Expression of the membrane attack complex of complement and its inhibitors during human liver allograft transplantation.

BACKGROUND/AIMS: In order to test the possible role of activated complement in human liver allograft rejection, we evaluated the expression of the membrane attack complex of complement, its soluble inhibitors clusterin and vitronectin and its membrane inhibitor protectin during the evolution of liver transplants.

METHODS

An indirect immunoperoxidase technique was applied to biopsy specimens obtained from liver allografts in 16 patients without complications, nine with acute rejection, four with chronic rejection and five with biliary complications.

RESULTS

Two types of membrane attack complex deposition were observed: (a) extracellular deposits in portal tracts and perisinusoidal matrix, associated with clusterin and vitronectin, similar to those found in the normal liver; and (b) intra-portal vascular deposits, devoid of clusterin and vitronectin. Vascular membrane attack complex deposition was detected in four clinically stable patients, three patients with chronic rejection and two patients with biliary complications. In clinically stable patients, vascular membrane attack complex deposition was restricted to large portal vessels and was detected in a minority of portal tracts. In patients with chronic rejection or biliary complications, vascular membrane attack complex deposition was detected along both large and small portal vessels and was present in the majority of portal tracts. Protectin induction on hepatocytes was detected in 33 cases.

CONCLUSIONS

Our results suggest that membrane attack complex deposition is unlikely to play a major role in the pathogenesis of acute liver allograft rejection but may contribute to the vascular and biliary lesions observed in chronic rejection.