Abstract
Background
Portal vein thrombosis (PVT) increases operative complexity and complication risks in liver transplantation (LT), but whether it compromises long-term survival with proper portal inflow reconstruction remains debated. This study aimed to evaluate the impact of preoperative PVT on perioperative and long-term outcomes after LT and to assess outcomes following individualized portal inflow reconstruction in patients with complex PVT.
Methods
Adult orthotopic LT recipients between 2016 and 2024 were retrospectively recruited and stratified into PVT (n=144) and non-PVT (n=373) groups. Baseline, operative, and survival data were compared.
Results
PVT patients had higher rates of Child-Pugh B/C (86.2% vs. 74.8%), hepatic encephalopathy (30.6% vs. 20.6%), upper gastrointestinal bleeding (UGIB; 57.6% vs. 35.9%), and prior splenectomy (16.7% vs. 2.4%; all P<0.05). Independent predictors of PVT included older age [odds ratio (OR) 1.03; 95% confidence interval (CI), 1.01–1.05; P=0.008], hepatitis B virus (HBV)-related cirrhosis (OR 2.12; 95% CI, 1.19–3.77; P=0.01) and prior splenectomy (OR 6.72; 95% CI, 2.85–15.85; P<0.001). PVT was associated with more deceased donor grafts (86.8% vs. 75.1%), longer operative time (453 vs. 405 min), greater blood loss (1,200 vs. 800 mL), and more red blood cell transfusions (800 vs. 600 mL; all P<0.01). Among 12 PVT patients undergoing non-anatomical reconstruction, 4 (33.3%) developed vascular complications. PV-related complications (16.2% vs. 3.5%) and 1-year renal dysfunction (52.5% vs. 39.4%) were more frequent in the PVT group (P<0.05). However, preoperative PVT was not an independent predictor of long-term survival in Kaplan-Meier or Cox regression.
Conclusions
Preoperative PVT did not compromise long-term survival after LT but increased operative complexity, PV-related complications, and renal dysfunction. When appropriately designed, a non-anatomical portal reconstruction strategy could achieve favorable outcomes in complex PVT cases.
Keywords: Portal vein thrombosis (PVT), liver transplantation (LT), non-anatomical reconstruction, physiological reconstruction, prognosis
Highlight box.
Key findings
• Preoperative portal vein thrombosis (PVT) increased operative complexity, portal vein-related complications, and postoperative renal dysfunction. However, when adequate portal inflow reconstruction was feasible, PVT was not an independent predictor of long-term survival. Selected patients with complex PVT achieved acceptable outcomes after individualized non-anatomical, physiological reconstruction.
What is known and what is new?
• PVT, particularly Yerdel grade III–IV disease, has been associated with technically demanding surgery and inferior outcomes after liver transplantation (LT). Outcomes increasingly appear to depend on the feasibility of restoring physiological splanchnic inflow rather than on PVT alone.
• This study provides recent single-center evidence that carefully selected patients with PVT can achieve survival comparable to those without PVT. It also highlights postoperative renal dysfunction as an important concern and describes individualized reconstruction, including multiple-vessel anastomosis, for complex PVT.
What is the implication, and what should change now?
• PVT should not be considered an absolute contraindication to LT when effective portal inflow reconstruction is technically achievable. Detailed preoperative vascular assessment, individualized surgical planning, and careful patient selection are essential. Complex cases should be managed in experienced centers with advanced reconstruction expertise, intensive Doppler surveillance, individualized anticoagulation, and close renal function monitoring.
Introduction
Liver transplantation (LT) is the only definitive treatment for end-stage liver disease, and reconstruction of the portal venous inflow is indispensable during the operation. Portal vein thrombosis (PVT) refers to thrombotic occlusion within the main portal vein (PV) and its tributaries [including the splenic vein (SpV) and superior mesenteric vein (SMV)] and is relatively common in LT candidates, with a reported prevalence ranging from approximately 8% to 26% (1-3). According to meta-analyses largely reflecting outcomes from earlier eras of LT, the presence of PVT was historically associated with increased surgical complexity, inferior postoperative vascular patency, graft function, and post-LT survival (4,5). Stratified analyses, however, showed that simple PVT (Yerdel grade I–II) is not significantly associated with post-LT mortality, whereas complex PVT (Yerdel grade III–IV) confers a higher risk of death and graft loss (4,6). Perioperatively, higher PVT stage predicts prolonged operative time and often necessitates advanced inflow reconstruction strategies (7).
Importantly, contemporary experience suggests that the unfavorable impact of complex PVT is not immutable. Recent multicenter cohort and registry-based data have shown that acceptable long-term survival can be achieved in patients with PVT, with outcomes increasingly determined by the feasibility of physiological portal inflow reconstruction rather than the mere presence of PVT (8,9). When physiological splanchnic venous inflow can be successfully restored, even patients with complete PV occlusion may achieve long-term survival comparable to those without PVT. When conventional thrombectomy and anatomical anastomosis are not feasible, non-anatomical revascularization techniques (e.g., portal-variceal anastomosis, portocaval transposition) are commonly employed to re-establish portal inflow (10). In extremely complex cases, our center proposed a non-anatomical, yet physiological multiple-vessel anastomosis to achieve appropriate portal inflow as well as sufficient splanchnic drainage (11). With all these approaches, the prognosis of LT recipients with PVT may be improved.
This retrospective study analyzed recent LT cases at our center managed with mature PVT management strategies to evaluate the impact of PVT on LT outcomes. Through this comprehensive assessment, we aimed to refine risk stratification, inform surgical decision-making, and optimize perioperative management for LT candidates with PVT. We present this article in accordance with the STROCSS reporting checklist (12) (available at https://tgh.amegroups.com/article/view/10.21037/tgh-2026-0127/rc).
