
Background & Aims: The Sundaram Acute-on-Chronic Liver Failure–Liver Transplant Mortality (SALT-M) score predicts 1-year post-transplant mortality in patients with severe ACLF undergoing deceased donor liver transplantation (DDLT). Its performance in living donor liver transplantation (LDLT) is unknown. Methods: We externally validated SALT-M in two independent ACLF-LDLT cohorts: King Faisal Specialist Hospital and Research Centre (KFSHRC), Riyadh (n=121), and a global International LDLT Registry cohort (n=57). Discrimination (AUROC with 95% CI), calibration (observed-to-expected [O:E] ratio, calibration slope and intercept), and association with observed outcomes were assessed overall and, in the KFSHRC cohort, separately in ACLF grade 1 and severe ACLF (grades 2–3). Results: In the KFSHRC cohort, ACLF grade was 1 in 47.9%, 2 in 43.0%, and 3 in 9.1%; 1-year mortality was 14.9% (global cohort 21.1%). SALT-M predicted ≤30% mortality in 95.9% of the KFSHRC and 98.2% of the global cohort. Discrimination was limited and statistically inconclusive: AUROC 0.56 (95% CI 0.40–0.72) overall, 0.62 (0.42–0.81) in severe ACLF, and 0.51 (0.25–0.76) in ACLF-1. Calibration-in-the-large was acceptable (O:E 1.18, 95% CI 0.74–1.87) but the calibration slope was shallow (0.16). None of the five SALT-M components was associated with 1-year mortality; white blood cell count (OR 1.14, p =0.03) and female sex (OR 3.49, p =0.02) were. MELD-Na and MELD 3.0 were higher in non-survivors in the global cohort ( p =0.03 and p =0.02). Conclusions: In LDLT-dominant ACLF cohorts — evaluated largely outside the severe-ACLF population for which SALT-M was derived — discrimination could not be confirmed, reflecting profound spectrum restriction and few outcome events rather than demonstrated model failure. SALT-M should be applied cautiously as an adjunctive risk-stratification tool, not as a universal threshold for transplant candidacy.
Thrombophilic states in the setting of living donor liver transplantation raises concerns regarding perioperative thromboembolism in the donor, as well as the potential transfer of inherited prothrombotic tendencies through mutated, hepatically synthesised coagulation factors. Screening practices for thrombophilia remain heterogeneous across centers and may result in donor exclusion based on local policies. However, accumulating evidence over the past decade suggests that most prospective donors are asymptomatic, and those with heterozygous inherited thrombophilias-such as Factor V Leiden or Prothrombin G20210A mutation-can safely undergo donation with standard perioperative thromboprophylaxis for recipient and donors. These states are unlikely to be transmitted to the recipient, as extrahepatic synthesis of coagulation proteins contributes to maintaining hemostatic balance. In contrast, donors with a prior history of thromboembolism, high-risk genotypes (e.g., homozygous or compound heterozygous states), or high-risk acquired thrombophilias should generally be excluded owing to an increased risk of thrombotic complications.