Background: Renal transplant recipients should be considered at high risk for development of Mycobacterium tuberculosis infection (tuberculosis, TB). TB is relatively more frequent among transplant recipients than general population, depending on its epidemicity in the geographic region. Clinical manifestations in this group of patients may be atypical and deserve aggressive investigations for diagnosis. Tuberculin skin test has several limitations regarding diagnosis in chronic renal failure patients. In this retrospective study, we aimed to explore the prevalence and clinical manifestations of TB in renal transplant patients. Materials and methods: We retrospectively analyzed the data for TB prevalence, clinical presentations, and patient and graft survivals of total 320 pediatric and adult renal transplant recipients in our center between 1992 and 2010. Results: The prevalence of TB was 2.8%. Five patients received kidney from living-donor related and four from cadaveric donors. Cadaveric-donor patients received antithymocyte globulin for induction, and four patients received pulse steroid for acute rejection. The median duration of time between transplantation and TB was 21 (1-150) months, and between induction/pulse therapy and infection was 5 (1-100) months. The immunosuppressive protocols included prednisolone and cyclosporine/rapamycin with or without mycophenolate mofetil/azathioprine. The major symptoms were fever (77%), cough (66%), and abdominal pain (22%). Extrapulmonary TB with intestinal (2/9), pericardial (1/9), lymph node (1/9), and cerebral (1/9) involvements developed in five patients. One patient had both pulmonary and testicular involvements. All patients received quartet of anti-TB therapy for a median duration of 9 months. One patient died at the second month of therapy because of dissemination of TB, and one patient returned to hemodialysis because of chronic allograft nephropathy. Conclusion: The prevalence of TB was 2.8% in our renal transplant patients. The quartet of anti-TB treatment including rifampicin resulted in success in a majority of patients.
Matrix metalloproteinases (MMPs) are enzymes that are responsible for degradation of extracellular matrix (ECM); they are involved in the pathogenesis of ischemia-re-perfusion (I-R) injury. We investigated the possible preventive effect of alpha-lipoic acid (LA) in a renal I-R injury model in rats by assessing its reducing effect on the expression and activation of MMP-2 and MMP-9 induced by I-R. Rats were assigned to four groups: control, sham-operated, I-R (saline, i.p.) and I-R+ LA (100 mg/kg, i.p.). After a right nephrectomy, I-R was induced by clamping the left renal pedicle for 1 h, followed by 6 h re-perfusion. In the sham group, a right nephrectomy was performed and left renal pedicles were dissected without clamping and the entire left kidney was excised after 6 h. LA pretreatment was started 30 min prior to induction of ischemia. Injury to tubules was evaluated using light and electron microscopy. The expressions of MMP-2 and MMP-9 were determined by immunohistochemistry and their activities were analyzed by gelatin zymography. Serum creatinine was measured using a quantitative kit based on the Jaffe colorimetric technique. Malondialdehyde (MDA) and glutathione (GSH) were analyzed using high performance liquid chromatography. Tissue inhibitor of metalloproteinase (TIMP)-2 and TIMP-1 were assessed using enzyme-linked immunosorbent assay (ELISA). I-R caused tubular dilatation and brush border loss. LA decreased both renal dysfunction and abnormal levels of MDA and GSH during I-R. Moreover, LA decreased significantly both MMP-2 and MMP-9 expressions and activations during I-R. TIMP-1 and TIMP-2 levels were increased significantly by LA administration. LA modulated increased MMP-2 and MMP-9 activities and decreased TIMP-1 and TIMP-2 levels during renal I-R.
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