabetes in Poland is similar to that observed in other European populations and has not changed over the last decade. The fact that every fourth person with diabetes is unaware of the disease creates important opportunities for screening and detection of the disease.

A novel programme to evaluate and communicate 10-year risk of CHD reduces predicted risk and improves patients' modifiable risk factor profile.

AIMS: We assessed whether a novel programme to evaluate/communicate predicted coronary heart disease (CHD) risk could lower patients' predicted Framingham CHD risk vs. usual care. METHODS: The Risk Evaluation and Communication Health Outcomes and Utilization Trial was a prospective, controlled, cluster-randomised trial in nine European countries, among patients at moderate cardiovascular risk. Following baseline assessments, physicians in the intervention group calculated patients' predicted CHD risk and were instructed to advise patients according to a risk evaluation/communication programme. Usual care physicians did not calculate patients' risk and provided usual care only. The primary end-point was Framingham 10-year CHD risk at 6 months with intervention vs. usual care. RESULTS: Of 1103 patients across 100 sites, 524 patients receiving intervention, and 461 receiving usual care, were analysed for efficacy. After 6 months, mean predicted risks were 12.5% with intervention, and 13.7% with usual care [odds ratio = 0.896; p = 0.001, adjusted for risk at baseline (17.2% intervention; 16.9% usual care) and other covariates]. The proportion of patients achieving both blood pressure and low-density lipoprotein cholesterol targets was significantly higher with intervention (25.4%) than usual care (14.1%; p < 0.001), and 29.3% of smokers in the intervention group quit smoking vs. 21.4% of those receiving usual care (p = 0.04). CONCLUSIONS: A physician-implemented CHD risk evaluation/communication programme improved patients' modifiable risk factor profile, and lowered predicted CHD risk compared with usual care. By combining this strategy with more intensive treatment to reduce residual modifiable risk, we believe that substantial improvements in cardiovascular disease prevention could be achieved in clinical practice.

Carbon monoxide may reduce ischemia reperfusion injury: a case report of complicated kidney transplantation from a carbon monoxide poisoned donor.

Carbon monoxide (CO), well known from clinical observation to be a deadly poisoning gas, in many animal experiments has revealed a beneficial effect to diminish ischemia/reperfusion injury and rejection of transplanted organs. Data on clinical transplantation of organs retrieved from poisoned persons are limited and discordant; some authors were reported good results, whereas others described high complication rates including death. We herein have described a case of organ transplantation retrieved from a CO-poisoned donor. Warm ischemia during the transplantation procedure was prolonged to 100 minutes, but no complications were observed in the posttransplant course. This report may represent CO preconditioning in clinical transplantation.

Locally Transplanted CD34+ Bone Marrow-Derived Cells Contribute to Vascular Healing After Vascular Injury.

INTRODUCTION: Vascular progenitor cells contribute to repair of injured vasculature. In this study, we aimed to investigate the role of bone marrow-derived cells in the intimal formation after arterial injury. METHODS AND RESULTS: Balloon injury of the femoral artery of wild-type mice was followed by local delivery of bone marrow-derived cells from GFP transgenic mice. The arteries were collected 1, 4, 7, and 14 days after injury and studied for morphology, localization, and phenotypes of delivered cells. Bone marrow-derived cells were present in the intima only at the early stages of arterial injury and expressed endothelial progenitor cell markers (CD31, CD34, and VEGFR-2). In the areas where intima was thicker, bone marrow-derived cells differentiated to intimal smooth muscle cells but they did not fuse with intimal cells. Delivery of CD34+ cells contributed to a 1.5-fold inhibition of intimal hyperplasia. CONCLUSION: Bone marrow-derived endothelial cells differentiated but did not fuse with vascular smooth muscle cells at the early stages of intimal formation and contributed to intimal hyperplasia.

Efficacy and safety of sibutramine in 2225 subjects with cardiovascular risk factors: short-term, open-label, observational study.

