Why is HIVAN or idiopathic collapsing glomerular disease different than standard FSGS? It is more proliferative compared to a podocytopenia seen in other forms of FSGS. The questions have been thrown out there multiple times. Studies in past have shown that the podocytes in the collapsing variant are premature form and then proliferate. Telomerase protein is responsible for aging. Two components called TERT and TERC are important. A study showed that transgenic TERT expression in mice induced up regulation of Wnt signaling and leading to disruption of glomerular structure and resulting in collapsing glomerulopathy. Then they showed that the humans and mice had increased expression of the TERT and activation of Wnt signaling in HIVAN models. This was inhibited by a Dkk1( inhibitor of the Wnt expression). The pathology changes were reversible. Interesting, as this suggests that the process might be reversible. Perhaps medications that use a Dkk1 might help? This adds to a novel understanding of collapsing GN that was not known before.
Take a look at this paper from Stanford and Columbia group
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