Tareev Clinic, Department of Nephrology, Sechenov First Moscow State Medical University, Moscow, Russia.
Adv Exp Med Biol. 2021;1306:81-99. doi: 10.1007/978-3-030-63908-2_6.
Chronic glomerulonephritis (CGN) is a disease with a steady progressive course that involves the development of nephrosclerosis, which is especially evident in clinical courses with incidences of high proteinuria (PU). Currently, proteinuria is considered the main laboratory feature (sign) of CGN activity and progression because proteinuria is closely related to the process of tubulointerstitial fibrosis, which is correlated with the grade of renal insufficiency. The injury to podocytes, which are key components of the filtration barrier, plays a central role in proteinuria development. The detachment of podocytes from the glomerular basement membrane leading to podocytopenia is suggested to induce glomerulosclerosis and hyalinosis with obliteration of capillary loops and the progression of chronic kidney disease. Urinary markers of podocyte dysfunction could serve as useful tools while monitoring the activity and prognosis of CGN. In this chapter, the most important mechanisms of podocyte loss and urinary markers of this process are discussed.
慢性肾小球肾炎 (CGN) 是一种进行性疾病，涉及肾硬化的发展，在蛋白尿 (PU) 发生率高的临床病程中尤为明显。目前，蛋白尿被认为是 CGN 活动和进展的主要实验室特征（迹象），因为蛋白尿与肾小管间质纤维化过程密切相关，而肾小管间质纤维化与肾功能不全的程度相关。足细胞是滤过屏障的关键组成部分，其损伤在蛋白尿的发展中起着核心作用。足细胞从肾小球基底膜脱落导致足细胞减少，被认为会导致肾小球硬化和玻璃样变，毛细血管袢闭塞，并导致慢性肾脏病的进展。足细胞功能障碍的尿标志物可以作为监测 CGN 活动和预后的有用工具。在本章中，讨论了足细胞丢失的最重要机制及其过程的尿标志物。
