Injury to podocytes and their slit diaphragms typically leads to marked proteinuria. Mutations
in the TRPC6 gene that codes for a slit diaphragm–associated, cation-permeable ion
channel have been shown recently to co-segregate with hereditary forms of progressive
kidney failure. Herein is shown that induced expression of wild-type TRPC6 is a common
feature of human proteinuric kidney diseases, with highest induction observed in
membranous nephropathy. Cultured podocytes that are exposed to complement upregulate …