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BACKGROUND: Chagas disease (ChD) is endemic in many parts of the world and can be transmitted through organ transplantation or reactivated by immunosuppression. Organs from infected donors are occasionally used for transplantation, and the best way of managing the recipients remains a subject of debate. METHODS: We present a single-center cohort study describing a 10-year experience of kidney transplantation in patients at risk of donor-derived ChD and or reactivation. Patients received prophylactic treatment with Benznidazole and were monitored for transmission or reactivation. Monitoring included assessing direct parasitemia, serology, and polymerase chain reaction (PCR). RESULTS: Fifty-seven kidney transplant recipients (KTRs) were enrolled in the study. Forty-four patients (77.2%) were at risk of primary ChD infection, nine patients (15.8%) were at risk of disease reactivation, and four patients (7.0%) were at risk of both. All patients received Benznidazole prophylaxis, starting on the first day after transplantation. Parasitemia was assessed in 51 patients (89.5%), serology also in 51 patients (89.5%), and PCR in 40 patients (70.2%). None of the patients exhibited clinically or laboratory-detectable signs of disease. A single patient experienced a significant side effect, a cutaneous rash with intense pruritus. At 1-year post-transplantation, the patient and graft survival rates were 96.5% and 93%, respectively. CONCLUSION: In this study, no donor-derived or reactivation of Trypanosoma cruzi infection occurred in KTRs receiving Benznidazole prophylaxis.
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PURPOSE: To evaluate the acute effect of aerobic exercise (AE) and resistance exercise (RE) on the release of endothelial progenitor cell (EPCs, CD34+/KDR+/CD45 dim) and vascular function in type 1 diabetes (T1DM). METHODS: Fourteen men with T1DM and 5 nondiabetic controls were randomly assigned to 40-min AE (60% VO 2peak) and RE sessions (60% 1-RM). The study had a crossover design, and interventions were 1 wk apart. Venous occlusion plethysmography (blood flow, reactive hyperemia, and vascular resistance) and blood collection (EPC levels, flow cytometry) were done immediately before and after exercise sessions. RESULTS: Patients were 30.3 ± 1.6 yr-old, HbA1c 7.7% ± 0.2%; controls were 26.8 ± 2.3 yr-old. Groups did not differ in EPC levels at baseline or in relation to exercise. Over time, exercise did not induce changes in patients with T1DM, whereas, in controls, EPCs were decreased after AE (-10.7%, P = 0.017) and increased after RE (+12.2%, P = 0.004). Compared with baseline, blood flow increased and vascular resistance decreased after RE in both groups. Reactive hyperemia was increased 10 min after AE and RE sessions in patients with T1DM (36.5% and 42.0%, respectively) and in controls (35.4% and 74.3%), but no group differences were observed between groups in response to exercise. CONCLUSIONS: Despite the increased vascular reactivity in both groups after both exercise sessions, EPCs were only influenced by exercise in controls. The unchanged number of EPCs in T1DM after exercise sessions might indicate a blunted endothelium regenerating capacity, revealing an early deterioration of the functional arterial characteristics not disclosed by only evaluating vascular functional variables.