A recent study published in the Feb JASN 2012 issue showed that there is an elevated soluble FLT-1 that is inhibiting the endothelial repair of PR3 ANCA vasculitis. This is very interesting as sFLT-1 now is not just associated with pre eclampsia. Vasculitis causes endothelial damage. VEGF is a factor that leads to endothelial repair. The authors show that in the PR3 ANCA vasculitis state, the VEGF factors are inhibited by sFLT-1 and leads to decreased endothelial repair and hence worse vasculitis.
sFLT1 are elevated in placental vascular dysfunction and pre eclampsia. sFLT1 is produced by placental cytotrophoblasts but also monocytes and endothelial cells and it inhibits VEGF. This study is interesting as it showed that sFLT1 was elevated in patients with PR3 ANCA vasculitis and this was due to monocyte activation activating the alternate complement components. They were increased in anti GBM and anti MPO disease but not significantly as in patients with anti PR3 related disease when compared to controls in their experiment. Interestingly, postulated that anti sFLT1 agents might be useful.
Take a look at the full reference
http://www.ncbi.nlm.nih.gov/pubmed/22034638
what can we learn from this and the fact that plasmapharesis help Anti GBM disease more universally and consistantly than ANCA vasculitis. Is TPE removing a different AB(Anti GBM) and not sFLT1 or simply removing abs that help repair the endothelium indiscrimnitly
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