1. In 2008, Savin et al. showed that galactose, a simple nontoxic sugar, binds with high affinity to the FSPF in vitro.(6) They also found that trace amounts of galactose (>10-12 M) inhibited glomerular permeability activity induced by FSPF in vitro. This series of in vitro experiments also demonstrated that the effect of FSPF activity in serum can be reversed by its incubation with galactose or alternatively by pre-incubation of glomeruli with galactose. Additionally, the authors describe significantly decreased permeability activity in vivo in a single patient with post-transplant FSGS in response to both IV and oral galactose. The FSPF activity in this patient decreased progressively during the 4 weeks of galactose ingestion (from 0.8 to 0.1), and persisted 4 weeks after discontinuation of oral galactose (0.2). The proposed mechanism for this action is that FSPF have galactose-binding sites which interact with galactose of the glomerular glycocalyx, activating signal transduction in podocytes. Introduction of free galactose may block the FSPF binding sites or alter the tertiary structure of the FSPF, thus inhibiting its activity.