高风险膜性肾病应首选抗CD20治疗。
Anti-CD20 should be the first-line treatment in high-risk membranous nephropathy.
发表日期:2023 Sep
作者:
Ladan Zand, Fernando C Fervenza
来源:
Clinical Kidney Journal
摘要:
膜性肾病(MN)是成人肾病综合征(NS)的常见原因,如果不治疗,可以进展为终末期肾脏病。被认为使患者处于高或非常高进展风险的因素包括基线时血清肌酐升高、肾功能下降、持续的重度蛋白尿(>8 g/24 h)或持续的NS、与NS相关的威胁生命的并发症(如静脉血栓栓塞事件)或非常高的抗-PLA2R抗体滴度(>150 RU/ml)。应对高或非常高进展风险的患者进行免疫抑制疗法治疗,以诱导蛋白尿缓解并避免肾功能逐渐丧失。传统的MN患者免疫抑制治疗包括使用波动疗程的皮质类固醇与环磷酰胺或钙调素酶抑制剂。这些治疗方式与显著的毒性相关,例如皮质类固醇(感染、糖尿病、体重增加)、环磷酰胺(不育、严重白细胞减少、恶性肿瘤)和钙调素酶抑制剂(高血压、肾毒性)。20世纪90年代末引入的抗CD20+ B细胞疗法改变了局面。在本文中,我们将主张在考虑到其疗效和副作用配置时,抗CD20+ B疗法应成为高/非常高进展风险的患者的首选治疗方案。© 2023年作者发表。由牛津大学出版社代表ERA发表。
Membranous nephropathy (MN) is a common cause of nephrotic syndrome (NS) in adults and if untreated can progress to endstage kidney disease. Factors considered to place a patient at high or very high risk for progression include elevated serum creatinine at baseline, declining kidney function, persistent heavy proteinuria (>8 g/24 h), or persistent NS, presence of life-threatening complications related to NS (such as venous thromboembolic events), or very high anti-PLA2R antibody titers (>150 RU/ml). Patients who are at high or very high risk of progression should be treated with immunosuppression therapy to induce remission of proteinuria and to avoid progressive loss of kidney function. Traditional forms of immunosuppression for patients with MN have included the use of cyclic courses of corticosteroids with cyclophosphamide or calcineurin inhibitors. These forms of therapy are associated with significant toxicity, e.g. corticosteroids (infections, diabetes, weight gain), cyclophosphamide (infertility, severe leukopenia, malignancy), and calcineurin inhibitors (hypertension, nephrotoxicity). The introduction of anti-CD20+ B-cell therapies in the late 1990s has changed the landscape. In this article we will argue that anti-CD20+ B therapy should be the treatment of choice for patients at high/very high risk of progression when considering its efficacy and side-effect profile.© The Author(s) 2023. Published by Oxford University Press on behalf of the ERA.