This study aims to determine the efficacy and tolerability of sibutramine hydrochloride in overweight and obese patients with cardiovascular risk factors. This was a 12-week, open-label, observational trial carried out in primary care settings. Patients' data were obtained from questionnaires received from 153 physicians. A total of 2225 overweight and obese (BMI> or =27 kg/m2) patients received sibutramine in single daily doses of 10 and/or 15 mg. The study population included patients in general good health and with controlled hypertension (41.2%), type II diabetes mellitus (15.6%), hyperlipidaemia (45.5%), and who were chronic tobacco users (smokers) (37.0%). The main outcome measures were changes in body weight, blood pressure and heart rate, and evaluation of reported adverse events. Reduction of body weight of at least >5% from baseline to week 12 was achieved in 2030 (91%) patients and >10% was achieved in 987 (44%) patients. Baseline differences in the percentages of male and female patients, presence or absence of hyperlipidaemia or smoking status did not appear to affect the rate of weight change. Weight loss was less in patients with type II diabetes mellitus and/or controlled systolic hypertension at baseline compared to those patients without these conditions. Mean systolic and diastolic blood pressure and heart rate decreased from baseline to week 12. Overall, sibutramine was well tolerated. In conclusions, treatment with sibutramine resulted in clinically significant weight loss during short-term therapy in obese adults with a range of cardiovascular risk factors..

Correction of posttransplant erythrocytosis with enalapril.

Erythrocytosis (i.e., elevation in red cell mass) frequently develops after renal transplantation and is associated with increased risk of thromboembolic incidents and hypertension. Because it has been reported that enalapril may induce anemia in renal allograft recipients, we have undertaken a prospective study to estimate the efficacy and safety of enalapril therapy for erythrocytosis and to establish the mechanism by which enalapril reduces red cell mass. Seventeen (12 male and 5 female) long-term renal allograft recipients with increased hematocrit value (> 55% for male and > 50% for female) and elevated red cell mass as determined with 51Cr-labeled autologous erythrocytes were treated with enalapril. After 3 months of therapy, enalapril was withdrawn and patients were observed in order to differentiate spontaneous remission of erythrocytosis from effects of enalapril therapy. After 3 months of the treatment, mean hematocrit decreased from 51.1% (range 47-56%) to 42.9% (range 37-51%; P < 0.01). Red cell mass significantly decreased during this period (from 46.7 ml/kg, range 32.5-60.7 ml/kg, to 32.9 ml/kg, range 20.1-60.1 ml/kg; P < 0.01). Serum erythropoietin levels also changed from 12.2 mIU/ml (range 1.0-33.0 mIU/ml) at baseline to 5.4 mIU/ml (range 0.7-24.2 mIU/ml; P < 0.05). During the following 3 months without enalapril treatment, an increase in hematocrit was noted, reaching 51.7% (range 46-58%; P < 0.05). No serious side effects of enalapril were observed during the study, but there was a need to reduce other hypotensive drugs in some patients. Serum creatinine did not change significantly during enalapril therapy (1.49 mg/dl, range 0.9-2.3 mg/dl, and 1.55 mg/dl, range 1.0-2.3 mg/dl; before and after 3 months of therapy, respectively). Our study proves that enalapril can be safely and effectively used to treat posttransplant erythrocytosis. The effect of enalapril on red cell mass results from reducing erythropoietin production.

Arteriosclerosis in rat aortic allografts: early changes in endothelial integrity and smooth muscle phenotype.

BACKGROUND: Transplant arteriosclerosis remains a limiting factor for the long-term survival of transplanted organs and effective treatment is lacking. A rat model of aortic allografts was used to analyze this process by electron microscopy and further characterize the phenotypic properties of the cells involved. METHODS: A segment of abdominal aorta was transplanted orthotopically from Fischer to Lewis rats. The animals were killed 1-12 weeks after the operation (four to six rats/group), and the grafts were removed and processed for microscopy. RESULTS: The first changes (1 week) included detachment of endothelial cells, adhesion of degranulating platelets to the subendothelial matrix, and modification of smooth muscle cells in the media. The latter process was distinguished by loss of myofilaments and formation of a prominent endoplasmic reticulum and Golgi complex (shift from contractile to synthetic phenotype). Subsequently, modified smooth muscle cells invaded the intima. In parallel, lymphocytes and monocytes/macrophages infiltrated the intima and adventitia. The neointima grew in size by cell proliferation and production of extracellular matrix (4-8 weeks). Smooth muscle cells and monocytes/macrophages in the neointima and media were also noted to accumulate cytoplasmic lipid droplets and eventually turn into foam cells and die. Within the lipid-rich cell remnants, calcification occurred. Finally (12 weeks), the growth in mass of the intimal lesions ceased and in some places reformation of an endothelial lining was detected. Few viable smooth muscle cells remained in the media and the inflammatory infiltrate in the adventitia was reduced. CONCLUSIONS: These observations highlight the importance of early changes in endothelial integrity and smooth muscle phenotype in the development of allograft vascular disease and form the basis for a partly modified model of the cellular mechanisms in this process.

