Graft Function In Liver Transplantation Research Articles

Living Donor Liver Transplant for Budd-Chiari Syndrome Without Caval Replacement: A Single-Center Study.

Adequate venous outflow is one of the most important factors responsible for optimal graft function in liver transplantation. Thrombosis of the inferior vena cava in cases of Budd-Chiari syndrome poses a major challenge to a transplant surgeon in establishing proper graft outflow. In deceased donor liver transplant, this problem can be dealt with relative ease as the liver graft includes donor inferior vena cava. However, this is not the case in living donor liver transplant. We present our findings of living donor liver transplant for Budd-Chiari syndrome and discuss techniques that have helped overcome this unique problem without the need for complete inferior vena cava replacement. Our retrospective analysis included living donor liver transplant recipients from November 2006 to March 2020 at our center and selected patients who underwent this transplant for Budd-Chiari syndrome. We studied the extent and severity of inferior vena cava involvement in these cases. We developed a classification that not only helped to stratify patterns of venacaval disease but also helped to plan the surgical technique. The role of interventional radiology combined with surgery in management of extensive inferior vena cava stenosis was studied. Among 2952 cases of liver transplant in our unit from November 2006 to March 2020, 36 patients had Budd-Chiari syndrome; 21 had significant level of inferior vena cava thrombosis, which was managed with inferior vena cava thrombectomy with either patchplasty (n = 20) or segmental replacement (n = 1). None of our patients showed recurrence of primary disease during the median follow-up of 36 months (range, 8-158 mo). Establishment of adequate venous ouflow in thrombosed inferior vena cava is possible with proper planning of surgical technique and timely involvement of interventional radiology-guided interventions in patients with Budd-Chiari syndrome.

The Impact of Deceased Donor Liver Extraction Time on Early Allograft Function in Adult Liver Transplant Recipients.

In liver transplantation, both cold and warm ischemia times are known to impact early graft function. The extraction time is a period during the initial phase of organ cooling which occurs during deceased donor procurement. During this time, the organ is at risk of suboptimal cooling. Whether donor extraction time, the time from donor aortic cross-clamp to removal of the donor organ from the body cavity has an effect on early graft function is not known. We investigated the effect of donor extraction time on early graft function in 292 recipients of liver grafts procured locally and transplanted at our center between June 2012 and December 2016. Early graft function was assessed using the model of early allograft function score in a multivariable regression model including donor extraction time, cold ischemia time, warm ischemia time, donor risk index, and terminal donor sodium. Donor extraction time had an independent effect on early graft function measured by the model of early allograft function score (coefficient, 0.021; 95% confidence interval, 0.007-0.035; P < 0.01; for each minute increase of donor extraction time). Besides donor extraction time, cold ischemia time, warm ischemia time, and donor risk index had a significant effect on early graft function. We demonstrate an independent effect of donor extraction time on graft function after liver transplantation. Efforts to minimize donor extraction time could improve early graft function in liver transplantation.

Complement Activation in Liver Transplantation: Role of Donor Macrosteatosis and Implications in Delayed Graft Function.

The complement system anchors the innate inflammatory response by triggering both cell-mediated and antibody-mediated immune responses against pathogens. The complement system also plays a critical role in sterile tissue injury by responding to damage-associated molecular patterns. The degree and duration of complement activation may be a critical variable controlling the balance between regenerative and destructive inflammation following sterile injury. Recent studies in kidney transplantation suggest that aberrant complement activation may play a significant role in delayed graft function following transplantation, confirming results obtained from rodent models of renal ischemia/reperfusion (I/R) injury. Deactivating the complement cascade through targeting anaphylatoxins (C3a/C5a) might be an effective clinical strategy to dampen reperfusion injury and reduce delayed graft function in liver transplantation. Targeting the complement cascade may be critical in donor livers with mild to moderate steatosis, where elevated lipid burden amplifies stress responses and increases hepatocyte turnover. Steatosis-driven complement activation in the donor liver may also have implications in rejection and thrombolytic complications following transplantation. This review focuses on the roles of complement activation in liver I/R injury, strategies to target complement activation in liver I/R, and potential opportunities to translate these strategies to transplanting donor livers with mild to moderate steatosis.

