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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
[Clinical approach to primary membranoproliferative glomerulonephritis]
1Service de néphrologie et d'immunologie, CHU de Nantes, 1, place Alexis-Ricordeau, 44000 Nantes, France; Inserm UMR S-1064, 30, boulevard Jean-Monnet, 44093 Nantes cedex 01, France; Institut de transplantation urologie-néphrologie (Itun), 30, boulevard Jean-Monnet, 44093 Nantes cedex 01, France.
Abstract:
Membranoproliferative glomerulonephritis represent a heterogeneous group of nephropathies. During the last five years, our understanding of membranoproliferative glomerulonephritis has greatly improved. Animal models and the study of complement genetics led to the dissection of the physiopathology of membranoproliferative glomerulonephritis, to the individualization of a new entity, C3 glomerulopathy, and to a new classification of these nephropathies. The study of large cohorts has also changed the clinical picture of membranoproliferative glomerulonephritis that has been long dominated by the severity of a single type of dense deposits disease. Finally, the rediscovery of complement through the study of the atypical haemolytic uremic syndrome and the availability in clinical practice of complement inhibitors have paved the way for new therapeutic approaches of membranoproliferative glomerulonephritis.
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