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Keywords. kidney transplantation, brain death, delayed graft function, lipocalins
Introduction. Development of delayed graft function is more prevalent in patients receiving a kidney allograft from brain-dead than living donors. This study aimed to evaluate the association between urine neutrophil gelatinase-associated lipocalin (NGAL) levels in brain-dead donors and subsequent allograft function.
Materials and Methods. Urine NGAL concentration was measured in urine samples obtained from 24 brain-dead kidney allograft donors before organ retrieval. The 24 kidney recipients were followed for 6 months. The immunosuppressive therapy was similar for all of the recipients. Following transplantation, plasma creatinine was recorded daily during the recipient's stay in the hospital and then at 1, 3, and 6 months after transplantation. Delayed graft function was defined as the need for dialysis in the first 7 days after transplantation.
Results. The mean age of the donors was 28.7 ± 11.2 years and 70.8% were men. Their median urine NGAL level was 7.4 ng/ml (range, 2 ng/mL to 45 ng/mL). Urine NGAL levels were only associated with the need for cardiopulmonary resuscitation (P = .007). On the 1st day after transplantation, 16.7% of the recipients developed delayed graft function, which was declined to 12.5% on the 2nd day and to 8.3% during the 3rd day and the following days. No significant association was observed between the donor's urine NGAL levels and graft function (P = .86).
Conclusions. Our results did not show any association between urine NGAL levels and outcome of allograft function obtained from brain-dead donors. Larger studies are required to confirm this finding.
IJKD 2015;9:394-9
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INTRODUCTION
Transplantation is the first choice of renal replacement therapy for patients with end-stage renal disease. Kidneys for transplantation can be obtained from either living related or unrelated donors or be donated by a brain- or cardiac-death victim. The process of brain death, however, could trigger a complex cascade of molecular and cellular events including the release of various pro-inflammatory mediators. Release of these mediators eventually leads to a pronounced inflammatory state, hemodynamic impairment, endothelial injury, and ultimately, an immunologically activated organ before transplantation.1,2 Moreover, vasoconstriction caused by both excessive secretion of catecoleamines and volume reduction increases the risk of hypoperfusion and ischemic injuries to the kidneys in brain-dead donors. On histological examination, these...