Stimulation and inhibition of hematopoiesis by the MLC reaction.

The effect of an MLC reaction on mouse and human hematopoiesis in vitro was studied. The growth of murine T- and B-lymphocyte colonies as well as myeloid colonies was enhanced during early days of MLC, while a marked decrease of colony formation was evident starting from day +4 of MLC. Allogeneic reaction initially stimulates hematopoiesis, while on its peak a marked inhibition of the proliferation and differentiation of progenitor cells occurs.

Effect of dietary sodium intake on intracellular calcium in lymphocytes of salt-sensitive hypertensive patients.

High dietary Na+ raises mean arterial pressure (MAP) by more than 10% in salt-sensitive (SS) patients with essential hypertension. To test whether the rise in MAP in these patients is caused by a Na(+)-linked increase in [Ca2+]i in vascular smooth muscle cells, we measured [Ca2+]i in the lymphocytes of 14 patients with essential hypertension kept on a Na+ intake of 20 mEq/day for 9 days, and 200-mEq/day for 14 days. Nifedipine gastrointestinal transport system (GITS) (30 mg/day) was given during the last 4 days of each diet. We isolated lymphocytes on Ficoll-Hypaque gradient and measured [Ca2+]i levels using Fura-2 fluorescent dye. During low Na+ intake, there was no difference in MAP (102 +/- 3.5 v 93 +/- 3.8 mm Hg) and in lymphocytes [Ca2+]i (80 +/- 3.0 v 87 +/- 5.4 nmol/L) between the seven salt-sensitive and the seven salt-resistant patients. During high Na+ intake, MAP (92 +/- 2.8 mm Hg) and [Ca2+]i (85 +/- 6.8 nmol/L) did not change in salt-resistant patients. On the contrary, MAP (115 +/- 3.4 mm Hg) and [Ca2+]i (130 +/- 11.1 nmol/L) increased significantly (P less than .01) in the salt-sensitive patients. Nifedipine did not significantly alter MAP and [Ca2+]i in both groups of patients during low Na+ and in salt-resistant patients during high Na+ intake. On the contrary, during high Na+ intake, nifedipine decreased significantly (P less than .01) both MAP (104 +/- 2.4 mm Hg) and [Ca2+]i (89 +/- 5.7 nmol/L) in salt-sensitive patients.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of thymosin (TEX) on antigen-induced primary and secondary antibody responses of mice.

Thymosin (TFX) administered in mice does not alter their primary IgM humoral responses, while it significantly increases the number of IgG plaque-forming cells and IgM PFC during the secondary response. In the thymectomized mice, thymosin partially restores primary and secondary IgM responses, but IgM production remains low.

TFX modulates the immunosuppressive effect of cyclophosphamide on antibody production in mice.

This study is a continuation of our previous work demonstrating the potentiating activity of TFX on cyclophosphamide-induced immunosuppression. Mice primed with TFX subsequently received cyclophosphamide and antigen and their B cell responses were evaluated with an aid of antigen-specific and reverse plaque forming cell assay. Cyclophosphamide-dependent inhibition of immunoglobulin synthesis was significantly stronger in mice pretreated with TFX than in controls. However, the synergistic immunosuppressive action of TFX with cyclophosphamide was evident only when polyclonal but not specific humoral response was studied.

Graft-induced polyclonal activation of B cells. I. Alloantigen-induced humoral response in mice.

