Kidney international最新文献

英文中文

Single-cell spatial transcriptomics reveal intraglomerular cell activation and ligand-receptor relationships in chronic, active antibody mediated rejection 单细胞空间转录组学揭示慢性活性抗体介导的排斥反应中肾小球内细胞活化和配体-受体关系

IF 12.6 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2026-01-01 DOI: 10.1016/j.kint.2025.08.042

Alessia Giarraputo , Evelyn Metzger , Nicole Brousaides , Jeremy Marcin , Claire Trivin-Avillach , R. Neal Smith , Joseph M. Beechem , Ivy A. Rosales , Robert B. Colvin

Introduction

Chronic active antibody-mediated rejection (CAMR) is a leading cause of late kidney allograft dysfunction, characterized by transplant glomerulopathy involving glomerular endothelial cells (GEC), natural killer (NK) cells, and macrophages. Mechanistic understanding remains limited due to the inability of bulk and single-cell RNA techniques to capture spatial molecular interactions.

Methods

Using spatial transcriptomics at single-cell resolution (CosMx Spatial Molecular Imager), we analyzed formalin fixed paraffin embedded kidney biopsies with CAMR and compared with controls without rejection.

Results

Cell typing, clustering, and dimensionality reduction identified 36 reference cell types, while selectively localizing GEC subtypes, NK cells, and macrophages in glomeruli. Cellular differential gene expression (DGE), cell proximity, and cell-to-cell ligand-receptor analyses elucidated candidate CAMR molecular mechanisms. Spatially resolved single-cell transcriptomics revealed upregulation of intraglomerular NK cell and macrophage genes in CAMR related to cytotoxicity, IgG Fc receptor and non-self-recognition. GEC subtypes developed distinctive transcript phenotypes that included upregulated genes related to complement protection, the MHC target of donor specific antibodies and IFNγ pathway and downregulation of sialyltransferase involved in protective glycocalyx synthesis and vascular integrity. Proximity of NK cells and macrophages with GEC revealed several potential ligand receptor interactions previously unappreciated, including GEC IL33→NK cell IL1RL1 and GEC HLA-DQA1→Macrophage FCGR3A, implicating NK cell and macrophage activation in endothelial injury.

Conclusions

High-resolution spatial transcriptomics provided novel and confirmatory insights into CAMR pathogenesis, highlighting cell-specific activation states, molecular interactions, and potential mechanistic pathways involving GECs, NK cells, and macrophages. Our findings advance understanding of CAMR and identify molecular targets for further investigation.

慢性活动性抗体介导的排斥反应（CAMR）是晚期异体肾移植功能障碍的主要原因，其特征是移植肾小球病变涉及肾小球内皮细胞（GEC）、自然杀伤细胞（NK）和巨噬细胞。由于体积和单细胞RNA技术无法捕获空间分子相互作用，机制理解仍然有限。方法采用单细胞分辨率空间转录组学技术（CosMx空间分子成像仪），用CAMR对福尔马林固定石蜡包埋肾活检组织进行分析，并与无排斥反应的对照组进行比较。结果细胞分型、聚类和降维鉴定了36种参考细胞类型，并选择性地定位了肾小球中的GEC亚型、NK细胞和巨噬细胞。细胞差异基因表达（DGE）、细胞接近性和细胞间配体受体分析阐明了候选CAMR的分子机制。空间分辨率单细胞转录组学显示CAMR中与细胞毒性、IgG Fc受体和非自我识别相关的肾小球内NK细胞和巨噬细胞基因上调。GEC亚型表现出独特的转录表型，包括与补体保护、供体特异性抗体MHC靶点和IFNγ途径相关的基因上调，以及参与保护性糖萼合成和血管完整性的唾液基转移酶的下调。NK细胞和巨噬细胞与GEC的接近揭示了以前未被发现的几种潜在的配体受体相互作用，包括GEC IL33→NK细胞IL1RL1和GEC HLA-DQA1→巨噬细胞FCGR3A，暗示NK细胞和巨噬细胞在内皮损伤中的激活。高分辨率的空间转录组学为CAMR的发病机制提供了新的和验证性的见解，突出了细胞特异性激活状态、分子相互作用以及涉及gec、NK细胞和巨噬细胞的潜在机制途径。我们的发现促进了对CAMR的理解，并确定了进一步研究的分子靶点。

