Treatment Of Cellular Rejection Research Articles

Polyclonal anti T-lymphocyte antibody therapy monitoring in kidney transplant recipients: comparison of CD3+ T cell and total lymphocyte counts.

ABSTRACTObjective:To investigate the correlation between total lymphocyte and CD3+ T cell counts in peripheral blood in renal transplant patients treated with anti-thymocyte globulin, and discuss related outcomes.Methods:A single-center, retrospective study involving 226 patients submitted to kidney transplant between 2008 and 2013, and treated with anti-thymocyte globulin for induction or treatment of cellular rejection. Doses were adjusted according to CD3+ T cell or total lymphocyte counts in peripheral blood.Results:A total of 664 paired samples were analyzed. The Spearman's correlation coefficient was 0.416 (p<0.001) for all samples combined; the overall Kappa coefficient was 0.267 (p<0.001). Diagnostic parameters estimated based on total lymphocyte counts were also calculated using the number of CD3+ T cells (gold standard), with a cut off of >20 cells/mm3.Conclusion:Total lymphocyte and CD3+ T cell counts in peripheral blood are not equivalent monitoring strategies in anti-thymocyte globulin therapy.

Rechazo agudo del trasplante renal: diagnóstico y alternativas terapéuticas

The main aim of renal transplantation is to achieve the longest patient and graft survival, in part by optimising immunological tolerance of the graft. Acute rejection decreases graft survival in the long term. The aim of this review is to describe the diagnosis criteria for acute rejection, the new classification tools, and its therapeutic alternatives.The diagnosis of acute kidney injury (AKI) in renal transplantation is a challenge, given the variability of serum creatinine results related to the titration of immunosuppressive drugs and the volume status. Serum creatinine as a biomarker of acute rejection has a low sensitivity and specificity.The diagnosis of rejection is made using the Banff criteria. The criteria for T-cell mediated rejection have not changed significantly in the past 10 years. However, the category of antibody-mediated rejection was modified in 2013 by adding rejection mediated by C4d-negative antibodies. For the diagnosis of antibody-mediated rejection, 3 main factors are required concomitantly: histological lesions, evidence of antibody-endothelium interaction, and specific donor antibodies.The quality of the evidence for the different options available for rejection treatment is low. The treatment of cellular rejection has not changed in the last decades and is based on corticosteroids and / or thymoglobulin. Treatment of antibody-mediated rejection is based on the removal of antibodies by immunoadsorption or plasmapheresis, with great variability between transplant centres in terms of complementary treatments (steroids, polyvalent human gammaglobulin, bortezomib, rituximab and/or eculizumab) in order to prevent their production.

Renal Allograft Aspergillus Infection Presenting With Obstructive Uropathy: A Case Report

BackgroundIsolated renal allograft aspergillosis is rare and usually presents with fever and decreased glomerular filtration rate. Presentation with obstructive uropathy caused by aspergillus fungal balls is much less common. We report a young male patient who presented with obstructive uropathy secondary to isolated renal allograft aspergillus infection 6 weeks after transplant. He was treated with nephrectomy and antifungal medications. Case presentationA 29-year-old Saudi male patient had a recent living non-related kidney transplantation in Pakistan. Early Post-transplant course was complicated by acute cellular rejection (Banff Class IB) which was managed successfully with pulse steroid and anti-thymocyte globulin. The patient presented again to our emergency room on fortieth day post-transplant with a complaint of decreased urine output and passing white particles in his urine. This presentation was three Three weeks after treatment for cellular rejection, the urine fungal culture showed growth of Aspergillus fumigatus, and ultrasound imaging of the allograft kidney revealed mild to moderate hydronephrosis with echogenic materials within the renal pelvis. Biopsy of the transplanted kidney showed severe necrotizing granulomatous inflammation and fungal elements consistent with aspergillus species. The patient was given voriconazole as an antifungal agent and was weaned from immunosuppressive medication. The patient eventually required intermittent hemodialysis and underwent surgical allograft nephrectomy. ConclusionSuboptimal environmental and infection prevention and control precautions can explain this type of infection. It is important for clinicians to have a high index of suspicion and to investigate for fungal infection as a rare cause of obstructive uropathy in high-risk patients.

