Table 1.

Data implicating a role for the PT in albumin processing and/or albuminuria

Process Implicated or Defective	Reference
d-Serine–induced PTC injury	Carone and Ganote, 197523
Megalin-cubilin complex	Birn, et al., 20005; Christensen and Birn, 20016; Wang et al., 200515
ClC-5 knockout	Piwon et al., 200013; Christensen et al., 200316
Total-body irradiation	Yammani et al., 200211
NHE-3 knockout	Gekle et al., 200412
Statins	Sidaway et al., 200420; Verhulst et al., 200421; Atthobari et al., 200622
Rab 38	Rangel-Filho et al., 200518; Williams et al., 201119; Rangel-Filho et al., 201317
Increased GSCs	Russo et al., 20077
Transcytosis	Russo et al., 2007,7 Sandoval et al., 20128
FcRn	Sarav et al., 2009100
Carbon nanotubes	Ruggiero et al., 2010126
Bardoxolone	Reisman et al., 201210
Diphtheria toxin–induced PTC injury	Grgic et al., 201225; Sekine et al., 201224; Zhang et al., 201226

Multiple PTC defects have been shown to lead to significant albuminuria. Notably, selective PTC injury using dophtheria toxin induction, essentially eliminating any PT uptake of albumin, resulted in severe, but reversible, albuminuria without histologic or electron microscopic changes.