Kidney failure leads to the retention of uremic toxins in the blood, a fraction of which have been quantified (Table ). Although the toxicity of all retained uremic toxins has not been established, several are toxic and cause systemic complications, like indoxyl sulfate, p-cresyl sulfate, urea, creatinine, and hippuric acid . It is unknown how the complex buildup of metabolites in the blood compartment affects the adsorption and activation of proteins adsorbed to surfaces. It has been observed that some metabolites trigger protein folding events , and their interactions with proteins alter the protein adsorption mode on surfaces Selected uremic toxins, mostly protein-bound, have been studied for adsorption to surfaces of different types but usually from the point of view of adsorbing the uremic toxin to clear it from blood rather than their effect on plasma protein-surface interactions .Hemodialysis allows for some uremic toxins to be cleared from the blood compartment and is universally used to treat those with kidney failure despite deplorable morbidity and mortality issues. Porous matrix development for the application to clearing toxins from blood has largely focused upon toxin adsorption, like our work on uremic toxin-laden plasma adsorption to 2-(methacryloyloxy)ethylphosphorylcholine-co-β-cyclodextrin (p(MPC-co-PMβCD)) films, leveraging MPC's inherent low-fouling characteristics and β-CD's capability to bind with uremic toxins . A more fundamental question regarding the effect plasma-borne uremic toxins have on the adsorption and activation of plasma proteins that can direct the host response to porous matrixes, however, remains woefully understudied.