Methods
Study design
The protocol for this research project was approved by the Ethics Committee of Beijing Friendship Hospital on 27th May 2024 (No. BFHHZS20240128), and this study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments and the International Conference on Harmonization Guideline for Good Clinical Practice. Informed consent was obtained from the subject(s) and/or guardian(s). The study has been registered on ClinicalTrials.gov (No. NCT06513780).
Patient selection
We retrospectively collected data from adult patients who underwent orthotopic LT at the Liver Transplantation Center between 1 January 2016 and 31 December 2024. Exclusion criteria were: (I) auxiliary LT, multi-organ transplantation, re-transplantation, or combined with other organ transplantation; (II) presence of PV tumor thrombus confirmed by postoperative pathology; (III) incomplete essential clinical data, defined as missing key variables for analysis.
PVT was graded according to the Yerdel grade: grade I, thrombus <50% of lumen (usually mural thrombus); grade II, thrombus >50% of lumen with patent proximal SMV; grade III, complete occlusion of the PV involving the proximal SMV with a patent distal SMV; grade IV, complete occlusion of the portal trunk and SMV. PVT patients were stratified as simple PVT (Yerdel I–II) and complex PVT (Yerdel III–IV) for subgroup analysis. All preoperative imaging studies were retrospectively and independently reviewed by two experienced abdominal radiologists. Any discrepancies were resolved by consensus after joint re-evaluation.
Each donation underwent ethics review by the hospital committee. None of the organs were sourced from executed prisoners or prisoners of conscience, and autonomous consent free from coercion was obtained from the donor(s) or their next of kin.
Data collection
Preoperative and postoperative variables were collected. The latest pretransplant laboratory values were used to calculate Child-Pugh grading, Model for End-Stage Liver Disease (MELD) score, MELD-Na, and MELD 3.0 (13). Follow-up included total hospital stay, intensive care unit (ICU) stay, PV-related complications, major complications (Clavien-Dindo grade ≥ III), and survival. PV-related complications were defined as postoperative PVT or PV stenosis. Renal dysfunction was defined as an estimated glomerular filtration rate (eGFR) <90 mL/min/1.73 m2.
LT surgical procedures
The entire surgical team evaluated and discussed each patient’s preoperative imaging, including contrast-enhanced computed tomography (CT), prior to the surgery. Based on the patient’s vascular condition, presence and degree of PVT, an individualized surgical and vascular reconstruction plan was devised. For patients with complex PVT, after thorough discussion and assessment, an alternative non-anatomical PV reconstruction plan was designed.
During LT, all PVT patients underwent PV dissection and thrombectomy attempts. The comprehensive thrombectomy technique, including eversion, rotation, and venotomy, was employed, while avoiding violent manipulation. Based on detailed preoperative imaging assessment and individualized surgical planning, satisfactory thrombectomy with adequate portal inflow was achieved in the vast majority of patients. When conventional thrombectomy was inadequate, but a patent retropancreatic portal venous segment remained available, the pull-out technique was preferentially performed to enable direct retropancreatic PV anastomosis. This procedure was classified as anatomical PV reconstruction. When adequate portal inflow could not be restored by thrombectomy or direct retropancreatic anastomosis, defined as no jet-like blood flow observed in the recipient PV upon the release of the clamp, individualized non-anatomical reconstruction was performed according to the preoperative plan, including porto-variceal, left renoportal, and multiple-vessel anastomoses using additional portal-system inflow sources (Figure 1). Post-anastomosis, PV flow was assessed via Doppler ultrasound, and a flow velocity greater than 20 cm/s was considered satisfactory to ensure adequate PV inflow. For some patients with anatomical PV reconstruction, if the post-anastomosis flow velocity was inadequate, an additional side-to-end porto-variceal anastomosis was performed. In some cases, large collateral vessels required ligation intraoperatively.
Figure 1.
Non-anatomical portal vein reconstruction. (A) End-to-end porto-variceal anastomosis; (B) end-to-end porto-portal anastomosis plus side-to-end porto-variceal anastomosis; (C) end-to-end left reno-portal anastomosis plus side-to-end porto-variceal anastomosis; (D) end-to-end graft portocaval anastomosis plus end-to-side recipient portocaval anastomosis; (E) end-to-side graft portocaval anastomosis (with narrowing of the IVC above the anastomosis) plus side-to-end graft porto-variceal anastomosis; (F) portocaval transposition. IVC, inferior vena cava.
Of note, LT was considered contraindicated at our center in patients with diffuse portomesenteric thrombosis, defined as complete, long-segment occlusion of the main PV, SpV, and SMV, accompanied by severe portal hypertension, recurrent refractory upper gastrointestinal bleeding (UGIB), and no surgically accessible collateral suitable for portal inflow reconstruction or splanchnic decompression on contrast-enhanced CT. Even when azygos-system collaterals were present, they were deeply located and unsuitable for safe anastomosis. Under these conditions, thrombectomy, jump grafting, cavoportal hemitransposition, or portocaval shunting was unlikely to provide effective splanchnic inflow or relieve portal hypertension.
