Midterm Results of Renal Transplantation From Controlled Cardiac Death Donors Are Similar to Those From Brain Death Donors

Lafuente, O; Sánchez‐Sobrino, Beatriz; Pérez, M.; López–Sánchez, Paula; Janeiro, Darío; Rubio, E. López; Huerta, Ana; Marqués, María; Llópez-Carratalá, M. Rosario; Rubio, Juan José Álvarez; Pórtoles, José

doi:10.1016/j.transproceed.2016.08.039

Cited by 3 publications

(1 citation statement)

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“…Still, the incidence of DGF in ECD recipients has progressively decreased over time from 35.2% in 2003 to 29.6% in 2011 in the USA, probably related to a better understanding of the donor risk profile along with improved allograft selection [ 3 ]. Cardiac death donors have also shown a higher rate of DGF [ 4 ]. Indeed, renal ischaemia/reperfusion (I/R) injury plays a critical role in DGF.…”

Section: Introductionmentioning

confidence: 99%

Genetic susceptibility to delayed graft function following kidney transplantation: a systematic review of the literature

Huart

Krzesinski

Jouret

2018

Clinical Kidney Journal

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Delayed graft function (DGF) is defined as the need for dialysis within 7 days following kidney transplantation (KTx). DGF is associated with increased costs, higher risk for acute rejection and decreased long-term graft function. Renal ischaemia/reperfusion (I/R) injury plays a major role in DGF occurrence. Single nucleotide polymorphisms (SNPs) in certain genes may aggravate kidney susceptibility to I/R injury, thereby worsening post-transplant outcomes. The present article proposes an extensive review of the literature about the putative impact of donor or recipient SNPs on DGF occurrence in kidney transplant recipients (KTRs). Among 30 relevant PubMed reports, 16 articles identified an association between 18 SNPs and DGF. These polymorphisms concern 14 different well-known genes and one not-yet-identified gene located on chromosome 18. They have been categorized into five groups according to the role of the corresponding proteins in I/R cascade: (i) oxidative stress, (ii) telomere shortening, (iii) chemokines, (iv) T-cell homeostasis and (v) metabolism of anti-inflammatory molecules. The remaining 14 studies failed to demonstrate any association between the studied SNPs and the occurrence of DGF. A better understanding of the genetic susceptibility to renal I/R injury may help prevent DGF and improve clinical outcomes in KTRs.

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Section: Introductionmentioning

confidence: 99%