Limitations of Use of the Noninvasive Clearance of Indocyanine Green as a Prognostic Indicator of Graft Function in Liver Transplantation

AimTo assess the prognostic value of noninvasive indocyanine green (ICG) clearance (ICG-pulse-densitometric method [PDR]) for the outcome of liver grafts after transplantation. MethodsICG-PDR, hepatic artery resistance index, cardiac output, transaminases, prothrombin time, bilirubin, albumin, hematocrit at 48 to 72 hours after transplantation were analyzed with reference to outcome among 59 liver graft recipients. ResultsTwo grafts were lost at 10 and 88 days during the initial hospitalization. These two patients only differed from the other recipients in the need for packing (1/2 versus 3/57) and degree of hypoproteinemia (46 ± 0 versus 51 ± 7.8 g/L), whereas they had similar ICG-PDR values (16.7%/min and 21.8%/min versus 17.3%/min ± 7.2%/min). Seven patients showed an ICG-PDR ≤ 8.8%/min, a previously identified cutoff for early postoperative complications. These patients versus the other 52 significantly differed in prothrombin index (47.9% ± 15.9% versus 64.3% ± 11.7%, P = .001) and bilirubin (8.3 ± 3.2 versus 3.3 ± 2.9 mg/dL, P = .0001). Early postoperative complications—primary graft nonfunction, hepatic artery thrombosis, or septic shock— responsible for an ICG-PDR ≤ 8.8%/min were observed in 2/7 patients. Interestingly, six cases developed an early (range: 3–15 days) rejection episode. In all the cases rejection suspected by analytical abnormalities was confirmed by liver biopsy. Among the overall series of patients, ICG-PDR significantly correlated with serum albumin (r = 0.345; P = .007), bilirubin (r = −0.514; P = .0001), and hematocrit (r = 0.462; P = .0001) but not with transaminases, prothrombin index, cardiac output, or hepatic artery resistance index. Actuarial 72-month probability of graft survival was 75%. Overall, 14 grafts were lost over a median follow-up of 78 months (range 1–99 m). There were no significant differences among early ICG-PDR values among grafts lost vs retained upon follow-up. ConclusionICG-PDR measured once early after liver transplantation did not offer relevant information to predict individual patient outcomes in the immediate postoperative phase. This lack of prognostic value may have been due to the multiple confounding factors involved in ICG metabolism after liver transplantation.

Indocyanine green clearance as a marker of graft function in liver transplantation

Indocyanine green clearance as a marker of graft function in liver transplantation

Hepatocyte degeneration as predictive of early graft function in liver transplantation.

Hepatocyte degeneration as predictive of early graft function in liver transplantation.

Donor des-gamma-carboxy prothrombin positivity is a risk factor for poor early graft function in liver transplantation.

Des-gamma-carboxy prothrombin (DCP) is an abnormal prothrombin that lacks coagulating activity. The aim of this study was to determine if the presence of DCP in the donor could be used as a marker of post-transplant graft function. We collected data and serum samples on 90 organ donors. DCP level was correlated with donor-specific factors and with graft function intraoperatively and in the early post-transplant period. Twenty-seven donors (30.0%) had positive DCP levels before harvesting. Although recipients were similar in demographics, preoperative liver function, and primary disease distribution, patients transplanted with livers from DCP-positive donors needed significantly more intraoperative transfusion. Furthermore, donor DCP positivity was identified as a preoperative risk factor for poor early graft function based on multivariate analysis (odds ratio = 6.58, P = 0.0032). Our findings suggest that DCP is another valuable marker for evaluating the quality of donor livers.

Donor des-gamma-carboxy prothrombin positivity is a risk factor for poor early graft function in liver transplantation

Abstract Des-gamma-carboxy prothrombin (DCP) is an abnormal prothrombin that lacks coagulating activity. The aim of this study was to determine if the presence of DCP in the donor could be used as a marker of post-transplant graft function. We collected data and serum samples on 90 organ donors. DCP level was correlated with donor-specific factors and with graft function intraoperatively and in the early post-transplant period. Twenty-seven donors (30.0%) had positive DCP levels before harvesting. Although recipients were similar in demographics, preoperative liver function, and primary disease distribution, patients transplanted with livers from DCP- positive donors needed significantly more intraoperative transfusion. Furthermore, donor DCP positivity was identified as a preoperative risk factor for poor early graft function based on multivariate analysis (odds ratio = 6.58, P= 0.0032). Our findings suggest that DCP is another valuable marker for evaluating the quality of donor livers.