Report of the experience with enteric-coated sodium mycophenolate in a de novo population of kidney transplant recipients at high risk for delayed graft function.
The introduction of mycophenolate as an adjuvant in immunosuppressive regimes has improved clinical outcomes of transplant patients due to a reduced incidence of acute rejection episodes. Nevertheless, the need for dose adjustments or therapy discontinuations (up to 45% in some series), have downgraded the efficacy of mycophenolate mofetil (MMF). From October 2003 to April 2005, 36 kidney transplantations were performed at our site. The immunosuppressive protocol included induction with basiliximab, administered on days 0 and 4 posttransplantation, cyclosporine microemulsion (CsA-ME) monitored by concentrations at 2 hours (C2), enteric-coated sodium mycophenolate (EC-MPS; 720 +/- 180 mg bid), and steroids. Mean follow-up time was 7.3 +/- 4.4 months. Fourteen patients (38.9%) experienced delayed graft function (DGF). Seven (19%) episodes of acute rejection included 5 graded as I-A, 1 as grade I-B, and 1 as grade II-A. There were discontinuations of EC-MPS. Regarding gastrointestinal (GI) adverse events, there were 2 episodes of noninfectious diarrhea, 1 gastritis, and 1 upper GI hemorrhage. There were 11 infections: 4 in the urinary tract; 3 in the lung; 3 in the GI tract; and 1 CMV infection. There were no discontinuations of EC-MPS reported [corrected] Two (6%) graft losses were reported to be due to sepsis. In this group of patients who experienced a high incidence of DGF, the combination of basiliximab, CsA-ME (monitored by C2), and EC-MPS resulted in low Banff grade acute rejection episodes which were all responsive to steroids. The incidence of GI adverse events was only 11%.[1]References
- Report of the experience with enteric-coated sodium mycophenolate in a de novo population of kidney transplant recipients at high risk for delayed graft function. Novoa, P., Rodríguez, L., Gutiérrez, L. Transplant. Proc. (2007) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
