Abstract
It has been reported that survival on mild hypoalbuminemia due to high albumin leakage did not worsen in patients on hemodialysis (HD) or online hemodiafiltration (OHDF) even though the level of serum albumin is a classic nutrition marker associated with mortality. Survival was also equivalent on HD and OHDF for patients with similar levels of albumin leakage and serum albumin. Furthermore, survival on HD using a super high-flux (SHF) albumin-leaking membrane was better than that on HD using a SHF membrane, and survival on SHF albumin-leaking HD with high albumin leakage was better than that on OHDF with low albumin leakage. The following hypothesis regarding crosstalk between α1-microglobulin (α1MG) and albumin is proposed that can explain the mechanism by which the level of serum human mercaptoalbumin (HMA) increases postdialysis and decreases predialysis. At initiation of and during dialysis, the production of free α1MG in the liver increases by upregulation of the α1MG-bikunin precursor gene. The free α1MG rapidly reacts with some substances that are reversibly bound to human nonmercaptoalbumin (HNA)-1, resulting in the conversion to HMA and free α1MG with reduced activity (i.e., free α1MG with reduced or no antioxidant capacity) during dialysis and in the increased serum HMA level postdialysis. In addition, it is possible that both hypoalbuminemia and the conversion of HNA-1 to HMA increase the free form of indoxyl sulfate, which is removed by diffusion. The antioxidant capacity in serum after dialysis is mainly due to the very large amount of HMA, resulting in the conversion to HNA and the decreased serum HMA level before dialysis. However, the very small amount of free α1MG produced in the liver has strong antioxidant activity after dialysis.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
