Daniela Macconi

TL;DR: Exposure to excess proteins in proximal tubular cells induces the formation of ROS, which is responsible for NF-kappaB activation and consequent induction of NF- kappaB-dependent inflammatory signals, according to real-time PCR data.

TL;DR: A biochemical explanation for defective NO activity and increased oxidative stress in preeclamptic placenta is provided, and a lower than normal l-arginine concentration caused by arginase II overexpression redirects ecNOS toward peroxynitrite.

TL;DR: It is suggested that reduction in podocyte number is an important determinant of podocyte dysfunction and progressive impairment of the glomerular permselectivity that lead to the development of massive proteinuria and ultimately to renal scarring.

TL;DR: Results document that spontaneous proteinuria in MWF rats develops without significant changes in the permeability of the GBM to water and albumin, or in the ultrastructure of the podocyte foot processes, but is associated with an important alteration in the distribution of ZO-1 at the glomerular level.

TL;DR: It appears that NO is a mediator of the bleeding tendency of uremia, as N-monomethyl-L-arginine (L-NMMA), a specific inhibitor of NO formation from L-argine, completely normalized bleeding time when given to uremic rats.