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1 Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, Tennessee; and William.Fissell@vanderbilt.edu minerj@wustl.edu.
2 Division of Nephrology, Washington University School of Medicine, St. Louis, Missouri William.Fissell@vanderbilt.edu minerj@wustl.edu.
1 Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, Tennessee; and William.Fissell@vanderbilt.edu minerj@wustl.edu.
2 Division of Nephrology, Washington University School of Medicine, St. Louis, Missouri William.Fissell@vanderbilt.edu minerj@wustl.edu.
A new model of the glomerular filtration barrier links glomerular basement membrane (GBM)…
Figure 1.
A new model of the glomerular filtration barrier links glomerular basement membrane (GBM) compression to permselectivity. Schematics of hydrodynamic forces in the glomerular capillary wall. In a healthy glomerulus (upper panel), water filtration (blue arrows) through the GBM (dark blue) compresses the GBM constituents (gold lines) against the podocyte foot processes (orange). Podocyte cell-cell attachment and contraction forces (large green double arrows) act to buttress (white arrows) the GBM against the distending force of circulation pressure. The compressed GBM cannot admit albumin (purple ovals) except possibly in the subendothelial space, where gel compression is least pronounced. In proteinuric glomerular disease with podocyte foot process effacement (lower panel), cell contraction is decreased (small green arrows), and podocytes no longer form as strong a buttress against which the GBM is compressed. With reduced gel compression, the mesh size of the GBM gel becomes large enough to allow albumin to transit through to Bowman’s space.