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引用次数: 0

Executive Summary of the KDIGO 2026 Clinical Practice Guideline for the Management of Anemia in Chronic Kidney Disease (CKD) 慢性肾脏疾病（CKD）贫血管理KDIGO 2026临床实践指南执行摘要

IF 12.6 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2026-01-01 DOI: 10.1016/j.kint.2025.06.005

Jodie L. Babitt , Jeffrey S. Berns , Biykem Bozkurt , Rebecca S. Cheung Khedairy , Yarieli Cuevas , Emmanuel E. Effa , Michele F. Eisenga , Steven Fishbane , Yelena Z. Ginzburg , Volker H. Haase , S. Susan Hedayati , Siah Kim , José A. Moura-Neto , Evi V. Nagler , Patrick Rossignol , Manisha Sahay , Tetsuhiro Tanaka , Angela Yee-Moon Wang , David C. Wheeler , Karen A. Robinson , Marcello Tonelli

The Kidney Disease: Improving Global Outcomes (KDIGO) 2026 Clinical Practice Guideline for the Management of Anemia in Chronic Kidney Disease (CKD) represents an update to the guideline published in 2012. Its scope includes diagnosis and evaluation of anemia; use of iron to treat iron deficiency and anemia in CKD; use of erythropoiesis-stimulating agents and hypoxia-inducible factor–prolyl hydroxylase inhibitors to treat anemia in CKD; and red blood cell transfusions to treat anemia in CKD. The guideline has been developed with patient partners, healthcare providers, and researchers around the world, with the goal to generate a useful resource for healthcare providers and patients by providing actionable recommendations. The development of this guideline followed an explicit process of evidence review and appraisal based on systematic reviews. The certainty of evidence and strength of recommendations follows the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. The guideline also provides practice points that provide clinical advice but are not supported by a systematic review. Limitations of the evidence are discussed. Research recommendations to address gaps in knowledge, and implications for policy and payment, are provided. The guideline targets a broad audience of healthcare providers, affected individuals, and stakeholders involved in the various aspects of anemia and CKD care.

肾脏疾病：改善全球结局（KDIGO） 2026慢性肾脏疾病（CKD）贫血管理临床实践指南是对2012年发布的指南的更新。其范围包括贫血的诊断和评价；用铁治疗慢性肾病缺铁性贫血；使用促红细胞生成剂和缺氧诱导因子-丙氨酸羟化酶抑制剂治疗慢性肾病贫血；以及红细胞输注来治疗慢性肾病中的贫血。该指南是与世界各地的患者合作伙伴、医疗保健提供者和研究人员共同制定的，其目标是通过提供可操作的建议，为医疗保健提供者和患者提供有用的资源。本指南的制定遵循了基于系统评价的证据审查和评价的明确过程。证据的确定性和建议的强度遵循建议评估，发展和评价（GRADE）方法的分级。该指南还提供了提供临床建议的实践要点，但没有得到系统评价的支持。讨论了证据的局限性。提出了解决知识差距及其对政策和支付的影响的研究建议。该指南的目标受众广泛的医疗保健提供者，受影响的个人，和利益相关者参与贫血和慢性肾病护理的各个方面。

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引用次数: 0

Insights into arteriovenous fistula (non)maturation: single-cell transcriptomics reveals new drivers of arteriovenous fistula remodeling 洞察动静脉瘘（非）成熟：单细胞转录组学揭示了动静脉瘘重塑的新驱动因素

IF 12.6 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2026-01-01 DOI: 10.1016/j.kint.2025.09.034

Andrew H. Baker , Margreet R. de Vries

Single-cell transcriptomics of arteriovenous fistulas reveal that failure is likely driven less by smooth muscle proliferation than by continuous inflammation, endothelial dysfunction, and fibroblast-driven fibrosis. These insights reframe current knowledge and highlight mechanistic pathways as to where future therapies could be targeted to improve arteriovenous fistula maturation kinetics and associated patency rates.

