Zununi Vahed Sepideh, Hosseiniyan Khatibi Seyed Mahdi, Ardalan Mohammadreza
Kidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Med Res Rev. 2025 Jan;45(1):144-163. doi: 10.1002/med.22074. Epub 2024 Aug 20.
Glomerulonephritis (GN) is an important cause of renal inflammation resulting from kidney-targeted adaptive and innate immune responses and consequent glomerular damage. Given the lack of autoantibodies, immune complexes, or the infiltrating immune cells in some forms of GN, for example, focal segmental glomerulosclerosis and minimal change disease, along with paraneoplastic syndrome and a special form of renal involvement in some viral infections, the likeliest causative scenario would be secreted factors, mainly cytokine(s). Since cytokines can modulate the inflammatory mechanisms, severity, and clinical outcomes of GN, it is rational to consider the umbrella term of cytokine GN as a new outlook to reclassify a group of previously known GN. We focus here, particularly, on cytokines that have the central "canonical effect" in the development of GN.
肾小球肾炎（GN）是由针对肾脏的适应性和先天性免疫反应以及随之而来的肾小球损伤导致的肾脏炎症的重要原因。鉴于在某些形式的GN（例如局灶节段性肾小球硬化症和微小病变病）中缺乏自身抗体、免疫复合物或浸润性免疫细胞，以及副肿瘤综合征和某些病毒感染中肾脏受累的特殊形式，最可能的致病情况是分泌因子，主要是细胞因子。由于细胞因子可以调节GN的炎症机制、严重程度和临床结果，因此将细胞因子性GN这一统称作为重新分类一组先前已知的GN的新观点是合理的。我们在此特别关注在GN发展过程中具有核心“典型效应”的细胞因子。
