Arizona Kidney Disease and Hypertension Center, 4511 North Campbell Avenue, Suite 100, Tucson, AZ 85718, USA.
Nat Rev Nephrol. 2011 Feb;7(2):85-95. doi: 10.1038/nrneph.2010.171. Epub 2010 Dec 14.
Paraneoplastic glomerulonephritis is a rare complication of malignancy that is frequently mistaken for idiopathic glomerulonephritis. Failure to recognize paraneoplastic glomerulonephritis can subject patients to ineffective and potentially harmful therapy. The pathology of paraneoplastic glomerulonephritis varies between different types of malignancies. This Review discusses the association of glomerulonephritis with both solid tumors and hematological malignancies. The pathogenetic mechanisms of many glomerular lesions seem to relate to altered immune responses in the presence of a malignancy. Studies in the Buffalo/Mna rat model of spontaneous thymoma and nephrotic syndrome indicate that polarization of the immune response toward a T-helper-2 (T(H)2) profile has an important role in the development of thymoma-associated glomerular lesions. Furthermore, overexpression of the T(H)2 cytokine interleukin 13 in rats induces minimal change disease. Such findings from experimental studies might facilitate the identification of biomarkers that can distinguish paraneoplastic glomerulonephritis from idiopathic and other secondary glomerulonephritides. This Review describes potential pathogenetic mechanisms for paraneoplastic glomerulonephritides associated with different malignancies and highlights the need for a multidisciplinary approach to the management of patients with paraneoplastic glomerulonephritis.
副肿瘤性肾小球肾炎是一种罕见的恶性肿瘤并发症，常被误诊为特发性肾小球肾炎。未能识别副肿瘤性肾小球肾炎可能导致患者接受无效且潜在有害的治疗。不同类型恶性肿瘤的副肿瘤性肾小球肾炎的病理学表现有所不同。这篇综述讨论了肾小球肾炎与实体瘤和血液恶性肿瘤的关联。许多肾小球病变的发病机制似乎与恶性肿瘤存在时改变的免疫反应有关。在自发性胸腺瘤和肾病综合征的布法罗/Mna 大鼠模型中的研究表明，免疫反应向辅助性 T 细胞 2（T(H)2）表型的极化在胸腺瘤相关肾小球病变的发展中起着重要作用。此外，在大鼠中过表达 T(H)2 细胞因子白细胞介素 13 可诱导微小病变性疾病。这些来自实验研究的发现可能有助于确定能够将副肿瘤性肾小球肾炎与特发性和其他继发性肾小球肾炎区分开来的生物标志物。本综述描述了与不同恶性肿瘤相关的副肿瘤性肾小球肾炎的潜在发病机制，并强调了需要对副肿瘤性肾小球肾炎患者进行多学科管理。