动静脉瘘的单细胞转录组学显示，失败可能不是由平滑肌增生引起的，而是由持续的炎症、内皮功能障碍和成纤维细胞驱动的纤维化引起的。这些见解重新构建了当前的知识，并强调了未来治疗可以靶向的机制途径，以改善动静脉瘘成熟动力学和相关的通畅率。

引用次数: 0

Intermittent dark urine in a school-aged boy: a case of alkaptonuria 学龄男孩间歇性尿色深：尿黑尿症1例

IF 12.6 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2026-01-01 DOI: 10.1016/j.kint.2025.07.035

Nora Abazi-Emini , Ardiana Beqiri-Jashari , Ivan Akimovski , Anja M. Billing , Markus M. Rinschen , Aleksandra Janchevska , Björn Reusch , Velibor Tasic , Bodo B. Beck

引用次数: 0

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IF 12.6 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2026-01-01 DOI: 10.1016/S0085-2538(25)00891-9

引用次数: 0

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IF 12.6 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2026-01-01 DOI: 10.1016/S0085-2538(25)00892-0

引用次数: 0

Critical role of transcription factor SOX4 in tubular epithelial cell dedifferentiation and fibroblast activation during kidney fibrosis 转录因子SOX4在肾纤维化过程中小管上皮细胞去分化和成纤维细胞活化中的关键作用。

IF 12.6 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2026-01-01 DOI: 10.1016/j.kint.2025.08.030

Hao Du , Baihai Jiao , Jian Xing , Dong Yang , Melanie Tran , Penghua Wang , Zhaoyong Hu , Véronique Lefebvre , Dong Zhou , Yanlin Wang

Introduction

Chronic kidney disease (CKD) is a widely prevalent health issue globally. A striking pathological feature of CKD is kidney fibrosis characterized by excessive production and deposition of extracellular matrix (ECM). Tubular epithelial cell (TEC) dedifferentiation and fibroblast activation contribute to the pathogenesis of kidney fibrosis. However, the molecular mechanisms underlying TEC dedifferentiation and fibroblast activation are not fully understood. Here, we investigated the role of SRY-box transcription factor 4 (SOX4) in regulating TEC dedifferentiation and fibroblast activation during the development of CKD.

Methods

We generated global, TEC-specific, and fibroblast-specific SOX4 knockout mice. These mice were subjected to three preclinical models of kidney fibrosis induced by unilateral ureteral obstruction, ischemia-reperfusion injury, or high-dose folic acid to examine the role of SOX4 in TEC dedifferentiation and fibroblast activation during the development of kidney fibrosis. Cultured TECs and fibroblasts were employed to determine the role and molecular mechanisms of SOX4 in regulating TEC dedifferentiation and fibroblast activation in vitro.

Results

SOX4 was induced in the injured kidneys but its deficiency inhibits TEC dedifferentiation, fibroblast activation and further impeded the development of kidney fibrosis in mice. In vitro, knockdown of SOX4 preserved the epithelial phenotype and inhibited fibroblast activation induced by transforming growth factor-β1 (TGF-β1). Mechanistically, SOX4 facilitated the TGF-β1-Smad3 signaling pathway to promote TEC dedifferentiation and fibroblast activation.

Conclusions

Our findings identify SOX4 as a critical factor in TEC dedifferentiation and fibroblast activation suggesting SOX4 may serve as a potential therapeutic target for the treatment of CKD.