Postoperative management: immunosuppression, anticoagulation, and ultrasound surveillance
Induction immunosuppression included basiliximab; standard triple therapy (methylprednisolone, a calcineurin inhibitor, and mycophenolate mofetil) was used postoperatively. After excluding contraindications related to bleeding risk, patients with preoperative PVT received intravenous heparin at an initial rate of 10 U/kg/h, generally starting approximately 1 week after LT. The dose was adjusted according to activated partial thromboplastin time (APTT), with a target range of 60–80 s. Anticoagulation was withheld or delayed when bleeding risk was considered unacceptable. Non-PVT recipients did not receive PVT-directed anticoagulation routinely; thromboprophylaxis in these patients followed standard institutional practice based on individualized bleeding and thrombosis risks. When liver function and the overall condition stabilized, usually around 2 weeks postoperatively, eligible patients were transitioned to oral warfarin, with a target international normalized ratio (INR) of 1.5–2.0 for at least 1 year. For patients who developed postoperative PVT or PV stenosis, oral anticoagulation was generally continued for at least 2 years and then reassessed by the treating team. All anticoagulation regimens were formulated by the same team. Dose reduction or discontinuation was considered for gingival bleeding, hematuria, gastrointestinal bleeding, or other clinically significant bleeding events. Postoperative Doppler ultrasound surveillance was performed daily during the first week after LT, with subsequent gradual extension of the follow-up intervals. Patients were monitored at least every 2–3 months within the first postoperative year.
Statistical analysis
Statistical analyses were performed using SPSS version 27.0. Continuous variables with normal distribution were presented as mean ± standard deviation (SD) and compared using Student’s t-test; non-normally distributed variables were presented as median [interquartile range (IQR)] and compared using the Mann-Whitney U test. Categorical variables were reported as n (%) and compared using the χ2 test or Fisher’s exact test as appropriate. Risk factors for preoperative PVT were analyzed using univariate followed by multivariable logistic regression. Survival analysis was performed using the Kaplan-Meier method, with between-group comparisons assessed by the log-rank test. To identify independent predictors of post-transplant mortality, multivariable Cox proportional hazards regression models were constructed. Variables with P<0.05 in univariate analysis or of clinical relevance were included in the multivariable models. P values were two-sided and considered significant at <0.05.
Results
Demographics and clinical characteristics
Between 1 January 2016 and 31 December 2024, our center performed 1,389 liver transplants. Applying inclusion/exclusion criteria, 517 adult patients were included in this analysis (Figure S1). Of these, 144 patients (27.9%) had preoperative PVT and 373 did not. Baseline characteristics were summarized (Table 1). Among the PVT cohort, Yerdel grade distribution was: grade I, 56 (38.9%); grade II, 54 (37.5%); grade III, 25 (17.4%); grade IV, 9 (6.3%). Median age in the PVT group was 55.1 (IQR, 47.9–61.2) years, which was significantly higher than 52.3 (IQR, 43.4–59.6) years in the non-PVT group (P=0.01). Both groups were predominantly male (PVT 68.8% vs. non-PVT 63.8%, P=0.29). The principal etiology in the PVT group was hepatitis B virus (HBV)-related cirrhosis (35.4%), whereas hepatocellular carcinoma (HCC) predominated in the non-PVT group (34.1%). Significant differences between groups were observed for Child-Pugh score, hepatic encephalopathy, UGIB, and prior splenectomy (all P<0.05).
Table 1. Demographics and clinical characteristics.
| Variables | Total (n=517) | Non-PVT (n=373) | PVT (n=144) | χ2/Z | P |
|---|---|---|---|---|---|
| Age (years) | 53.1 (44.7–60.2) | 52.3 (43.4–59.6) | 55.1 (47.9–61.2) | −2.48 | 0.01 |
| Gender | 1.12 | 0.29 | |||
| Male | 337 (65.2) | 238 (63.8) | 99 (68.8) | ||
| Female | 180 (34.8) | 135 (36.2) | 45 (32.2) | ||
| Disease duration (months) | 84.0 (24.0–204.0) | 60.0 (18.0–168.0) | 120.0 (60.0–240.0) | −5.20 | <0.001 |
| Diagnosis | 21.98 | <0.001 | |||
| HCC | 166 (32.1) | 127 (34.1) | 39 (27.1) | ||
| HBV-related cirrhosis | 117 (22.6) | 66 (17.7) | 51 (35.4) | ||
| PBC | 66 (12.8) | 55 (14.8) | 11 (7.6) | ||
| Alcoholic cirrhosis | 50 (9.7) | 34 (9.1) | 16 (11.1) | ||
| Other | 118 (22.8) | 91 (24.4) | 27 (18.8) | ||
| Child-Pugh | 11.08 | 0.004 | |||
| A | 114 (22.1) | 94 (25.2) | 20 (13.9) | ||
| B | 175 (33.9) | 113 (30.3) | 62 (43.1) | ||
| C | 228 (44.1) | 166 (44.5) | 62 (43.1) | ||
| MELD | 15.0 (11.0–21.0) | 15.0 (11.0–22.0) | 14.0 (11.0–18.0) | −1.14 | 0.25 |
| MELD-Na | 16.0 (13.0–23.0) | 17.0 (13.0–24.0) | 16.0 (13.0–20.0) | −1.14 | 0.25 |
| MELD 3.0 | 15.0 (10.0–21.0) | 15.0 (10.0–22.0) | 14.0 (11.0–18.0) | −1.18 | 0.24 |
| Yerdel grade | 517.00 | <0.001 | |||
| 0 | 373 (72.2) | 373 (100.0) | 0 (0.0) | ||
| 1 | 56 (10.8) | 0 (0.0) | 56 (38.9) | ||
| 2 | 54 (10.4) | 0 (0.0) | 54 (37.5) | ||
| 3 | 25 (4.8) | 0 (0.0) | 25 (17.4) | ||
| 4 | 9 (1.7) | 0 (0.0) | 9 (6.3) | ||
| HE | 5.69 | 0.02 | |||
| No | 396 (76.6) | 296 (79.4) | 100 (69.4) | ||
| Yes | 121 (23.4) | 77 (20.6) | 44 (30.6) | ||
| History of UGIB | 20.11 | <0.001 | |||
| No | 300 (58.0) | 239 (64.1) | 61 (42.4) | ||
| Yes | 217 (42.0) | 134 (35.9) | 83 (57.6) | ||
| History of prior splenectomy | 35.32 | <0.001 | |||
| No | 484 (93.6) | 364 (97.6) | 120 (83.3) | ||
| Yes | 33 (6.4) | 9 (2.4) | 24 (16.7) | ||
| TIPS | 0.87 | 0.352 | |||
| No | 492 (95.2) | 357 (95.7) | 135 (93.8) | ||
| Yes | 25 (4.8) | 16 (4.3) | 9 (6.3) |
Data are presented as median (interquartile range) or number (percentage). HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HE, hepatic encephalopathy; MELD, Model for End-Stage Liver Disease; PBC, primary biliary cholangitis; PVT, portal vein thrombosis; TIPS, transjugular intrahepatic portosystemic shunt; UGIB, upper gastrointestinal bleeding.