In recent years evidence has accumulated pointing out that graft rejection may be mediated not only by cellular but also humoral mechanisms. To study this problem in some detail, humoral responses were studied in mice subjected to skin grafting across the H-2 locus. B cell reactivity was measured during the first and second set reactions on consecutive days after transplantation until graft rejection. In vitro B cell activity was assessed by means of the reverse plaque-forming cell assay (PFC) using cells obtained from the lymph nodes and spleens. The results indicate that polyclonal activation of B cells is an integral part of the immune response to skin transplantation in mice. However, no correlation was found between the level of activation as demonstrated by the PFC and the time of graft rejection.

Graft-induced polyclonal activation of B cells. II. Humoral response of renal allograft recipients (RAR).

Ig production by peripheral blood lymphocytes of renal allograft recipients was studied. It was demonstrated that lymphocytes of patients with acute graft rejection produce elevated numbers of PFC in culture in response to PWM (a T-cell dependent stimulus) and Salmonella paratyphi B (a T-cell independent stimulus) as well as spontaneously. PFC responses were significantly higher in patients with acute rejection than in a group of patients with stable graft function. The B cells of the recipients with stable graft function showed a normal humoral response in vitro. During chronic rejection no significant changes were found in the production of antibodies by B cells.

Deficiency of short-lived suppressor cells controlling T-lymphocyte colony formation in acute lymphoblastic leukemia.

Short-lived suppressor cell (SLSC) activity controlling T-lymphocyte colony formation in vitro was evaluated in patients with acute lymphoblastic leukemia (ALL). No SLSC activity was found in patients in acute phase of the disease. On the other hand, patients in remission frequently had higher SLSC activity than controls. No correlation between colony count and thymidine incorporation as well as T-cell numbers was found in ALL patients.

Fucoidan improves the renal blood flow in the early stage of renal ischemia/reperfusion injury in the rat.

It has been shown that monoclonal anti-P-selectin antibody administration protects renal function in an ischemic model of acute renal failure. This study was designed to evaluate the effect of administration of fucoidan, P-selectin inhibitor, on reduction in renal blood flow induced by ischemia/reperfusion injury in the rat. Experiments were performed on male Wistar rats weighting 35-400 g. The systemic blood pressure (mm Hg) (BP) and renal blood flow (RBF) were monitored continuously and renal vascular resistance (RVR) was calculated. After 20 min period of stabilization animals (6 rats in each group) received one of the following agents administered by continuous i.v. infusion during 165 min: 1 mg/kg of body weight of fucoidan (F1), 10 mg/kg of fucoidan (F10), 100 mg/kg of fucoidan (F100), 10 mg/kg of heparin (H), or 0.9% NaCl solution (control). After 15 min of drug administration the renal vessels of the both kidney were occluded with vascular clamps for 60 min. There were no significant changes in the initial values of RBF, RVR and BP between groups. None procedure affected significantly BP during all experiments. In F10 RBF returned to the initial values in 70th min of reperfusion and did not change up to 90th min. This value was significantly higher than respective value in the control group. In F1 group RBF in 90th min was also higher than in the control group, but it was not statistically significant. The dose of heparine and fucoidan used in the H and F100 groups failed to preserve RBF during reperfusion. In the present study we found that administration of fucoidan--P-selectin inhibitor, increases significantly postischemic renal blood flow and may have renoprotective activity.

Do high levels of serum triglycerides in pancreas graft recipients before transplantation promote graft pancreatitis?

OBJECTIVE: Graft pancreatitis is a serious complication following pancreas transplantation. The aim of this study was to evaluate the influence of pretransplant serum lipid levels on the development of graft pancreatitis among patients undergoing simultaneous pancreas and kidney transplantation (spkTx). METHODS: We reviewed data from spkTx patients engrafted between 1999 and 2002. Group 1 consisted of 10 recipients with well-established pancreas and kidney graft function without postoperative pancreatitis; group 2 5 spkTx recipients who developed fatal graft pancreatitis in the first posttransplant month. The lipid parameters evaluated within 1 hour before transplantation and after hemodialysis included total cholesterol, HDL, LDL, VLDL, triglicerides and apoproteins A and B. RESULTS: Triglycerides, apoprotein B and VLDL were significantly increased just before transplantation among patients who developed fatal pancreatitis compared to those patients with good graft function. CONCLUSION: Recipient hypertriglyceridemia promotes graft pancreatitis in previously injured pancreatic graft.

