Mutations in the canonical transient receptor potential cation channel 6 (TRPC6) are
responsible for familial forms of adult onset focal segmental glomerulosclerosis (FSGS). The
mechanisms by which TRPC6 mutations cause kidney disease are not well understood. We
used TRPC6-deficient mice to examine the function of TRPC6 in the kidney. We found that
adult TRPC6-deficient mice had BP and albumin excretion rates similar to wild-type animals.
Glomerular histomorphology revealed no abnormalities on both light and electron …