Calcific Uremic Arteriolopathy in Peritoneal Dialysis Populations

Figure 4

Schematic representation for the pathogenic mechanisms of CUA development and the potential sites of action for therapeutic intervention, where (+) indicates augmentation and (−) indicated inhibition; STS, sodium thiosulfate; HBO, hyperbaric oxygen; PO₄⁻, phosphate; Ca⁺⁺, calcium; NDPT, sodium-dependent phosphate cotransporter (Pit-1); vSMC, vascular smooth muscle cell; Cbfa-1, core-binding factor alpha 1; NFκB, nuclear factor κ−B; RANK(L), receptor activator of NFκB (ligand); OPG, osteoprotegerin; TNF-α, tumour necrosis factor alpha; IL-1 interleukin 1; BMP, bone morphogenic protein; ESKD, end-stage kidney disease; MGP, matrix G1a protein; ASHG, α-2 Heremans-Schmid glycoprotein.