Kriz Wilhelm
lnstitut für Anatomie and Zellbiologle, Universität Heidelberg, Heidelberg, Germany.
Nephrol Dial Transplant. 2003 Aug;18 Suppl 6:vi39-44. doi: 10.1093/ndt/gfg1064.
The present paper summarizes the evidence for the hypothesis that the development of focal segmental glomerulosclerosis (FSGS-'classic' type) is initiated and maintained by injury to podocytes. Loss of podocytes leads to the formation of tuft adhesions to Bowman's capsule, followed-with a certain probability-by misdirected filtration. This leads to a sequence of events resulting in degeneration of the entire nephron. The way by which the nephron undergoes destruction in this process assures that the destructive effects remain confined to the initially affected nephron. There is no nephron-to-nephron transfer of the disease at the level of the tubular interstitium.
局灶节段性肾小球硬化（“经典”型）的发生和维持是由足细胞损伤引发和推动的。足细胞的丢失导致肾小球毛细血管袢与鲍曼囊粘连，随后在一定概率下会出现滤过方向错误。这会引发一系列事件，导致整个肾单位退化。在此过程中肾单位遭到破坏的方式确保了破坏作用局限于最初受影响的肾单位。在肾小管间质水平不存在疾病在肾单位之间的转移。