慢性肾脏疾病（CKD）是全球广泛流行的健康问题。CKD的一个显著病理特征是肾纤维化，其特征是细胞外基质（ECM）的过度产生和沉积。肾小管上皮细胞（TEC）去分化和成纤维细胞活化参与肾纤维化的发病机制。然而，TEC去分化和成纤维细胞活化的分子机制尚不完全清楚。在这里，我们研究了SRY-box转录因子4 （SOX4）在CKD发展过程中调节TEC去分化和成纤维细胞激活中的作用。方法制备了全局、tec特异性和成纤维细胞特异性的SOX4基因敲除小鼠。采用单侧输尿管梗阻、缺血再灌注损伤和高剂量叶酸诱导的三种肾纤维化临床前模型，观察SOX4在肾纤维化发展过程中TEC去分化和成纤维细胞活化中的作用。采用体外培养的TEC和成纤维细胞，研究SOX4在体外调节TEC去分化和成纤维细胞活化中的作用和分子机制。结果sox4可诱导损伤肾，但缺乏sox4可抑制TEC去分化、成纤维细胞活化，进一步抑制小鼠肾纤维化的发展。在体外，敲除SOX4保留了上皮表型，抑制了转化生长因子-β1 （TGF-β1）诱导的成纤维细胞活化。机制上，SOX4促进TGF-β1-Smad3信号通路促进TEC去分化和成纤维细胞活化。结论SOX4是TEC去分化和成纤维细胞活化的关键因子，提示SOX4可能是CKD治疗的潜在靶点。

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引用次数: 0

Mouse Alport podocytes are susceptible to AAV9 transduction in vivo 小鼠Alport足细胞在体内易受AAV9转导

IF 12.6 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2026-01-01 DOI: 10.1016/j.kint.2025.09.027

Meei-Hua Lin , Kohei Omachi , Joshua F. Begin , Jennifer L. Richardson , Jeffrey H. Miner

Introduction

Alport syndrome features a defective glomerular basement membrane (GBM) due to variants in COL4A3, COL4A4, and COL4A5. The most severe forms, which lack the GBM’s collagen α3α4α5(IV) network, progress from hematuria in early childhood to proteinuria, chronic kidney disease, and kidney failure by the age of ∼30. As a monogenic disease without specific treatments, and with podocytes being the only glomerular cells that synthesize collagen α3α4α5(IV), the ability to efficiently deliver genes to Alport podocytes could open up new possibilities for treatment.

Methods

As a proof-of-concept study, we investigated whether podocytes in X-linked Alport mice were susceptible to transduction by adeno-associated virus (AAV)9. ssAAV9-CAG-tdTomato and scAAV9-CMV-Cre were intravenously injected into Col4a5^-/y and Col4a5^-/y; Ai14 (Cre-activatable tdTomato) Alport mice, respectively. The kidneys were collected two weeks later and subjected to quantification of podocyte transduction by fluorescence assays using synaptopodin as a podocyte marker.

Results

ssAAV9-CAG-tdTomato delivered to controls failed to transduce podocytes, but heterozygous female and hemizygous male Alport podocytes showed a range of transduction efficiencies, from 1.8% to 26%, which correlated positively with levels of albuminuria. Similar correlation between podocyte transduction and albuminuria was observed in the more sensitive Ai14 system with scAAV9-CMV-Cre administration. A subset of tubular and mesangial cells could also be transduced, the former in Alport mice and the latter in both Alport and control mice.

Conclusions

The Alport GBM becomes leaky to AAV9 as mice mature, allowing viruses to reach and transduce a substantial subset of podocytes. This is promising for someday using AAV9 or other vehicles in gene therapy for patients with Alport syndrome. Interestingly, mesangial cells of control and young Alport mice were moderately susceptible to transduction, demonstrating that gene delivery to mesangial cells in mice is a viable approach for investigating mesangial cell biology in any context.

