Pretransplant inflammation: A risk factor for delayed graft function?

Ricardo Lauzurica, Mari Cruz Pastor, Beatriz Bayés, Jose María Hernández, Josep Bonet, María Doladé, Maru Navarro, Ramón Romero

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22 Citations (Scopus)

Abstract

Background: Inflammation plays an important role in the pathogenesis of ischemic acute kidney injury (IAKI). In this study, we hypothesize that transplant recipients with pretransplant inflammation may have a greater chance of developing delayed graft function (DGF), an example of IAKI. Patients and methods: We analyzed 178 patients who had undergone their first transplant using cadaveric donors. Blood samples were extracted from transplant recipients prior to transplantation. C-reactive protein (CRP) (nephelometry); interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) (automatized enzyme chemiluminescence immunometric assay); and pregnancy-associated plasma protein A (PAPP-A) (enzyme-linked immunosorbent assay) were determined using the pretransplant blood samples. The risk factors analyzed included cold ischemia, type and time of dialysis, donor and recipient age and HLA compatibility. Results: Sixty-one patients (34.3%) developed DGF. Pretransplant TNF-α (9.31 ± 2.57 vs. 10.56 ± 3.82 pg/mL; p=0.039) and PAPP-A (1.25 ± 0.74 vs. 1.90 ± 1.56 mU/L; p=0.002) were significantly elevated in the group of patients with DGF. Univariate analysis showed that PAPP-A, TNF-α, cold ischemia, type of dialysis (hemodialysis) and donor age were associated with DGF. Multivariate analysis showed that PAPP-A (p=0.006), cold ischemia (p=0.009) and type of dialysis (p=0.046) were independent risk factors for DGF. Conclusions: Pretransplant inflammation (TNF-α, PAPP-A) in transplant recipients could be a risk factor for the development of DGF. © Società Italiana di Nefrologia.
Original languageEnglish
Pages (from-to)221-228
JournalJournal of Nephrology
Volume21
Issue number2
Publication statusPublished - 1 Mar 2008

Keywords

  • CRP
  • Delayed graft function
  • IL-6
  • PAPP-A
  • Pre TR inflammation
  • TIVF-alpha

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