Initial graft function following liver transplantation is a major determinant of postoperative survival and morbidity. Primary graft nonfunction (PNF) is uncommon; however, it is one of the most serious and life-threatening conditions in the immediate postoperative period. The risk factors associated with PNF and short-term outcome have been previously reported, but there are no reports of long-term follow-up after retransplant for PNF. At our institution, 52 liver transplants had PNF (2.22%) among 2,341 orthotopic liver transplants in 2,130 patients from 1984 to 2003. PNF occurred more often in the retransplant setting. Female donors, donor age, donor days in the intensive care unit, cold ischemia time, and operating room time were significant factors for PNF. Patient as well as graft survival of retransplant for PNF was not different compared to retransplant for other causes. However, PNF for a second or third transplant did not demonstrate long-term survival, and hospital mortality was 57%.In conclusion, retransplant for PNF in the initial transplant can achieve relatively good long-term survival; however, if another transplant is needed in the setting of a second PNF, the third retransplant should probably not be done due to poor expected outcome. Liver Transpl 13:227-233, 2007.

In addition to patient demographic features, donor factors, including suboptimal organ quality and the need for more intense immunosuppression, were associated with an increased risk of fractures during the first 5 years after a renal transplant.

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1 Activated hepatic stellate cells play a major role in the pathophysiology of chronic liver disease. They can in¯uence the metabolism of hepatocytes by producing a variety of cytokines and growth factors. Upon stimulation with endotoxin, stellate cells also synthesize nitric oxide (NO), a potent mediator of growth of several cell types including hepatocytes. 2 We investigated the eect of serum-free medium conditioned by activated stellate cells in the absence and presence of endotoxin on NO and DNA synthesis in hepatocytes. Stellate cells and hepatocytes were isolated by enzymatic digestion of the liver. Stellate cells were cultured for 10 days after which the majority exhibited a-smooth muscle actin (a marker for activated cells); hepatocytes were used after overnight culture. 3 While the medium conditioned by stellate cells in the absence of endotoxin stimulated DNA synthesis in hepatocytes, medium conditioned in its presence inhibited this process in an endotoxin concentration-dependent manner (10 ± 1000 ng ml 71). Endotoxin-conditioned stellate cell medium also stimulated NO synthesis in hepatocytes; the eect was consistent with increased protein and mRNA expression of inducible NO synthase (iNOS). However, inhibition of DNA synthesis in hepatocytes caused by endotoxin-conditioned stellate cell medium was unaected by the NOS inhibitor, L-N G -monomethylarginine (L-NMMA), guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), and neutralizing antibodies for TGF-b, IL-1b, IL-6 and TNF-a. 4 These results indicate that factors other than these cytokines produced by activated stellate cells upon stimulation with endotoxin or by hepatocytes challenged with endotoxin-conditioned stellate cell medium inhibit DNA synthesis in hepatocytes.