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See Latest ArticlesTubulointerstitial nephritis without glomerular lesions in three patients with myeloperoxidase-ANCA-associated vasculitis
Clinical and Experimental Nephrology, 06/11/09
Nakabayashi K et al. - Based on the findings, the loss of CD34 vascular endothelial markers occurs in the early phase of the disease because of the MPO, which is presumed to have burst out from the infiltrated, activated neutrophils. This MPO, which releases proteolytic enzymes and radical oxygen species, acts on tissue destruction, namely the lysis of endothelial cell membranes as well as vascular basement membranes in the peritubular capillary. This mechanism eventually proceeds to the destruction of the peritubular capillary walls (vasculitis). This pathogenesis is thought to play an important role in the pathogenesis of TI nephritis, which is associated with MPO–ANCA vasculitis.
Kimimasa Nakabayashi, 06/13/09
| Thank you for the presentation of our article on the MD Linx.com site. Our article disclosed the loss of CD34 vascular endothelial marker on the peritubular capillary without the CD34 loss of glomerular capillary in the three cases with MPO-ANCA-associated TI nephritis. These three cases had not glomerular lesion, and had the reservation of CD34 marker in glomeruli. Accordingly, these data suggest that the peritubular capillaritis in the interstitium plays an important role in the pathogenesis of primary MPO-ANCA associated TI nephritis. In addition, tubulitis accompanied with TBM lysis was also observed in these cases, even though the TBM lysis is not usually demonstrated in general tubulitis (this observation is written in the text). Therefore, primary two different pathogenetic mechanisms operate in the pathogenesis of MPO-ANCA-associated TI nephritis. |
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