Risk factors for PVT
Univariate and multivariate logistic regression analyses identified the following factors as independent predictors of preoperative PVT: age [odds ratio (OR) 1.03; 95% confidence interval (CI), 1.01–1.05; P=0.008], HBV-related cirrhosis (OR 2.12; 95% CI, 1.19–3.77; P=0.01), prior splenectomy (OR 6.72; 95% CI, 2.85–15.85; P<0.001, Table S1).
LT surgical procedures
The proportion of deceased donor liver transplantation (DDLT) was higher in the PVT group (86.8% vs. 75.1%, P=0.004) (Table 2). Two patients in the PVT group died intraoperatively due to cardiac arrest.
Table 2. Liver transplantation surgical procedures.
| Variables | Total (n=517) | Non-PVT (n=373) | PVT (n=144) | χ2/Z | P |
|---|---|---|---|---|---|
| Graft type | 8.44 | 0.004 | |||
| DDLT | 405 (78.3) | 280 (75.1) | 125 (86.8) | ||
| LDLT | 112 (21.7) | 93 (24.9) | 19 (13.2) | ||
| GRWR | 1.73 (1.12–2.22) | 1.70 (1.07–2.28) | 1.78 (1.31–2.10) | −0.57 | 0.57 |
| Portal vein anastomosis | <0.001 | ||||
| Anatomical reconstruction | 503 (97.7) | 373 (100.0) | 130 (91.6) | ||
| Porto-variceal anastomosis | 5 (0.97) | 0 | 5 (3.52) | ||
| Portocaval hemi-transposition | 5 (0.97) | 0 | 5 (3.52) | ||
| Portocaval transposition | 2 (0.39) | 0 | 2 (1.41) | ||
| Vascular graft† | 6.84 | 0.009 | |||
| No | 509 (98.8) | 372 (99.7) | 137 (96.5) | ||
| Yes | 6 (1.2) | 1 (0.3) | 5 (3.5) | ||
| Operative time (min) | 420.0 (350.0–510.0) | 405.0 (340.0–507.5) | 453.0 (390.0–530.0) | −3.65 | <0.001 |
| Warm ischemia time (min) | 3.0 (2.0–5.0) | 3.0 (2.0–5.0) | 3.0 (2.0–5.0) | −0.56 | 0.57 |
| Cold ischemia time (min) | 430.0 (202.5–540.0) | 405.0 (162.0–532.0) | 480.0 (358.5–556.3) | −3.28 | 0.001 |
| Intraoperative blood loss (mL) | 900.0 (590.0–1,350.0) | 800.0 (500.0–1,200.0) | 1,200.0 (800.0–1,800.0) | −5.91 | <0.001 |
| Intraoperative RBC transfusion (mL) | 600.0 (0.0–1,200.0) | 600.0 (0.0–900.0) | 800.0 (250.0–1,200.0) | −3.52 | <0.001 |
| Intraoperative platelets (mL) | 0.0 (0.0–0.0) | 0.0 (0.0–0.0) | 0.0 (0.0–0.0) | −0.45 | 0.65 |
| Intraoperative plasma (mL) | 600.0 (0.0–1,000.0) | 600.0 (0.0–1,000.0) | 600.0 (0.0–800.0) | −1.68 | 0.09 |
Data are presented as median (interquartile range) or number (percentage). †, the vascular grafts reported in this table were used for portal venous reconstruction procedures, and no grafts were used for portal jump grafting. DDLT, deceased-donor liver transplantation; GRWR, graft-to-recipient weight ratio; LDLT, living-donor liver transplantation; PVT, portal vein thrombosis; RBC, red blood cell.
Compared with the non-PVT group, the PVT group required more vascular grafts [5 (3.5%) vs. 1 (0.3%), P=0.009]. All patients underwent hepatic artery end-to-end anastomosis; biliary reconstruction (duct-to-duct or choledochojejunostomy) was performed according to intraoperative biliary anatomy.
Operative time was significantly longer in the PVT group [453.0 (IQR, 390.0–530.0) vs. 405.0 (IQR, 340.0–507.5) minutes, P<0.001]. Intraoperative blood loss [1,200.0 (IQR, 800.0–1,800.0) vs. 800.0 (IQR, 500.0–1,200.0) mL, P<0.001] and red blood cell transfusion volume [800.0 (IQR, 250.0–1,200.0) vs. 600.0 (IQR, 0.0–900.0) mL, P<0.001] were both significantly higher in the PVT group.
