Lai Kar Neng, Tang Sydney C W, Leung Joseph C K
Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, SAR, China.
Adv Otorhinolaryngol. 2011;72:40-4. doi: 10.1159/000324593. Epub 2011 Aug 18.
IgA nephropathy (IgAN) is characterized by mesangial deposition of pathogenic polymeric IgA1 with rare deposits in the tubular epithelial cells (TEC). Recently, a novel mechanism involving a glomerulopodocytictubular cross-talk in the development of tubulointerstitial damage in IgAN has been revealed. Podocytes are positioned strategically along the glomerulotubular axis and plays an important role in mediating the glomerulotubular cross-talk. In IgAN, podocyte markers are reduced in the glomeruli. In vitro study implicates humoral factors (predominantly tumor necrosis factor-α and transforming growth factor-β) released from mesangial cells alter the glomerular permeability in the event of proteinuria and tubulointerstitial injury in IgAN. These mediators released from mesangial cells after IgA deposition further activate TEC leading to subsequent inflammatory changes in the renal tubulointerstitium.
IgA肾病（IgAN）的特征是致病性聚合IgA1在系膜沉积，在肾小管上皮细胞（TEC）中沉积罕见。最近，一种涉及IgAN肾小管间质损伤发展过程中肾小球足细胞-肾小管相互作用的新机制已被揭示。足细胞沿肾小球-肾小管轴呈战略性定位，在介导肾小球-肾小管相互作用中起重要作用。在IgAN中，肾小球中足细胞标志物减少。体外研究表明，系膜细胞释放的体液因子（主要是肿瘤坏死因子-α和转化生长因子-β）在IgAN出现蛋白尿和肾小管间质损伤时会改变肾小球通透性。IgA沉积后系膜细胞释放的这些介质进一步激活肾小管上皮细胞，导致肾小管间质随后发生炎症变化。
