Sustained proteinuria and tubulointerstitial damage have been closely linked with
progressive renal failure. Upon excess protein endocytosis, tubular epithelial cells are
thought to produce mediators that promote inflammation, tubular degeneration, and fibrosis.
This concept was tested in a transgenic mouse model with megalin deficiency. Application of
an anti–glomerular basement membrane serum to transgenic megalin-deficient mice [Cre
(+)/GN] and megalin-positive littermates [Cre (−)/GN] produced the typical …