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      Identifying specific causes of kidney allograft loss.

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          Abstract

          The causes of kidney allograft loss remain unclear. Herein we investigated these causes in 1317 conventional kidney recipients. The cause of graft loss was determined by reviewing clinical and histologic information the latter available in 98% of cases. During 50.3 +/- 32.6 months of follow-up, 330 grafts were lost (25.0%), 138 (10.4%) due to death with function, 39 (2.9%) due to primary nonfunction and 153 (11.6%) due to graft failure censored for death. The latter group was subdivided by cause into: glomerular diseases (n = 56, 36.6%); fibrosis/atrophy (n = 47, 30.7%); medical/surgical conditions (n = 25, 16.3%); acute rejection (n = 18, 11.8%); and unclassifiable (n = 7, 4.6%). Glomerular pathologies leading to failure included recurrent disease (n = 23), transplant glomerulopathy (n = 23) and presumed nonrecurrent disease (n = 10). In cases with fibrosis/atrophy a specific cause(s) was identified in 81% and it was rarely attributable to calcineurin inhibitor (CNI) toxicity alone (n = 1, 0.7%). Contrary to current concepts, most cases of kidney graft loss have an identifiable cause that is not idiopathic fibrosis/atrophy or CNI toxicity. Glomerular pathologies cause the largest proportion of graft loss and alloinmunity remains the most common mechanism leading to failure. This study identifies targets for investigation and intervention that may result in improved kidney transplantation outcomes.

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          Author and article information

          Journal
          Am J Transplant
          American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
          Wiley
          1600-6143
          1600-6135
          Mar 2009
          : 9
          : 3
          Affiliations
          [1 ] Department of Internal Medicine, Division of Nephrology and Hypertension and William von Liebig Transplant Center, Mayo Clinic, Rochester, MN, USA.
          Article
          AJT2519
          10.1111/j.1600-6143.2008.02519.x
          19191769
          cb125a0f-60b8-4571-8b34-705f3589531e
          History

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