Protease administration decreases enhanced transforming growth factor-beta 1 content in isolated glomeruli of diabetic rats.

Overproduction of transforming growth factor (TGF)-beta 1 messenger RNA is of fundamental importance in the pathogenesis of diabetic nephropathy. In vitro studies have recently shown that the serine protease trypsin diminishes the enhanced TGF-beta 1-expression induced by advanced glycation end products. Moreover, proteolytic enzymes may accelerate the removal of TGF-beta 1 from renal tissue via a protease-induced activation of alpha 2-macroglobulin (alpha 2M). This activation results in the binding of numerous cytokines, including TGF-beta 1 and is followed by enhanced plasma clearance of the protease alpha 2M-cytokine complex. In the present study in streptozotocin-diabetic rats we investigated whether the administration of Phlogenzym, a fixed combination of the proteases trypsin and bromelain combined with the antioxidant rutosid, modulates renal hypertrophy and the formation of TGF-beta 1 in isolated glomeruli. Three weeks after induction of diabetes, renal hypertrophy developed with an enhanced kidney/body weight ratio. When compared with normal rats, an elevated content of intraglomerular TGF-beta 1 (44.25 +/- 21.9 vs. 71.1 +/- 23.4 ng/microgram DNA, p < 0.05) as well as fibronectin (2.62 +/- 0.49 vs. 3.42 +/- 0.62 ng/microgram DNA, p < 0.05) was observed. In the diabetic rats, treatment with intraperitoneal proteases prevented the rise of intraglomerular TGF-beta 1 content (34.9 +/- 22.2 ng/microgram DNA, p < 0.01) and attenuated the rise of fibronectin (3.03 +/- 1.12 ng/microgram DNA NS). Furthermore, a decrease in the kidney/body weight ratio (p < 0.01) was achieved. Protease administration did not affect blood glucose concentration and was without visible adverse effects.

The effect of chronic allograft rejection on plasma regulators of fibrinolysis.

Chronic renal allograft rejection is often associated with the presence of fibrin thrombi in the microcirculation. Our purpose was to evaluate the influence of chronic rejection on fibrinolytic regulators in plasma of renal allograft recipients. We evaluated the concentration and activities of tPA, uPA and PAI-I in plasma from kidney allograft recipients. We studied 64 patients who underwent kidney transplantation from cadaveric allograft donors. At the time of the study 38 patients had stable graft function for at least 6 months proceeding the study, and 26 recipients had biopsy-proven chronic rejection of the kidney transplant. Control group included 30 healthy blood donors. In kidney transplant recipients we found significantly higher plasma tPA activity (median: 0.99 IU/ml; range: 0-3.8 IU/ml) in comparison to healthy controls (median: 0.15 IU/ml; range: 0-2.8 IU/ml) (p = 0.002) as well as significantly lower plasma PAI-I activity (median: 7.06 U/ml; range: 0-33.2 U/ml) in comparison to healthy controls (median: 21.8 U/ml; range: 0-36.7 U/ml), (p = 0.0001). Among transplant recipients, PAI-I plasma activity in recipients with chronic graft rejection (median: 10.16 U/ml; range: 0-33.2 U/ml) was significantly higher than in patients with stable graft function (median: 4.83 U/ml; range: 0-22.9 U/ml), (p = 0.01). In transplant recipients with stable graft function and poorly controlled hypertension we found significantly higher PAI-I plasma activity in comparison to recipients with normal blood pressure (p = 0.006). In kidney transplant recipients there was a positive correlation between the dose of prednisone and PAI-I activity in plasma (p = 0.01) and an association between BMI value and plasma PAI-I activity (p = 0.008), as well as an association between BMI value and plasma tPA-Ant concentration (p = 0.006). Among transplant recipients, patients treated with ACE inhibitors had significantly lower uPA plasma activity than the rest of the group (p = 0.003). In recipients with stable graft function we found a correlation between CsA concentration and tPA activity (p = 0.04), as well as an association between the dose of CsA and uPA-Ant concentration in plasma (p = 0.049). In patients with chronic graft rejection we found a negative correlation between the dose of prednisone and uPA-Ant plasma level (p = 0.004). Renal allograft recipients have higher tPA and lower PAI-I activities in plasma in comparison to healthy individuals. Chronic allograft rejection, is as well as poorly controlled hypertension, seem to be associated with an increase PAI-I plasma activity. In kidney graft recipients there is a relation between the value of BMI and the activity and concentration of tPA-Ant as well as the value of BMI and the PAI-I activity in plasma. Poorly controlled hypertension is associated with an increase in PAI-I plasma activity. The results of our study suggest a stimulatory effect of CsA on tPA and PAI-I plasma activities as well as on uPA-Ant concentration, while prednisone in turn seems to enhance PAI-I activity in plasma and decrease uPA expression. In renal allograft recipients ACE inhibitors seem to reduce uPA plasma activity.