alport综合征的特点是由于COL4A3、COL4A4和COL4A5的变异导致肾小球基底膜（GBM）缺陷。最严重的形式，缺乏GBM的胶原α3α4α5（IV）网络，从儿童早期的血尿发展到蛋白尿、慢性肾脏疾病和30岁左右的肾衰竭。作为一种无特异性治疗的单基因疾病，足细胞是唯一能够合成胶原α3α4α5（IV）的肾小球细胞，将基因高效传递到Alport足细胞的能力为治疗开辟了新的可能性。方法作为一项概念验证性研究，我们研究了x连锁Alport小鼠足细胞是否易受腺相关病毒（AAV）9的转导。将ssAAV9-CAG-tdTomato和scAAV9-CMV-Cre静脉注射到Col4a5-/y和Col4a5-/y；Ai14 (crea -activatable tdTomato) Alport小鼠。两周后收集肾脏，用synaptopodin作为足细胞标记物，用荧光法定量测定足细胞转导。结果saav9 - cag - tdtomato不能转导足细胞，但杂合子雌性和半合子雄性Alport足细胞的转导效率在1.8% ~ 26%之间，与蛋白尿水平呈正相关。在给予scAAV9-CMV-Cre的更敏感的Ai14系统中，足细胞转导与蛋白尿之间也存在类似的相关性。小管细胞和系膜细胞的一部分也可以被转导，前者在Alport小鼠中，后者在Alport小鼠和对照小鼠中都可以被转导。结论随着小鼠成熟，Alport GBM会渗漏到AAV9，使病毒能够到达并转导大量足细胞。这很有希望在将来使用AAV9或其他载体对阿尔波特综合征患者进行基因治疗。有趣的是，对照小鼠和年轻Alport小鼠的系膜细胞对转导具有中度易感性，这表明基因传递到小鼠系膜细胞是在任何情况下研究系膜细胞生物学的可行方法。

{"title":"Mouse Alport podocytes are susceptible to AAV9 transduction in vivo","authors":"Meei-Hua Lin , Kohei Omachi , Joshua F. Begin , Jennifer L. Richardson , Jeffrey H. Miner","doi":"10.1016/j.kint.2025.09.027","DOIUrl":"10.1016/j.kint.2025.09.027","url":null,"abstract":"<div><h3>Introduction</h3><div>Alport syndrome features a defective glomerular basement membrane (GBM) due to variants in <em>COL4A3</em>, <em>COL4A4</em>, and <em>COL4A5</em>. The most severe forms, which lack the GBM’s collagen α3α4α5(IV) network, progress from hematuria in early childhood to proteinuria, chronic kidney disease, and kidney failure by the age of ∼30. As a monogenic disease without specific treatments, and with podocytes being the only glomerular cells that synthesize collagen α3α4α5(IV), the ability to efficiently deliver genes to Alport podocytes could open up new possibilities for treatment.</div></div><div><h3>Methods</h3><div>As a proof-of-concept study, we investigated whether podocytes in X-linked Alport mice were susceptible to transduction by adeno-associated virus (AAV)9. ssAAV9-CAG-tdTomato and scAAV9-CMV-Cre were intravenously injected into <em>Col4a5</em><sup><em>-/y</em></sup> and <em>Col4a5</em><sup><em>-/y</em></sup>; Ai14 (Cre-activatable tdTomato) Alport mice, respectively. The kidneys were collected two weeks later and subjected to quantification of podocyte transduction by fluorescence assays using synaptopodin as a podocyte marker.</div></div><div><h3>Results</h3><div>ssAAV9-CAG-tdTomato delivered to controls failed to transduce podocytes, but heterozygous female and hemizygous male Alport podocytes showed a range of transduction efficiencies, from 1.8% to 26%, which correlated positively with levels of albuminuria. Similar correlation between podocyte transduction and albuminuria was observed in the more sensitive Ai14 system with scAAV9-CMV-Cre administration. A subset of tubular and mesangial cells could also be transduced, the former in Alport mice and the latter in both Alport and control mice.</div></div><div><h3>Conclusions</h3><div>The Alport GBM becomes leaky to AAV9 as mice mature, allowing viruses to reach and transduce a substantial subset of podocytes. This is promising for someday using AAV9 or other vehicles in gene therapy for patients with Alport syndrome. Interestingly, mesangial cells of control and young Alport mice were moderately susceptible to transduction, demonstrating that gene delivery to mesangial cells in mice is a viable approach for investigating mesangial cell biology in any context.</div></div>","PeriodicalId":17801,"journal":{"name":"Kidney international","volume":"109 1","pages":"Pages 129-138"},"PeriodicalIF":12.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145412272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanistic insights from transcript analysis of long-term pig to non-human primate kidney xenografts. 从长期猪到非人灵长类动物肾脏异种移植的转录物分析的机制见解。

IF 12.6 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-12-30 DOI: 10.1016/j.kint.2025.11.018

Ivy A Rosales, Alessia Giarraputo, Claire Trivin-Avillach, Ahmad Karadagi, Christina Laguerre, Toru Goto, Jeremy Marcin, Nicole Brousaides, Tatsuo Kawai, Robert B Colvin

Introduction: Porcine xenografts are a potential future organ source. Limited short-term clinical studies have suggested different mechanisms in xenografts than allografts. Here, we sought further insights from transcript analysis of xenografts in non-human primates that achieved up to two years of survival.

