AI Article Synopsis

  • Poor early graft function (EGF) after living donor kidney transplantation (LDKT) is understudied compared to deceased donor transplantations, with data from 469 cases revealing 4.7% incidence of delayed graft function (DGF) and 10.7% for slow graft function (SGF).
  • Diabetic causes and longer warm ischemia times (WIT) were identified as significant risk factors for poor EGF, with WIT increasing the risk of poor functioning by 1.05 for each additional minute.
  • Although poor EGF itself didn't directly reduce graft survival or 1-year function, it was linked to a higher chance of acute rejection, indicating that stronger immunosuppression is needed during these cases to protect

Article Abstract

Poor early graft function (EGF) after deceased donor kidney transplantation (DDKT) has been intensely studied. Much less is known about poor EGF after living donor kidney transplantation (LDKT). Data were collected on 469 LDKTs performed between 1/1/97 and 12/31/01 to determine risk factors for and outcomes associated with poor EGF, defined as either delayed or slow graft function (DGF or SGF). The incidence of DGF and SGF were 4.7% and 10.7%, respectively. Diabetic etiology (OR 2.22; p = 0.021) and warm ischemia time (WIT) (OR 1.05 per min increment; p = 0.0025) emerged as independently associated with poor EGF. Neither functional graft survival nor 1-year graft function differed among the EGF groups. However, DGF and SGF strongly predisposed to acute rejection (AR), which compromised functional graft survival (p = 0.0007) and 1-year graft function. Therefore, we conclude that diabetic etiology of renal disease and WIT are the dominant risk factors for poor EGF after LDKT. Poor EGF did not directly compromise functional graft survival but strongly predisposed to AR. We suggest that immunosuppression should be intensified in the poor EGF setting to maximize LDKT longevity, as AR does impair functional graft survival.

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Source
http://dx.doi.org/10.1111/j.1600-6143.2004.00441.xDOI Listing

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