Kidney international最新文献

英文中文

A kidney organoid-based readout to assess disease activity in primary and recurrent focal segmental glomerulosclerosis.

IF 14.8 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-02-04 DOI: 10.1016/j.kint.2025.01.018

Ashwani Kumar Gupta, Ekta Minocha, Kyle M Koss, Bilal A Naved, Luisa Safar-Boueri, Jason A Wertheim, Lorenzo Gallon

Primary Focal Segmental Glomerulosclerosis (pFSGS) is an acquired kidney disorder that frequently leads to kidney failure and confers an elevated risk of recurrence after kidney transplantation, termed recurrent pFSGS. Unfortunately, there is no diagnostic method to foresee recurrence of pFSGS after kidney transplantation. Progress in developing assays to test disease activity is hampered by few preclinical models to replicate disease and inability of in vitro cultured primary podocytes to remain terminally differentiated. In recent years, advancements in kidney organoid biology have led to the development of kidney tissues with glomeruli and major nephron segments including podocytes. To develop a pFSGS model, we studied the effect of plasma from patients diagnosed with pFSGS on kidney organoids differentiated from human pluripotent stem cells. The pFSGS plasma treatment induced podocytopathy, extracellular matrix protein deposition, fibrosis and apoptosis within organoids, whereas non-recurrent plasma did not affect organoid structure. pFSGS plasma also led to loss of normal expression patterns of podocyte specific proteins, nephrin and podocin within podocytes. Further, cytokine array profiling revealed that pFSGS plasma induced secretion of cytokines associated with inflammation and angiogenesis. Additionally, kidney organoids treated with plasma obtained after therapeutic plasma exchange for recurrent pFSGS led to lower cell death in organoids after sequential exchanges with the final exchange showing the least apoptotic cells without morphological abnormality. Overall, our results demonstrate the potential of kidney organoids in advancing kidney disease modeling. These insights could be applied in clinical settings to assist in gauging FSGS recurrence risk prior to kidney transplantation.

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Prenatal and preimplantation genetic testing for monogenic kidney disorders 单基因肾脏疾病的产前和植入前检测。

IF 14.8 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-02-01 DOI: 10.1016/j.kint.2024.06.031

Nine V.A.M. Knoers

In recent years, advances in genetic sequencing techniques and in the analysis of sequencing data have significantly improved our ability to diagnose genetic kidney diseases. Identification of the disease-causing genetic variant(s) is crucial not only for prognostication and personalized management, but also for providing genetic counseling and guiding family planning decisions. It is particularly important that patients desiring children receive advice on their reproductive choices early, ideally before conception. This concise review focuses on the options available for prenatal and preimplantation genetic testing in the context of monogenic kidney diseases, including the latest progress and the legal and ethical issues associated with these reproductive technologies. Although these tests could be performed for all monogenic disorders where the disease-causing variant(s) has (have) been identified in the index patient, invasive prenatal testing is currently primarily performed for severe childhood-onset monogenic kidney disorders. Noninvasive prenatal diagnosis for monogenic disorders is a rapidly developing field that promises to provide an accurate and acceptable alternative to invasive procedures once several technical challenges have been addressed. Preimplantation genetic testing allows for the selection and implantation of embryos free from the disease-causing genetic variants, significantly lowering the risk of affected pregnancies. This option is becoming more popular among individuals with monogenic kidney diseases, particularly those with disorders that manifest later in life, such as autosomal dominant polycystic kidney disease. This review covers the procedure, its outcomes, and the technical, ethical and legal challenges of preimplantation genetic testing for monogenic kidney diseases.

近年来，基因测序技术和测序数据分析的进步大大提高了我们诊断遗传性肾脏疾病的能力。确定致病基因变异不仅对预后和个性化管理至关重要，而且对提供遗传咨询和指导计划生育决策也至关重要。尤其重要的是，希望生育的患者应尽早获得有关生育选择的建议，最好是在受孕之前。这篇简明综述重点介绍了单基因肾病产前和植入前基因检测的可选方案，包括最新进展以及与这些生殖技术相关的法律和伦理问题。虽然这些检测可用于所有已在指标患者中发现致病变异体的单基因疾病，但目前有创产前检测主要用于严重的儿童期单基因肾脏疾病。单基因遗传病的无创产前诊断是一个快速发展的领域，一旦一些技术难题得到解决，有望为有创产前诊断提供准确、可接受的替代方案。植入前基因检测可以选择和植入不含致病基因变异的胚胎，从而大大降低受影响妊娠的风险。这种方法越来越受到单基因肾病患者的青睐，尤其是那些晚期表现的疾病，如常染色体显性多囊肾。这篇综述涵盖了单基因肾病植入前基因检测的程序、结果以及技术、伦理和法律方面的挑战。

