Livingston, David

Background. Aorto-hepatic conduits can provide arterial inflow for liver transplants in cases where the native hepatic artery is unsuitable for use. Methods. Clinical outcomes of all patients undergoing liver transplantation (LT) with an aorto-hepatic conduit between 2000 and 2016 were included. Recipients were divided into 2 groups: those with a supraceliac (SC) aortic conduit (N = 22) and those with an infrarenal (IR) aortic conduit (N = 82). Results. There was no difference in calculated model for end-stage liver disease score between the 2 groups. The SC group received grafts with a higher mean donor risk index (1.69 versus 1.48; P = 0.02). Early allograft dysfunction was 18.2% in the SC group and 29.3% in the IR group (P = 0.30). In the SC group, 10.5% of patients required initiation of postoperative continuous renal replacement therapy compared to 12.1% of patients in the IR group (P = 0.69). No difference in the rate of postoperative acute kidney injury was seen between the 2 groups (P = 0.54). No significant difference in median creatinine at 1 year was seen between the SC (1.2 mg/dL; IQR 1–1.3) and IR (1.2 mg/dL; IQR 0.9–1.5) groups (P = 0.85). At a median follow-up of 5.3 years, thrombosis of the aortic conduit occurred in 0% of patients in the SC group and 6.1% of patients in the IR group (P = 0.24). Graft survival was not significantly different between the 2 groups (P = 0.47). Conclusions. No difference in renal dysfunction as demonstrated by need for post-LT continuous renal replacement therapy, acute kidney injury, or creatinine at 1 year post-LT was seen between SC and IR aortic conduits. A slight trend of higher conduit thrombosis rate was seen with IR compared to SC aortic conduits; however, this did not reach statistical significance. Both SC and IR aortic conduits represent reasonable options when the native hepatic artery is unsuitable for use.

It has been suggested that microsteatosis does not negatively impact graft survival following liver transplantation (LT). The present study represents the largest series on donor livers with significant microsteatosis and investigates the impact of microsteatosis on perioperative factors such as postreperfusion syndrome (PRS), early allograft dysfunction (EAD), and postoperative renal dysfunction. Clinical outcomes of all patients undergoing LT with donor livers with isolated microsteatosis (≥30%; n = 239) between 2000 and 2017 were compared with a propensity score–matched cohort of patients undergoing LT with donor livers with no steatosis (n = 239). Patients in the microsteatosis group had a higher rate of PRS (33.1% versus 24.2%; P = 0.03), EAD (38.2% versus 23.0%; P < 0.001), and continuous renal replacement therapy (CRRT) requirement following LT (10.9% versus 3.6%; P = 0.002) than the no steatosis group. No difference in patient (P = 0.33) or graft survival (P = 0.18) was observed between the 2 groups. On multivariate regression, livers with microsteatosis had an increased risk of graft loss with retransplant recipients (hazard ratio [HR], 1.59; P < 0.001), increasing Model for End‐Stage Liver Disease (MELD) score (HR, 1.13; P = 0.01), and organs from donation after circulatory death donors (HR, 1.46; P = 0.003). In conclusion, recipients of donor livers with significant microsteatosis are at an increased risk of PRS, EAD, and postoperative renal dysfunction requiring CRRT. Livers with significant microsteatosis should be avoided in retransplant recipients and in recipients with high biological MELD scores. Once appropriately selected recipients of these livers are able to overcome the initial perioperative implications of using these donor livers, longterm patient and graft survival is similar to recipients receiving grafts with no steatosis.

Nephrocalcinosis consists of deposition of calcium in the renal parenchyma. Renal cortical calcification is a rare entity in comparison to calcium deposits in the medulla and is seen only in a handful of pathologies with corresponding characteristic patterns on imaging. Thin linear calcifications may get deposited in the peripheral renal cortex suggestive of cortical necrosis due to a vascular insult (vasculitis), and rarely due to glomerulonephritis. This pattern of calcification has also been referred to as the “tramline” or “railroad track” sign.