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具有肾脏意义的克隆性单核细胞增多症。

Clonal monocytosis of renal significance.

发表日期:2024 Sep 18
作者: Anuya A Natu, Ishan Gupta, Nelson Leung, Mariam P Alexander, Mrinal M Patnaik
来源: KIDNEY INTERNATIONAL

摘要:

克隆性单核细胞增多反映了在没有反应性原因的情况下绝对单核细胞计数的肿瘤前或肿瘤持续增加。克隆性单核细胞增多症的原因包括伴有单核细胞增多症的克隆性血细胞减少症以及急性和慢性骨髓肿瘤。慢性粒单核细胞白血病是成人中典型的骨髓增生异常/骨髓增殖性重叠肿​​瘤,其特征是持续的外周血单核细胞增多。肾脏异常,包括急性肾损伤和慢性肾脏疾病,在慢性粒单核细胞白血病患者中很常见,并且是更糟糕结果的预测因素。此外,急性肾损伤/慢性肾病常常限制同种异体干细胞移植或临床试验招募的资格。在这篇综述中,我们重点介绍了导致急性肾损伤和慢性肾脏疾病的克隆单核细胞增多症相关病因,特别强调慢性粒单核细胞白血病和溶菌酶诱导的肾病。单核细胞产生溶菌酶,过量时会积聚并损伤近端肾小管上皮。及早识别病因并及时减少单核细胞计数可以挽救肾功能。与克隆性单核细胞增多症相关的肾损伤的其他病因包括单核细胞直接肾浸润、肾髓外造血、骨髓增生性肿瘤相关性肾小球病、自身免疫性(膜性肾病、微小病变)和副肿瘤表现、血栓性微血管病、骨髓增生引起的梗阻性肾病和尿酸盐肿瘤溶解综合征引起的肾病。我们建议将这些肾损伤的机制病因归为具有肾脏意义的克隆性单核细胞增多症,并为其诊断和治疗提供指导。版权所有 © 2024 国际肾病学会。由爱思唯尔公司出版。保留所有权利。
Clonal monocytosis reflects a preneoplastic or neoplastic sustained increase in the absolute monocyte count in the absence of reactive causes. Causes of clonal monocytosis include clonal cytopenias with monocytosis and acute and chronic myeloid neoplasms. Chronic myelomonocytic leukemia is a prototypical myelodysplastic/myeloproliferative overlap neoplasm in adults, characterized by sustained peripheral blood monocytosis. Renal abnormalities, including acute kidney injury and chronic kidney disease, are frequent in patients with chronic myelomonocytic leukemia and are predictors of worse outcomes. In addition, acute kidney injury/chronic kidney disease often limits eligibility for allogeneic stem cell transplantation or enrollment in clinical trials. In this review, we highlight clonal monocytosis-related etiologies that give rise to acute kidney injury and chronic kidney disease, with special emphasis on chronic myelomonocytic leukemia and lysozyme-induced nephropathy. Monocytes produce lysozyme, which, in excess, can accumulate in and damage the proximal renal tubular epithelium. Early identification of this etiology and a timely reduction in monocyte counts can salvage renal function. Other etiologies of renal injury associated with clonal monocytosis include direct renal infiltration by monocytes, renal extramedullary hematopoiesis, myeloproliferative neoplasm-associated glomerulopathy, autoimmune (membranous nephropathy, minimal change disease) and paraneoplastic manifestations, thrombotic microangiopathy, obstructive nephropathy due to myeloproliferation, and urate nephropathy due to tumor lysis syndrome. We propose to group these mechanistic etiologies of renal injury as clonal monocytosis of renal significance and provide guidance on their diagnosis and management.Copyright © 2024 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.