Higher exposure to cyclosporine A with unchanged tolerability in patients converted from Sandimmun to Sandimmun Neoral.

Neoral (NEO) is claimed to have better pharmacokinetics than standard preparation of cyclosporine (SIM) thus providing more reliable immunosuppression. We estimated safety and tolerability of NEO and compared pharmacokinetic parameters in 20 stable renal allograft recipients (RARs) converted from SIM to NEO treatment. Another 20 stable RARs continuously treated with SIM created a control group. Whole blood through CsA level (C0) did not differ after conversion (SIM: 136.2 +/- 33 ng/ml and NEO: 142.6 +/- 34 ng/ml). During therapy with NEO peak blood concentration (Cmax) was significantly higher (935.6 +/- 368 ng/ml) and occurred earlier (Tmax 1 hr. 36 min. +/- 30 min) as compared to the period on SIM (Cmax 598 +/- 309 ng/ml, p = 0.01), Tmax = 3 hr. +/- 1 h 36 min., (p = 0.01) respectively. AUC increased from 2975.4 +/- 1020 ngxhr/ml to 4236.1 +/- 1188 ngxhr/ml (p < 0.0001). Correlation coefficient between AUC and C0 was higher during NEO (r = 0.52) than SIM therapy (r = 0.32). The only noticeable change in laboratory tests after switch to NEO was slight increase of serum triglyceride concentration (119.5 +/- 44.7 mg/dL vs. 148.4 +/- 67.0 mg/dl). The mean serum creatinine concentration did not change significantly (1.42 +/- 0.32 mg/dL and 1.46 +/- 0.31 mg/dL). Tolerance of NEO was good and 1:1 switch from SIM to NEO is clinically safe. Higher bioavailability of NEO was not associated with decreased tolerability or increased nephrotoxicity. Better correlation between C0 and AUC during NEO administration makes CsA treatment monitoring more reliable.

Factors affecting reactivation of Epstein-Barr virus infection after kidney allograft transplantation.

OBJECTIVES: Reactivation of Epstein-Barr virus (EBV) infection in renal transplant recipients may cause significant morbidity and mortality. To evaluate factors associated with activation of EBV replication we followed prospectively a group of 65 recipients of cadaveric kidney for 12 months. METHODS: Sera were collected periodically from these patients and analyzed for the presence of specific anti-EBV antibodies. Control group consisted of renal (n=35) and healthy blood donors (n=35). Enzyme-linked immunoassays based on recombinant EBV proteins were used to detect the following antibody specificities: early antigen (EA) IgA, IgM, and IgG, nuclear antigen (EBNA) IgG. RESULTS: During first year after transplantation, primary infection developed in 4 (6.15%) recipients and reactivation occurred in 18 (27.7%) recipients. Analysis did not show the association of reactivation with type of basic immunosuppressive therapy, prophylactic or therapeutic use of anti-lymphocyte antibodies, as well as acute rejection episodes. There was a borderline association (p=0.068) between the incidence of CMV infection and EBV reactivation. CONCLUSIONS: Our data suggest casual relationship between CMV infection and EBV reactivation.