Postoperative outcomes
Median follow-up was 45.6 (IQR, 20.5–75.7) months (Table 3). There were no significant differences in total hospital stay or ICU stay between groups. The incidence of PV-related complications in the PVT and non-PVT groups was 16.2% vs. 3.5% (P<0.001). Postoperative PVT occurred in 12.7% of the PVT group vs. 2.7% of the non-PVT group (P<0.001). Notably, 11 patients (7.8%) in the PVT group had partially organized chronic PVT on postoperative ultrasound. PV stenosis occurred in 8 patients (5.6%) in the PVT group and 4 patients (1.1%) in the non-PVT group (P=0.006). Among the six patients who underwent multiple-vessel anastomoses, one developed PVT 14 days postoperatively, which resolved after anticoagulation therapy. Another patient developed PV anastomotic stenosis 6 months after surgery and received interventional balloon dilation and thrombectomy, but eventually died of septic shock. The remaining four patients maintained satisfactory PV patency with favorable outcomes. There was no significant difference in the incidence of major complications between the two groups (P=0.41). Most PV-related complications were managed with anticoagulation (24/36), interventional procedures (9/36), or surgery (1/36), and only 3 patients eventually died as a direct result of unsuccessful treatment of their PV complications.
Table 3. Follow-up and prognosis.
| Variables | Total (n=517) | Non-PVT (n=373) | PVT (n=144) | χ2/Z | P |
|---|---|---|---|---|---|
| Follow-up (months) | 45.6 (20.5–75.7) | 45.6 (20.3–76.5) | 45.3 (23.8–73.9) | −0.61 | 0.54 |
| Total hospital stay (days) | 24.0 (18.0–36.0) | 24.0 (18.0–36.0) | 24.0 (19.0–36.0) | −0.60 | 0.55 |
| ICU stay (days) | 3.0 (2.0–4.0) | 3.0 (2.0–4.0) | 3.5 (2.3–5.0) | −1.71 | 0.09 |
| 30-day mortality | 21 (4.1) | 13 (3.5) | 8 (5.6) | 1.14 | 0.28 |
| Outcome | 0.04 | 0.85 | |||
| Survival | 405 (78.3) | 293 (78.6) | 112 (77.8) | ||
| Death | 112 (21.7) | 80 (21.4) | 32 (22.2) | ||
| Postoperative PVT† | 51.29 | <0.001 | |||
| None | 476 (92.4) | 363 (97.3) | 113 (79.6) | ||
| Recurrent PVT | 28 (5.5) | 10 (2.7) | 18 (12.7) | ||
| Chronic residual PVT | 11 (2.1) | 0 (0.0) | 11 (7.8) | ||
| Postoperative PV stenosis | 7.51 | 0.006 | |||
| No | 503 (97.7) | 369 (98.9) | 134 (94.4) | ||
| Yes | 12 (2.3) | 4 (1.1) | 8 (5.6) | ||
| PV-related complications | 23.88 | <0.001 | |||
| No | 479 (93.0) | 360 (96.5) | 119 (83.8) | ||
| Yes | 36 (7.0) | 13 (3.5) | 23 (16.2) | ||
| Major complications (Clavien-Dindo ≥ III) | 1.11 | 0.29 | |||
| No | 404 (78.4) | 297 (79.6) | 107 (75.4) | ||
| Yes | 111 (21.6) | 76 (20.4) | 35 (24.6) |
Data are presented as median (interquartile range) or number (percentage). †, two patients experienced intraoperative cardiac arrest and died (not salvageable). ICU, intensive care unit; PV, portal vein; PVT, portal vein thrombosis.
Renal function was also evaluated longitudinally. The eGFR was measured both preoperatively and at predefined postoperative time points. The PVT group exhibited consistently lower eGFR values compared with the non-PVT group at both preoperative and postoperative assessments, with the difference becoming more pronounced at 6 months and 1 year after LT (Table 4). Postoperative renal dysfunction was significantly more frequent in the PVT group at both 6 months and 1 year after transplantation. Specifically, at 6 months, 46.2% of patients in the PVT group experienced renal dysfunction compared to 33.7% in the non-PVT group (P=0.01, Table 5). Similarly, at 1 year, the PVT group had a significantly higher incidence of renal dysfunction (52.5% vs. 39.4%, P=0.01). The overall 30-day mortality rate was 4.06% (21/517). Thirty-day mortality was numerically higher in the PVT group than in the non-PVT group [5.56% (8/144) vs. 3.49% (13/373)], although the difference was not statistically significant (P=0.28). The 1-, 3-, and 5-year overall survival rates in the PVT and non-PVT groups were 88.9%, 82.6%, and 78.5% versus 88.5%, 82.0%, and 80.4%, respectively. Kaplan-Meier survival analysis demonstrated no statistically significant difference between the survival curves of the two groups (P=0.94, Figure 2).
Table 4. Pre- and post-LT eGFR.
| eGFR (mL/min/1.73 m2) | Total (n=517) | Non-PVT (n=373) | PVT (n=144) | Z | P |
|---|---|---|---|---|---|
| Pre-LT | 104.5 (93.2–114.0) | 104.7 (93.9–114.7) | 103.8 (88.4–110.0) | −1.97 | 0.048 |
| Post-LT 1 month | 102.7 (87.8–112.6) | 103.1 (89.7–114.0) | 101.3 (79.2–109.6) | −2.00 | 0.046 |
| Post-LT 6 months | 98.8 (79.1–108.1) | 100.0 (82.0–109.8) | 92.1 (70.6–106.5) | −2.75 | 0.006 |
| Post-LT 1 year | 95.7 (78.3–107.1) | 97.7 (80.9–108.5) | 89.5 (74.6–104.2) | −2.48 | 0.01 |
Data are presented as median (interquartile range). eGFR, estimated glomerular filtration rate; LT, liver transplantation; PVT, portal vein thrombosis.
