Editorial
Copyright ©The Author(s) 2015.
World J Nephrol. Nov 6, 2015; 4(5): 487-491
Published online Nov 6, 2015. doi: 10.5527/wjn.v4.i5.487
Figure 1
Figure 1 Graft injury and clinical presentation after development of de novo donor specific antibody. The pathologic injury of ABMR starts from microvascular inflammation, including peritubular capillaritis, C4d staining in allograft, and glomerulitis, to interstitial fibrosis/tubular atrophy (IF/TA) and transplant glomerulopathy (TG). GFR: Glomerular filtration rate; ABMR: Antibody mediated rejection; DSA: Donor specific antibody.
Figure 2
Figure 2 Comparing the mechanism of acute tubular necrosis and rejection. The rejection causes tubular damage similar to ATN but lymphocytes infiltration can leads to elevation of urinary IP-10 in rejection. ATN: Acute tubular necrosis; Cr: Creatinine; IP-10: Interferon-gamma induced protein of 10 kDa.