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When two signals cross paths: cGAS-STING and ER stress in kidney disease progression

IF 14.8 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-02-01 DOI: 10.1016/j.kint.2024.11.023

Ryo Yamada , Motoko Yanagita

Previous reports have suggested that both the endoplasmic reticulum (ER) stress and cyclic guanosine monophosphate–adenosine monophosphate synthase–stimulator of interferon genes pathways contribute to the progression of chronic kidney disease; however, the relationship between these 2 pathways in kidney injury has not been fully elucidated. Andrade-Silva et al. revealed that the cyclic guanosine monophosphate–adenosine monophosphate synthase–stimulator of interferon genes pathway can enhance ER stress through the protein kinase R-like ER kinase (PERK)–mediated signaling cascade in kidney tubular epithelial cells and sequentially augment fibrosis during kidney injury. Further studies are needed to elucidate the precise mechanisms by which the cyclic guanosine monophosphate–adenosine monophosphate synthase–stimulator of interferon genes pathway activates PERK-dependent ER stress in kidney tubular epithelial cells post injury.

引用次数: 0

KDIGO 2025 clinical practice guideline for the evaluation, management, and treatment of autosomal dominant polycystic kidney disease (ADPKD): executive summary

IF 14.8 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-02-01 DOI: 10.1016/j.kint.2024.07.010

Vicente E. Torres , Curie Ahn , Thijs R.M. Barten , Godela Brosnahan , Melissa A. Cadnapaphornchai , Arlene B. Chapman , Emilie Cornec-Le Gall , Joost P.H. Drenth , Ron T. Gansevoort , Peter C. Harris , Tess Harris , Shigeo Horie , Max C. Liebau , Michele Liew , Andrew J. Mallett , Changlin Mei , Djalila Mekahli , Dwight Odland , Albert C.M. Ong , Luiz F. Onuchic , Olivier Devuyst

The Kidney Disease: Improving Global Outcomes (KDIGO) 2025 Clinical Practice Guideline for the Evaluation, Management, and Treatment of Autosomal Dominant Polycystic Kidney Disease (ADPKD) represents the first KDIGO guideline on this subject. Its scope includes nomenclature, diagnosis, prognosis, and prevalence; kidney manifestations; chronic kidney disease (CKD) management and progression, kidney failure, and kidney replacement therapy; therapies to delay progression of kidney disease; polycystic liver disease; intracranial aneurysms and other extrarenal manifestations; lifestyle and psychosocial aspects; pregnancy and reproductive issues; pediatric issues; and approaches to the management of people with ADPKD. The guideline has been developed with patient partners, clinicians, 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 a rigorous, formal systematic literature review. The strength of recommendations follows the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. The guideline also provides practice points serving to direct clinical care or activities relating to areas for which a systematic review was not conducted. 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, people living with ADPKD, and stakeholders involved in the various aspects of ADPKD care.

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引用次数: 0

KDIGO 2025 Clinical Practice Guideline for the Evaluation, Management, and Treatment of Autosomal Dominant Polycystic Kidney Disease (ADPKD)

IF 14.8 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-02-01 DOI: 10.1016/j.kint.2024.07.009

引用次数: 0

PI3Kα in the pathogenesis and treatment of lupus nephritis 狼疮肾炎发病机制和治疗中的 PI3Kα

IF 14.8 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-02-01 DOI: 10.1016/j.kint.2024.11.004

Vivek Kasinath , George C. Tsokos

引用次数: 0

Challenges in maturation and integration of kidney organoids for stem cell–based renal replacement therapy 基于干细胞的肾脏替代疗法中肾脏器官组织的成熟和整合所面临的挑战。

IF 14.8 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-02-01 DOI: 10.1016/j.kint.2024.10.028

Cathelijne W. van den Berg , Sébastien J. Dumas , Melissa H. Little , Ton J. Rabelink

Human pluripotent stem cell–derived kidney organoids hold promise for future applications in regenerative medicine. However, significant biological hurdles need to be overcome to enable their use as a transplantable stem cell–derived therapeutic graft. Current kidney organoid protocols do not recapitulate a complete integrated developing kidney, but embryonic kidney transplantations have provided clues for advancing maturation and functionality of kidney organoids. Transplantation, subsequent vascularization, and blood perfusion of kidney organoids improve nephron patterning and maturation, suggesting a role for angiocrine factors as well as metabolic wiring in these processes. Transplanted organoids exhibit filtration, but the resulting filtrate has no apparent exit path for excretion. Improved in vitro patterning of kidney organoids may be required such that a more structurally correct tissue is formed before transplant. Here we review current progress with transplantation of kidney organoids, as well as their engraftment and integration, and identify the key obstacles to therapeutic success and how these might be achieved.

