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异基因造血干细胞移植后肾损伤患者的微生物组变化

Changes in Microbiome in Patients with Kidney Injury after Allogeneic Hematopoietic Stem Cell Transplantation.

作者信息

Abramson Matthew H, Sathick Insara Jaffer, Knezevic Andrea, Perales Miguel-Angel, Jaimes Edgar A

机构信息

Renal Service, Memorial Sloan Kettering Cancer Center, New York, New York.

Icahn School of Medicine at Mount Sinai, New York, New York.

出版信息

Kidney360. 2025 Jan 1;6(1):58-68. doi: 10.34067/KID.0000000627. Epub 2024 Oct 24.

DOI:10.34067/KID.0000000627
PMID:39446483
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11793185/
Abstract

KEY POINTS

Changes in microbiome diversity index are common in patients with stem cell transplant. Changes in microbiome diversity do not explain the high incidence of AKI in patients with stem cell transplant.

BACKGROUND

AKI is a common complication of allogeneic hematopoietic cell transplantation (allo-HCT) that increases the risk of mortality. By contrast, higher diversity of intestinal microbiota at the time of neutrophil engraftment has been associated with lower mortality. We aimed to better understand kidney outcomes in relation to changes in gut diversity in this patient population, hypothesizing that patients with lower microbiome diversity at baseline and at engraftment were at higher risk of developing kidney complications.

METHODS

We performed a single-center retrospective study of 419 hematopoietic cell transplant recipients from 2014 to 2017 at our institution whose gut microbiota were analyzed. We defined AKI and CKD on the basis of Kidney Disease Improving Global Outcomes criteria and eGFR using the CKD Epidemiology Collaboration equation. We defined gut microbiome diversity using Shannon and Simpson reciprocal diversity indices, with higher levels indicating more diverse microbiota.

RESULTS

Simpson reciprocal diversity index and Shannon diversity index were 21.8 (interquartile range [IQR], 13.7–35.2; range, 1.6–102.5) and 3.7 (IQR, 3.2–4.2; range, 0.7–5.2) in our cohort at baseline and 6.3 (IQR, 3.7–10.4) and 2.3 (IQR, 1.7–2.8) at periengraftment, respectively. Of the 419, 263 patients (63%) developed any grade AKI in 100 days after hematopoietic cell transplantation and 114 (27%) developed grade 2+ AKI. There were no significant differences in microbiome diversity at baseline or periengraftment in patients who developed post-transplant AKI or CKD, respectively, in comparison with those who did not develop kidney complications.

CONCLUSIONS

Our findings do not support the existence of a link between baseline or periengraftment gut diversity and the risk of development of AKI or CKD in patients undergoing allo-HCT. This study highlights the complex and multifactorial etiology of AKI in allo-HCT recipients and the need for additional prospective and mechanistic studies.

摘要

关键点

微生物群多样性指数的变化在干细胞移植患者中很常见。微生物群多样性的变化并不能解释干细胞移植患者急性肾损伤的高发病率。

背景

急性肾损伤(AKI)是异基因造血细胞移植(allo-HCT)的常见并发症,会增加死亡风险。相比之下,中性粒细胞植入时肠道微生物群多样性较高与较低的死亡率相关。我们旨在更好地了解该患者群体中与肠道多样性变化相关的肾脏结局,假设基线和植入时微生物群多样性较低的患者发生肾脏并发症的风险更高。

方法

我们对2014年至2017年在我们机构接受造血细胞移植的419名患者进行了单中心回顾性研究,分析了他们的肠道微生物群。我们根据改善全球肾脏病预后(KDIGO)标准定义AKI和慢性肾脏病(CKD),并使用CKD流行病学协作组方程计算估算肾小球滤过率(eGFR)。我们使用香农多样性指数和辛普森倒数多样性指数定义肠道微生物群多样性,指数越高表明微生物群越多样。

结果

在我们的队列中,基线时辛普森倒数多样性指数和香农多样性指数分别为21.8(四分位间距[IQR],13.7 - 35.2;范围,1.6 - 102.5)和3.7(IQR,3.2 - 4.2;范围,0.7 - 5.2),植入期分别为6.3(IQR,3.7 - 10.4)和2.3(IQR,1.7 - 2.8)。在419名患者中,263名(63%)在造血细胞移植后100天内发生了任何级别的AKI,114名(27%)发生了2级及以上AKI。与未发生肾脏并发症的患者相比,发生移植后AKI或CKD的患者在基线或植入期的微生物群多样性没有显著差异。

结论

我们的研究结果不支持基线或植入期肠道多样性与接受allo-HCT患者发生AKI或CKD风险之间存在关联。这项研究强调了allo-HCT受者中AKI病因的复杂性和多因素性,以及进行更多前瞻性和机制性研究的必要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/04558216ab2c/kidney360-6-058-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/36b186bed166/kidney360-6-058-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/64ce7d70801e/kidney360-6-058-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/1a47d17dd5a9/kidney360-6-058-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/dad7504139e4/kidney360-6-058-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/99c1e7fb9318/kidney360-6-058-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/3792f38202d1/kidney360-6-058-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/04558216ab2c/kidney360-6-058-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/36b186bed166/kidney360-6-058-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/64ce7d70801e/kidney360-6-058-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/1a47d17dd5a9/kidney360-6-058-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/dad7504139e4/kidney360-6-058-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/99c1e7fb9318/kidney360-6-058-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/3792f38202d1/kidney360-6-058-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c8d/11793185/04558216ab2c/kidney360-6-058-g007.jpg

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