Hemorrhagic Cystitis in a Liver Transplant Recipient Secondary to BK Virus

Introduction: Solid organ transplant recipients are at increased risk of infections. Knowledge of clinical presentation and risk factors allows early diagnosis and directed therapy. We present the case of a 53-year-old liver transplant recipient male who developed hemorrhagic cystitis due to BK virus while undergoing treatment for acute cellular rejection. Case Description: Our patent is a 53-year-old male who underwent liver transplantation for cirrhosis secondary to hepatitis C. He was treated for hepatitis C post-transplant and achieved Sustained Virologic Response (SVR). The patient also had a history of Chronic Kidney Disease Stage 3. He was hospitalized for worsening liver function tests 2 years after his transplant. A liver biopsy revealed acute cellular rejection (ACR). He was treated with high dose IV steroids followed by oral taper and dual immunosuppression therapy with tacrolimus and mycophenolate. Owing no improvement in liver function tests, a repeat liver biopsy was done and showed findings consistent with severe rejection. The patient was given a second cycle of high dose IV steroids followed by 4 doses of antithymoglobulin antibody. He responded to the treatment with improvement in liver function tests, however developed gross hematuria with bladder spasms. Urine analysis showed moderate blood and pyuria. Urine cultures were negative. Treatment with broad-spectrum antibiotics failed to improve his symptoms. Cystoscopy showed diffusely inflamed bladder with no masses identified. High titers of BK virus (>5,000,000 copies /ml) were identified in urine and low level viremia was also noted by blood PCR (1,200 copies /ml). Adenovirus, another agent responsible for cystitis in immunocompromised induvial was ruled out by negative PCR. Supportive care with IV hydration and pain control resulted in gradual resolution of symptoms over two weeks. As patient was being treated for ACR, immunosuppression regimen was not changed. Kidney functions remained stable throughout hospitalization. Discussion: Cystitis secondary to viruses like BK and adenovirus has been described in renal and allogeneic hematopoietic cells transplantation. Presentation in liver transplant recipients, either at time of transplantation or during treatment of cellular rejection has not been well documented. Our case suggests that BK virus infection should be considered as the potential cause of cystitis in solid organ transplant recipients.

Evolving Trends in the Costs Associated With Hospital Use of Immunosuppressive Drugs

Evolving Trends in the Costs Associated With Hospital Use of Immunosuppressive Drugs

Impact of immunosuppression and acute rejection on recurrence of hepatitis C: results of the National Institute of Diabetes and Digestive and Kidney Diseases Liver Transplantation Database.

Whereas the impact of early (first 6 postoperative weeks) acute cellular rejection on patient survival among liver transplant recipients as a whole has been reported to be favorable, we hypothesized treatment for acute cellular rejection may have differing impacts on patient and graft survival in hepatitis C virus (HCV)-infected and HCV-negative transplant recipients. We studied the impact of immunosuppression and rejection on patient and graft survival among the 166 HCV-infected and 602 HCV-negative transplant recipients enrolled onto the National Institute of Diabetes and Digestive and Kidney Diseases Liver Transplantation Database. All data were collected prospectively. The association of early acute cellular rejection with mortality was determined using a Cox proportional hazards model with a time-dependent covariate. Median follow-up was 5.0 years for HCV-infected and 5.2 years for HCV-negative transplant recipients. HCV-infected transplant recipients experienced similar frequencies of acute cellular and steroid-resistant rejection as patients undergoing liver transplantation for most other indications. The mortality risk was significantly increased (relative risk = 2.4; P =.03) for HCV-infected transplant recipients who developed early acute cellular rejection compared with HCV-negative transplant recipients. None of the HCV-infected transplant recipients developed allograft failure secondary to chronic rejection. The choice of calcineurin inhibitor did not affect posttransplantation outcomes. Early acute cellular rejection occurs at similar frequencies in HCV-infected and HCV-negative transplant recipients. Although an episode of early acute cellular rejection is associated with a lower cumulative mortality among HCV-negative transplant recipients, the opposite is true for HCV-infected transplant recipients, who experience an increased risk for mortality after an episode of early acute cellular rejection. The adverse impact of early acute cellular rejection on patient survival should be considered in developing primary immunosuppression and acute cellular rejection treatment protocols for HCV-infected transplant recipients.