Contribution of renal secreted complement C3 to the circulating pool in humans.

摘要: Complement C3 produced within the kidney may be an important mediator of local inflammatory and immunological injury. The overall level renal production consequently its contribution to total circulating are, however, unknown. This was investigated by using conversion from recipient donor allotype following transplantation. F S allotypes 80 consecutive donor-recipient pairs (148 individuals) were determined amplification refractory mutation system analysis. extent in F/S mismatched recipients quantified at different stages after transplantation, enzyme-linked immunosorbent assay specific for HAV 4-1 polymorphism that is strongly associated with C3F. Twenty-one eighty potentially informative, i.e., SS FF or FS kidneys. In early postoperative period, donor-derived (HAV 4-1-positive) undetectable, increasing 9.6% times acute allograft rejection. When graft dysfunction occurred causes other than rejection, remained undetectable. After stable function attained (3–13 mo transplantation), made up 4.5% pool. Our findings demonstrate human transplant resting state a significant source extrahepatic C3. Its heightened synthesis during rejection episodes suggests possible pathogenic role this process.