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Review
. 2022 Jan 4:12:779881.
doi: 10.3389/fimmu.2021.779881. eCollection 2021.

Recent Advances of Acute Kidney Injury in Hematopoietic Cell Transplantation

Affiliations
Review

Recent Advances of Acute Kidney Injury in Hematopoietic Cell Transplantation

Masahiro Miyata et al. Front Immunol. .

Abstract

Acute kidney injury (AKI) is a common complication of allogeneic hematopoietic cell transplantation (allo-HCT) and is associated with non-relapse mortality (NRM) and quality of life (QOL). Multiple factors may contribute to AKI during allo-HCT and are often present at the same time making it difficult to determine the cause of AKI in each patient. Nephrotoxic drugs, infections, thrombotic microangiopathy (TMA), and sinusoidal obstruction syndrome (SOS) are well described causes of AKI during allo-HCT. Acute graft-versus-host disease (aGVHD) is a major complication of allo-HCT that mainly targets the intestines, liver, and skin. However, recent studies suggest aGVHD may also attack the kidney and contribute to AKI following allo-HCT. For example, severe aGVHD is associated with AKI, suggesting a link between the two. In addition, animal models have shown donor immune cell infiltration and increased expression of inflammatory cytokines in recipient kidneys after allo-HCT. Therefore, aGVHD may also target the kidney and contribute to AKI following allo-HCT. Herein, we describe the etiology, diagnosis, risk factors, pathophysiology, prevention, and treatment of renal injury after allo-HCT. In addition, we highlight emerging evidence that aGVHD may contribute to the development of AKI after allo-HCT.

Keywords: GvHD; acute kidney injury; allogeneic hematologic stem cell transplantation; calcinurin inhibitors; cytokine; experimental BMT; thrombotic microagiopathy.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Overview of the pathophysiology of AKI after HCT. AKI, acute kidney injury; HCT, hematopoietic cell transplantation; IL, interleukin; IFN, interferon; TNF, tumor necrosis factor; Treg, regulatory T cell; SOS, sinusoidal obstruction syndrome; CNI, calcineurin inhibitor; TA-TMA, transplantation associated-thrombotic microangiopathy.

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