Table 5. Pre- and post-LT renal dysfunction.
| Variables | Total (n=517) | Non-PVT (n=373) | PVT (n=144) | χ2 | P |
|---|---|---|---|---|---|
| Pre-LT, n (%) | 2.96 | 0.08 | |||
| No | 404 (78.6) | 298 (80.5) | 106 (73.6) | ||
| Yes | 110 (21.4) | 72 (19.5) | 38 (26.4) | ||
| Post-LT 1 month, n (%) | 3.03 | 0.08 | |||
| No | 359 (72.4) | 269 (74.5) | 90 (66.7) | ||
| Yes | 137 (27.6) | 92 (25.5) | 45 (33.3) | ||
| Post-LT 6 months, n (%) | 6.33 | 0.01 | |||
| No | 295 (62.8) | 224 (66.3) | 71 (53.8) | ||
| Yes | 175 (37.2) | 114 (33.7) | 61 (46.2) | ||
| Post-LT 1 year, n (%) | 6.12 | 0.01 | |||
| No | 248 (57.0) | 191 (60.6) | 57 (47.5) | ||
| Yes | 187 (43.0) | 124 (39.4) | 63 (52.5) |
LT, liver transplantation; PVT, portal vein thrombosis.
Figure 2.
Overall survival according to preoperative PVT status. Kaplan-Meier survival curves comparing overall survival between liver transplant recipients with and without preoperative PVT. Overall survival was comparable between the PVT and non-PVT groups, with no statistically significant difference observed by log-rank test (P=0.94; HR, 1.015; 95% CI, 0.674–1.530). Numbers at risk are shown below the plot. CI, confidence interval; HR, hazard ratio; PVT, portal vein thrombosis.
Etiology-stratified survival and multivariable mortality analysis
We also performed Kaplan-Meier survival analyses stratified by the presence of HCC. In both the HCC and non-HCC strata, survival curves between PVT and non-PVT patients did not differ significantly (Figure S2A,S2B). A multivariable Cox proportional hazards regression model was constructed to identify independent predictors of all-cause mortality in the entire cohort (Table S2). After adjusting for relevant clinical variables, HCC, MELD-3.0 score and ICU stay were identified as independent risk factors for all-cause death. Notably, preoperative PVT status was not a significant independent predictor of survival in this adjusted model.
PVT subgroup comparison (simple vs. complex)
PVT patients were stratified as simple PVT (Yerdel I–II, n=108) and complex PVT (Yerdel III–IV, n=34) (Table S3). Baseline characteristics were similar between the subgroups. Intraoperatively, complex PVT had a significantly higher vascular graft usage rate (11.8% vs. 0.9%, P=0.01; Table 6). In the non-PVT group, all patients underwent anatomical PV reconstruction. Among the 142 patients with PVT who completed transplantation, 130 (91.6%) underwent anatomical reconstruction and 12 (8.4%) received non-anatomical reconstruction (including portal-variceal anastomosis in 5 patients, portocaval hemi-transposition in 5 patients, and portocaval transposition in 2 patients) (Figure 1). The remaining two patients died from intraoperative cardiac arrest and were included in the mortality analyses but not in the reconstruction or postoperative complication analyses. No patient underwent portal inflow reconstruction using a jump graft. Among the 12 non-anatomical reconstructions, six patients required additional anastomoses from supplemental portal sources because a single anastomosis provided insufficient inflow (Table S4): in porto-variceal reconstructions, Case 1 combined an end-to-end porto-portal anastomosis plus a side-to-end porto-variceal anastomosis (Figure 1B). In portocaval hemi-transposition cases, Cases 2-4 had end-to-end left reno-portal anastomosis plus a side-to-end porto-variceal anastomosis (Figure 1C); Case 5 had end-to-end graft portocaval anastomosis plus end-to-side recipient portocaval anastomosis (Figure 1D); Case 6 had end-to-side graft portocaval anastomosis [with narrowing of the inferior vena cava (IVC) above the anastomosis] plus side-to-end graft porto-variceal anastomosis (Figure 1E).
Table 6. Liver transplantation surgical procedures (simple vs. complex PVT).