人类多能干细胞衍生的肾脏器官组织有望在未来的再生医学中得到应用。然而，要将其用作可移植的干细胞衍生治疗移植物，还需要克服重大的生物学障碍。目前的肾脏类器官方案不能再现完整的综合发育肾脏，但胚胎肾脏移植为促进肾脏类器官的成熟和功能提供了线索。移植后，肾脏器官组织的血管化和血液灌注改善了肾小球的形态和成熟，这表明血管内分泌因子和代谢线路在这些过程中发挥了作用。移植的器官组织具有过滤功能，但所产生的滤液没有明显的排泄途径。可能需要改进肾脏器官组织的体外模式，以便在移植前形成结构更正确的组织。在此，我们回顾了肾脏类器官移植、其移植和整合的当前进展，并指出了治疗成功的关键障碍以及如何实现这些障碍。

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The authors reply

IF 14.8 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-02-01 DOI: 10.1016/j.kint.2024.11.010

Yoshio Funahashi , Seung Hun Park , Jessica F. Hebert , Mahaba B. Eiwaz , Adam C. Munhall , Tahnee Groat , Lingxue Zeng , Jonghan Kim , Hak Soo Choi , Michael P. Hutchens

引用次数: 0

The autoimmune architecture of childhood idiopathic nephrotic syndrome 儿童特发性肾病综合征的自身免疫结构。

IF 14.8 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-02-01 DOI: 10.1016/j.kint.2024.10.027

Tho-Alfakar Al-Aubodah , Ciriaco A. Piccirillo , Howard Trachtman , Tomoko Takano

Idiopathic nephrotic syndrome, the most common glomerular disorder in children, has long been considered an immune-mediated disease based on the efficacy of glucocorticoids at inducing remission. Nevertheless, the immune processes leading to podocytopathy have largely remained elusive. The success of B-cell depletion with rituximab, descriptions of B-cell dysregulation during active disease, and the most recent discovery of autoantibodies targeting the major podocyte antigen nephrin point to an autoimmune humoral etiology for idiopathic nephrotic syndrome. Investigations of the immune factors involved in idiopathic nephrotic syndrome pathogenesis have uncovered common features with other autoimmune disorders that will aid in prognostication and in guiding the expansion of our glucocorticoid-sparing therapeutic arsenal. In this review, we discuss the emerging autoimmune architecture of idiopathic nephrotic syndrome, with a specific focus on pediatric steroid-sensitive disease, including the podocyte-reactive B-cell response that causes anti-podocyte antibodies, the predisposing genetic factors that shape the podocyte-reactive immune landscape, and the immune triggers driving active disease.

特发性肾病综合征（INS）是儿童中最常见的肾小球疾病，长期以来一直被认为是一种免疫介导的疾病，因为糖皮质激素能有效诱导病情缓解。然而，导致荚膜细胞病变的免疫过程在很大程度上仍然难以捉摸。利妥昔单抗成功地清除了 B 细胞，描述了疾病活动期 B 细胞失调的情况，以及最近发现的针对主要荚膜抗原 Nephrin 的自身抗体，都表明 INS 的病因是自身免疫体液病。对参与 INS 发病机制的免疫因素的研究发现了 INS 与其他自身免疫性疾病的共同特征，这将有助于预后判断，并指导我们扩大糖皮质激素节约型疗法的范围。在这篇综述中，我们将讨论 INS 新出现的自身免疫结构，特别关注儿科类固醇敏感性疾病，包括引起抗荚膜细胞抗体 (APA) 的荚膜细胞反应性 B 细胞反应、形成荚膜细胞反应性免疫结构的易感遗传因素以及驱动活动性疾病的免疫诱因。

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IF 14.8 1区医学 Q1 UROLOGY & NEPHROLOGY

Kidney international

Pub Date : 2025-02-01 DOI: 10.1016/j.kint.2024.11.024

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