Abstract

Acute kidney injury (AKI) is a common finding in kidney donors and recipients. AKI in kidney donor, which increases the risk of delayed graft function (DGF), may not by itself jeopardize the short- and long-term outcome of transplantation. However, some forms of AKI may induce graft rejection, fibrosis, and eventually graft dysfunction. Therefore, various strategies have been proposed to identify conditions at highest risk of AKI-induced DGF, that can be treated by targeting the donor, the recipient, or even the graft itself with the use of perfusion machines. AKI that occurs early post-transplant after a period of initial recovery of graft function may reflect serious and often occult systemic complications that may require prompt intervention to prevent graft loss. AKI that develops long after transplantation is often related to nephrotoxic drug reactions. In symptomatic patients, AKI is usually associated with various systemic medical complications and could represent a risk of mortality. Electronic systems have been developed to alert transplant physicians that AKI has occurred in a transplant recipient during long-term outpatient follow-up. Herein, we will review most recent understandings of pathophysiology, diagnosis, therapeutic approach, and short- and long-term consequences of AKI occurring in both the donor and in the kidney transplant recipient.

Highlights

  • Acute kidney injury (AKI), a common problem in kidney transplantation, can take place both in the donor before organ harvesting, and in the recipient early after transplantation

  • According to recently published data, AKI affects 30% of kidneys coming from deceased donors and 50% of those coming from deceased donors after cardiac death (DCD) [2,3]

  • Graft failure at 1 year was greater for donors with AKI than for those without, and PNF rates were significantly higher for AKI Network (AKIN) stage 3 kidneys (9% vs. 4%, p = 0.04) [13]

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Summary

Introduction

Acute kidney injury (AKI), a common problem in kidney transplantation, can take place both in the donor before organ harvesting, and in the recipient early after transplantation. It manifests as delayed graft function (DGF) or de novo post-transplant acute deterioration of graft function. AKI may develop post-transplantation after an initial recovery of kidney function or may occur late after transplantation. In both settings, AKI can originate from severe and often unrecognized clinical conditions that may require a prompt intervention to prevent graft loss. The present review focuses on the etiology, diagnosis, prognosis, and treatment of AKI in both the donor and the recipient, both in the short and long term

Acute Kidney Injury in the Donor DGF and Risk of Graft Failure
Recipient with AKI Early Post-Transplantation
Biomarkers of DGF
Organ-Targeted Therapy
Early AKI in the Transplant Recipient after Initial Recovery
Long-Term AKI in the Transplant Recipient
COVID-19-Associated AKI in Kidney Transplant Recipients
Findings
Conclusions
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