| Variables | Total (n=142) | Simple PVT (n=108) | Complex PVT (n=34) | χ2/Z | P |
|---|---|---|---|---|---|
| Graft type | 0.00 | >0.99 | |||
| DDLT | 123 (86.6) | 94 (87.0) | 29 (85.3) | ||
| LDLT | 19 (13.4) | 14 (13.0) | 5 (14.7) | ||
| GRWR | 1.76 (1.31–2.04) | 1.81 (1.29–2.18) | 1.66 (1.32–2.00) | −0.89 | 0.37 |
| Portal vein anastomosis | – | <0.001 | |||
| Anatomical reconstruction | 128 (91.4) | 104 (98.1) | 24 (70.6) | ||
| Porto-variceal anastomosis | 5 (3.6) | 2 (1.9) | 3 (8.8) | ||
| Portocaval hemi-transposition | 5 (3.6) | 0 (0.0) | 5 (14.7) | ||
| Portocaval transposition | 2 (1.4) | 0 (0.0) | 2 (5.9) | ||
| Vascular graft | 5.89 | 0.01 | |||
| No | 135 (96.4) | 105 (99.1) | 30 (88.2) | ||
| Yes | 5 (3.6) | 1 (0.9) | 4 (11.8) | ||
| Operative time (min) | 455.0 (395.0–530.0) | 430.0 (385.0–502.5) | 502.5 (448.8–563.8) | −3.10 | 0.002 |
| Warm ischemia time (min) | 3.0 (2.0–5.0) | 3.0 (2.0–5.0) | 3.0 (2.0–5.0) | −0.47 | 0.64 |
| Cold ischemia time (min) | 480.0 (360.0–558.8) | 480.0 (331.5–558.8) | 478.0 (375.0–533.8) | −0.14 | 0.89 |
| Intraoperative blood loss (mL) | 1,200.0 (800.0–1,800.0) | 1,200.0 (800.0–1,800.0) | 1,350.0 (900.0–2,000.0) | −1.00 | 0.32 |
| Intraoperative packed RBC transfusion (mL) | 800.0 (255.0–1,230.0) | 800.0 (280.0–1,200.0) | 850.0 (187.5–1,525.0) | −0.63 | 0.53 |
| Intraoperative platelets (mL) | 0.0 (0.0–0.0) | 0.0 (0.0–0.0) | 0.0 (0.0–0.0) | −0.18 | 0.86 |
| Intraoperative plasma (mL) | 600.0 (0.0–820.0) | 600.0 (0.0–800.0) | 700.0 (400.0–1,200.0) | −1.01 | 0.31 |
Data are presented as median (interquartile range) or number (percentage). Two patients experienced intraoperative cardiac arrest and died (not salvageable). DDLT, deceased-donor liver transplantation; GRWR, graft-to-recipient weight ratio; LDLT, living-donor liver transplantation; PVT, portal vein thrombosis; RBC, red blood cell.
There were no significant differences between simple and complex PVT in total hospital stay, ICU stay, PV-related complications, major complications, or 30-day mortality (Table S5). Thirty-day mortality did not differ significantly between the simple and complex PVT groups [7.3% (8 patients) vs. 0% (0 patients), P=0.23]. All eight deaths within 30 days occurred in the simple PVT group. However, this finding should be interpreted cautiously because of the small complex PVT subgroup, the limited number of early deaths, and the strict selection of patients with advanced PVT. Kaplan-Meier analysis demonstrated no statistically significant survival difference (P=0.11, Figure S3). We also performed Kaplan-Meier survival analyses stratified by the presence of HCC. Whether in the HCC group or the non-HCC group, survival curves between simple PVT and complex PVT patients did not differ significantly (Figure S4A,S4B). Multivariate Cox regression analysis identified the MELD 3.0 score [hazard ratio (HR) =1.08, 95% CI, 1.04–1.13; P<0.001] and length of ICU stay (HR =1.08, 95% CI, 1.02–1.15; P=0.008) as independent predictors of mortality risk (Table S6). Although included in the model, PVT grade remained a non-significant factor.
Discussion
In this large single-center Chinese cohort, preoperative PVT was associated with greater operative complexity, more PV-related complications, and persistent renal dysfunction. However, 30-day mortality and adjusted long-term survival were comparable between the PVT and non-PVT groups. No early deaths occurred in the complex PVT subgroup, but this finding should be interpreted cautiously because of the small sample size and strict patient selection. Long-term survival remained comparable between PVT and non-PVT recipients after multivariable adjustment. Nevertheless, selected patients undergoing non-anatomical yet physiological multi-vessel PV reconstruction achieved outcomes comparable to those with simple PVT.
The prevalence of PVT reported among LT candidates ranges from 8% to 26%. Our observed PVT prevalence was higher, potentially related to: (I) longer waiting times for LT attributable to advances in endoscopic and interventional management; (II) referral bias with more complex PVT patients presenting to our experienced center; and (III) more comprehensive imaging surveillance improving detection rates.
Pathophysiologically, PVT is linked to Virchow’s triad (endothelial injury, hemodynamic changes, and hypercoagulability) (14). Splenectomy could reduce portal flow and predispose to thrombosis, which emphasizes the value of preoperative imaging for risk stratification. Some etiologies, such as cryptogenic cirrhosis and nonalcoholic steatohepatitis, may confer additional risk due to procoagulant imbalance (15). In our cohort, HBV-related cirrhosis emerged as a risk factor, possibly reflecting chronic inflammation associated with long-standing HBV infection. HBV-related cirrhosis is frequently observed among Asian patients with PVT, and recent evidence further suggests that adverse virological responses and higher hepatitis B surface antigen (HBsAg) levels are associated with an increased risk of PVT in patients with chronic hepatitis B (16).
PVT compromises intraoperative PV reconstruction and its hemodynamics, particularly in complex PVT defined as Yerdel grade III or higher, where complete thrombectomy is technically challenging and operative difficulty is substantially increased (17). In some patients, thrombi are calcified and not amenable to complete removal, and postoperative ultrasonography may reveal residual, chronic calcified PVT. In our prior work, calcified PVT was associated with unsatisfactory thrombectomy outcomes (11). Overall rates of major postoperative complications following LT did not differ between PVT and non-PVT patients in this study, which is in agreement with other reports (8,18).
Postoperative PVT and PV stenosis are common postoperative complications, and the presence of preoperative PVT increases these risks (19). This study confirmed that PVT significantly increases the incidence of postoperative PV-related complications. This elevated risk necessitates a structured and vigilant postoperative management protocol. In clinical practice, our findings underscore the importance of enhanced surveillance through regular Doppler ultrasonography to enable early detection and intervention for vascular complications. Additionally, anticoagulation strategy must be carefully individualized and requires meticulous monitoring.