Methods: Transcript analysis was performed on 58 samples from eGenesis pig kidney xenografts in Cynomolgus monkeys, including donor, post-perfusion, protocol, and terminal samples, using the Banff Human Organ Transplant panel, supplemented with 35 pig specific probes. Glomerular regions of interest in donor and terminal samples were analyzed using the GeoMx Immune Pathways Panel and 10 custom probes. Antibodies that distinguish donor and recipient molecules were used to confirm protein expression.

Results: Protocol biopsies with no histologic evidence of rejection had a marked rise in CD45 transcripts compared with donor samples, similar to CD45 levels in stable human allografts that did not portend rejection. Terminal samples showed increases in antibody and T cell mediated rejection gene sets and prominence of alternatively activated macrophages. Reduction of VEGFA transcripts correlated with transplant glomerulopathy and glomerular thrombotic microangiopathy and was localized to glomeruli by spatial transcriptomics. Loss of donor and gain of recipient endothelial transcripts were detected in the graft, with widespread expression of recipient PECAM1, vWF, and MHC class I and II proteins in xenograft endothelium.

Conclusions: Marked transcript elevation occurred in stable grafts probably due to repopulation by recipient leukocytes. VEGFA loss in podocytes preceded and potentially contributed to thrombotic microangiopathy. Loss of donor endothelial transcripts contrasts with antibody mediated rejection in allografts. Unexpected gain of recipient endothelial transcripts and proteins was shown, a novel process detected in the xenograft.

猪异种移植是未来潜在的器官来源。有限的短期临床研究表明异种移植物与同种异体移植物的机制不同。在这里，我们从非人类灵长类动物的异种移植物的转录本分析中寻求进一步的见解，这些移植物的存活率高达两年。方法：使用Banff人类器官移植面板，并辅以35个猪特异性探针，对58份eGenesis猪肾异种移植食食猴样本进行转录分析，包括供体样本、灌注后样本、方案样本和终端样本。使用GeoMx免疫途径小组和10个定制探针分析供体和终末样品的肾小球感兴趣区域。区分供体和受体分子的抗体被用来确认蛋白质的表达。结果：与供体样本相比，没有组织学排斥证据的方案活检的CD45转录本明显上升，类似于稳定的人类同种异体移植物的CD45水平，没有预示排斥。终端样品显示抗体和T细胞介导的排斥基因组增加，选择性活化的巨噬细胞突出。VEGFA转录物的减少与移植肾小球病变和肾小球血栓性微血管病相关，并通过空间转录组学定位于肾小球。在移植物中检测到供体内皮转录本的缺失和受体内皮转录本的获得，受体PECAM1、vWF和MHC I类和II类蛋白在异种移植物内皮中广泛表达。结论：稳定移植物中转录物显著升高可能是由于受体白细胞的再增殖。足细胞中VEGFA的缺失先于血栓性微血管病变，并可能导致血栓性微血管病变。同种异体移植中供体内皮转录物的丢失与抗体介导的排斥反应不同。受体内皮转录本和蛋白质的意外增益显示，在异种移植物中检测到一个新的过程。

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引用次数: 0

Key drivers and potential therapeutic targets in the AKI-to-CKD transition: roles of kidney-resident macrophages and neutrophils. aki向ckd转变的关键驱动因素和潜在治疗靶点：肾内巨噬细胞和中性粒细胞的作用。

IF 12.6 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-12-30 DOI: 10.1016/j.kint.2025.12.018

Kensei Taguchi, Kei Fukami

引用次数: 0

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