School of Science & Technology, University of New England, NSW, Australia.
Department of Surgery and Obstetrics, Faculty of Veterinary Science, Bangladesh Agricultural University, Mymensingh, Bangladesh.
Pathog Dis. 2024 Feb 7;82. doi: 10.1093/femspd/ftae024.
Post-streptococcal glomerulonephritis (PSGN) is primarily associated with preceding group A streptococcal skin or throat infections, now mainly observed in economically disadvantaged communities. This condition significantly predisposes individuals to later-life chronic kidney disease and concurrent renal complications, with the elderly experiencing increased severity and less favourable outcomes. Streptococcal pyrogenic exotoxin B and nephritis-associated plasmin receptor are identified nephritogenic antigens (nephritogens). Pathogenesis of PSGN is multifactorial. It can involve the formation of antigen-antibody immune complexes, causing inflammatory damage to renal glomeruli. Deposition of circulating immune complexes or in situ formation of immune complexes in glomeruli, or both, results in glomerulonephritis. Additionally, molecular mimicry is hypothesized as a mechanism, wherein cross-reactivity between anti-streptococcal antibodies and glomerular intrinsic matrix proteins leads to glomerulonephritis. Besides, as observed in clinical studies, streptococcal inhibitor of complement, a streptococcal-secreted protein, can also be associated with PSGN. However, the interplay between these streptococcal antigens in the pathogenesis of PSGN necessitates further investigation. Despite the clinical significance of PSGN, the lack of credible animal models poses challenges in understanding the association between streptococcal antigens and the disease process. This review outlines the postulated mechanisms implicated in the development of PSGN with possible therapeutic approaches.
链球菌后肾小球肾炎 (PSGN) 主要与 A 组链球菌皮肤或咽喉感染有关，现在主要发生在经济条件较差的社区。这种情况使个体极易在以后的生活中患上慢性肾病和并发的肾脏并发症，老年人的病情更严重，预后更差。链球菌致热外毒素 B 和肾炎相关纤溶酶受体被鉴定为致肾炎抗原（肾炎原）。PSGN 的发病机制是多因素的。它可能涉及抗原抗体免疫复合物的形成，导致肾脏肾小球的炎症损伤。循环免疫复合物的沉积或原位形成免疫复合物，或两者兼而有之，导致肾小球肾炎。此外，分子模拟被认为是一种机制，其中抗链球菌抗体与肾小球固有基质蛋白之间的交叉反应导致肾小球肾炎。此外，正如临床研究中观察到的，链球菌补体抑制剂，一种链球菌分泌的蛋白，也与 PSGN 有关。然而，这些链球菌抗原在 PSGN 发病机制中的相互作用需要进一步研究。尽管 PSGN 具有临床意义，但缺乏可靠的动物模型使得难以理解链球菌抗原与疾病过程之间的关系。这篇综述概述了 PSGN 发展中涉及的假定机制，并提出了可能的治疗方法。