The post-LT prognosis of PVT patients is therefore of considerable concern to surgeons. Prior investigations have largely focused on postoperative patient survival and PV patency. In our study, patients with preoperative PVT exhibited lower eGFR levels both before and after LT compared to those without PVT. The incidence of renal dysfunction was significantly higher in the PVT group at 6 months and 1 year, highlighting the sustained impact of preoperative PVT on renal function even after the initial postoperative period. The underlying mechanisms are likely multifactorial. PVT can reduce renal perfusion by increasing systemic vascular resistance, further impairing kidney function and lowering preoperative eGFR. Moreover, the complex vascular conditions in PVT patients often lead to longer operative time, greater intraoperative blood loss, and higher transfusion requirements (20,21). These factors can contribute to perioperative hemodynamic instability and fluctuations in effective circulating volume, potentially resulting in renal hypoperfusion and even acute kidney injury. More importantly, PVT patients are at a significantly higher risk of postoperative recurrent PVT or PV stenosis. These vascular complications can lead to persistent or recurrent portal hypertension, which may adversely affect renal function. Therefore, for LT recipients with PVT, it is crucial not only to focus on the prevention and management of vascular complications but also to emphasize perioperative renal monitoring and protection.
PVT was once considered an absolute contraindication to LT, but advances in medical and surgical techniques have rendered it no longer universally prohibitive. The method of PV reconstruction is critical for restoring PV patency and ultimately influences patient prognosis. To maximize the likelihood of anatomical PV reconstruction, surgeons employ thrombectomy techniques such as eversion, pull-out, and pull-through (22,23). However, for extensive or severely calcified complex PVT, complete thrombus removal may be impossible and satisfactory portal inflow cannot be guaranteed. In these situations, strategies intended to achieve non-anatomical but physiological PV inflow, such as jump grafts, porto-variceal anastomosis, or portocaval hemi-transposition/transposition (24-26), have been attempted to maximize portal-system blood delivery to the graft while simultaneously decompressing portal hypertension. For complex PVT not amenable to conventional anastomosis, the multiple-vessel anastomosis strategy used in this study sought to achieve partial physiological reconstruction by augmenting graft inflow with additional portal-system sources. This approach was intended to ensure adequate graft perfusion while improving splanchnic venous drainage. Increased portal inflow supports graft perfusion and metabolic function and may also reduce flow stasis and turbulence, both of which promote thrombus formation. This hemodynamic optimization may explain the comparable long-term outcomes despite greater anatomical complexity.
Current consensus holds that outcomes after LT for simple PVT are comparable to those for patients without PVT, whereas complex PVT has been linked to higher mortality and complication rates (6,27). In our series, overall prognosis was similar between PVT and non-PVT patients, and survival outcomes in complex PVT were comparable to those observed in simple PVT. As noted in our protocol, patients with diffuse portomesenteric thrombosis accompanied by severe portal hypertension and no surgically accessible collateral were considered absolute contraindications to LT at our center. This selection bias fundamentally limits the generalizability of our favorable results for complex PVT and underscores that our conclusions are not applicable to patients with the most advanced, diffuse forms of the condition. For this subset of patients, multivisceral transplantation may represent a last-resort option, but it is currently performed only in a few highly experienced centers (28,29).
Pretransplant portal vein recanalization with transjugular intrahepatic portosystemic shunt (PVR-TIPS) may facilitate physiologic PV reconstruction during subsequent LT (30,31). Some series report that PVR-TIPS increases rates of transplantation and physiologic portal reconstruction in patients with chronic obliterative PVT (32). Our center initiated the use of PVR-TIPS during the study period with encouraging preliminary results, supporting the role of multidisciplinary, individualized preoperative interventional strategies.
Study limitations include the single-center retrospective design with potential selection bias, and a small sample size for the multiple-vessel anastomosis subgroup, which limits the generalizability of conclusions regarding this technique. Larger prospective and multicenter studies are needed to validate these findings.
Conclusions
Preoperative PVT was associated with greater operative complexity, more PV-related complications, and a higher incidence of postoperative renal dysfunction after LT. However, in carefully selected patients in whom adequate portal inflow reconstruction was technically feasible, PVT was not independently associated with inferior long-term survival. Individualized anatomical or non-anatomical physiological reconstruction may achieve acceptable outcomes in complex PVT.
Supplementary
The article’s supplementary files as
Acknowledgments
We thank Siqi Liu, Junshan Liu, Rili Li, and Fanghui Cui for their invaluable efforts in maintenance of Beijing Friendship Hospital database of China Liver Transplant Registry.
Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments and the International Conference on Harmonization Guideline for Good Clinical Practice. The protocol for this research project has been approved by the Ethics Committee of Beijing Friendship Hospital (No. BFHHZS20240128). All informed consent was obtained from the subject(s) and/or guardian(s).
Footnotes
Reporting Checklist: The authors have completed the STROCSS reporting checklist. Available at https://tgh.amegroups.com/article/view/10.21037/tgh-2026-0127/rc
Funding: This work was supported by Capital’s Funds for Health Improvement and Research (No. 2024-1-2022) and National Natural Science Foundation of China (No. 82400697).
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tgh.amegroups.com/article/view/10.21037/tgh-2026-0127/coif). The authors have no conflicts of interest to declare.
Data Sharing Statement
Available at https://tgh.amegroups.com/article/view/10.21037/tgh-2026-0127/dss
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