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Acute kidney injury following haplo stem cell transplantation: incidence, risk factors and outcome

Bone Marrow Transplantation volume 53, pages 483–486 (2018)Cite this article

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Organ damage is a common complication in the process of HSCT. Among targeted organ, the incidence of acute kidney injury is high, ranging from 26.4 to 62.2% [1,2,3,4,5,6,7] during HLA-identical matched HSCT. Despite the overall improvement in outcomes after hematopoietic-cell transplantation, acute kidney injury remains a frequent complication and contributes to the morbidity and mortality [1, 2, 4, 8]. In the recent decades, haplo-HSCT developed rapidly and could achieve outcomes similar to those of matched-sibling donor (MSD) HSCT for many diseases such as intermediate and high risk acute myelogenous leukaemia, high-risk acute lymphoblastic leukaemia and so on [9, 10]. However, until to now, studies of AKI on the field of haplo-HSCT are lacking.

This was a single institution, retrospective study which aim to explore the incidence, risk factors, clinical characteristics of acute kidney injury (AKI) within 100 days and impact on the prognosis of haplo hematopoietic stem cell transplantation. Data for all patients who received haplo-HSCT were reviewed between 1 May 2013 and 30 June 2014. The exclusion criteria were: (1) patients who received second stem cell transplantation (4 patients); (2) alive patients whose follow-up was less than 180 days (8 patients) and (3) donor–recipient HLA matching locus was 6/6 (4 patients). Thus, there were 353 consecutive patients evaluated for renal function in the first 100 days, where 201 patients developed AKI and 152 cases were the control group. Baseline creatinine was evaluated 1 week before pre-conditioning, and renal function was re-evaluated after HSCT at least twice a week. According to serum creatinine concentration, AKI was classified as follows: grade 0, normal renal function; grade 1, renal dysfunction corresponded to a less than 1.5-fold rise in baseline serum creatinine; grade 2, renal dysfunction corresponded to greater than or equal to a twofold rise in baseline serum creatinine; grade 3, renal dysfunction corresponded to greater than or equal to a three fold rise in baseline serum creatinine. The urine output or glomerular filtrate rate (GFR) was not a basis for judging AKI. The predominant preconditioning regimen consisted of cytarabine (4 g/[m2 day] on −10 to −9 days), busulfan (BU, 3.2 mg/[kg day] on −8 to −6 days), cyclophosphamide (CY, 1.8 g/[m2 day] on −5 to −4 days), simustine (250 mg/m2 on day −3), and rabbit antithymocyte globulin (ATG; thymoglobulin, 2.5 mg/kg, −5 to −2 days; Sanofi, France). Thirteen patients also received total body irradiation, as part of the conditioning regimen. Five patients received a preconditioning regimen consisting of cytarabine (4 g/[m2 day] −10 to −9 days), busulfan (BU, 3.2 mg/[kg day] on −8 to −6 days), fludarabine (30–35 mg/[m2 day] on −6 to −2 days), simustine (250 mg/m2 on day −3), and rabbit ATG (2.5 mg/kg, −5 to −2 days). One patient received a preconditioning regimen that consisted of fludarabine, cyclophosphamide and rabbit ATG. One patient received reduced-intensity conditioning, which consisted of cytarabine (4 g/[m2 day] −10 to −9 days), busulfan (BU, 3.2 mg/[kg day] on −8 to −6 days), fludarabine (30 mg/[m2 day] on −6 to −2 days), cyclophosphamide (CY 1.4 g/[m2 day] on −5 to −4 days), and rabbit ATG (2.5 mg/kg on −5 to −2 days). GVHD prevention and treatment were as follows: all patients received cyclosporine A, mycophenolate mofetil, and short-term methotrexate for GVHD prophylaxis. The first-line treatment for acute GVHD treatment includes adjusting cyclosporine concentration to effective target and 1–2 mg/kg/d methylprednisolone. When first-line treatment fails (any disease progression in one or more organs after 3 days, or no improvement after 5 days), tacrolimus, CD25 antibody, mycophenolate mofetil, ATG, or mesenchymal stem cells, would then be used.

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Acknowledgements

Support: This work was supported by the Foundation for Innovative Research Groups of the National Natural Science Foundation of China (81621001), the National Natural Science Foundation of China (81530046), and the Science and Technology Project of Guangdong Province of China (2016B030230003).

Author contributions

Research idea and study design: YL and XH. Data acquisition and analysis, statistical analysis: YL. Each author contributed important intellectual content during manuscript draughting or revision and accepts accountability for the overall work by ensuring that questions pertaining to the accuracy or integrity of any portion of the work are appropriately investigated and resolved.

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Authors and Affiliations

  1. Peking University People’s Hospital, Peking University Institute of Hematology, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, Beijing, China

    Yang Liu, Lanping Xu, Xiaohui Zhang, Yu Wang, Kaiyan Liu, Huan Chen, Yuhong Chen, Wei Han, Chenhua Yan & Xiaojun Huang

  2. Peking-Tsinghua Center for Life Sciences, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China

    Xiaojun Huang

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Liu, Y., Xu, L., Zhang, X. et al. Acute kidney injury following haplo stem cell transplantation: incidence, risk factors and outcome. Bone Marrow Transplant 53, 483–486 (2018). https://doi.org/10.1038/s41409-017-0030-3

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