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Case Reports
. 2018 Nov 23:11:321-327.
doi: 10.2147/IJNRD.S185520. eCollection 2018.

Successful salvage of allograft dysfunction triggered by transplant renal vein thrombosis immediately after kidney transplantation: a case report

Affiliations
Case Reports

Successful salvage of allograft dysfunction triggered by transplant renal vein thrombosis immediately after kidney transplantation: a case report

Shunta Hori et al. Int J Nephrol Renovasc Dis. .

Abstract

Background: Transplant renal vein thrombosis (TRVT) is a severe vascular complication and is caused by various factors, including recipient factors, donor factors, immunosuppression regimens, and surgical techniques. Despite adequate interventions, including thrombolytic therapy or surgical thrombectomy, successful salvage of the allograft is often difficult. We observed a case of TRVT induced by compression of the renal vein immediately after intraoperative abdominal closure.

Case presentation: A 41-year-old male underwent ABO-compatible living kidney transplantation. The donor was his 45-year-old sister, and her right kidney was donated. The allograft had a single artery and vein. One of the preoperative recipient problems was obesity (body mass index, 33.4 kg/m2). Intraoperative Doppler ultrasonography (US) revealed sufficient blood flow throughout the allograft, and urine output was also observed. After surgery, hematuria was observed; the urine output decreased and serum creatinine levels increased to 7.0 mg/dL. Doppler US showed a decrease in diastolic flow and an elevated resistive index, which were similar findings to those noted in acute rejection. Although steroid pulse therapy was initiated, allograft dysfunction was worsening. On postoperative day 4, surgical exploration revealed TRVT; consequently, thrombectomy was performed. The urine output increased, and serum creatinine levels decreased to 1.8 mg/dL. The cause of TRVT development may be that the transplant renal vein was relatively short, due to the right kidney being compressed by surrounding tissues after abdominal closure, and that TRVT was gradually developing due to stagnant blood flow.

Conclusion: Although TRVT is induced by multiple factors, an accurate diagnosis is often difficult. Understanding these factors, including obesity, and considering TRVT as a cause of allograft dysfunction are important during the pre-, peri-, and postoperative periods. Knowledge of TRVT can lead to early and accurate diagnosis and intervention, resulting in better outcomes for the patients with allograft dysfunction.

Keywords: kidney transplantation; surgical exploration; thrombectomy; transplant renal vein thrombosis.

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Conflict of interest statement

Disclosure The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
Representative allograft images of Doppler US and CT before surgical exploration. Notes: Doppler US revealed a decrease in end-diastolic blood velocity (4.2 cm/s) and an elevated RI (0.85) (A). CT revealed a hematoma with air in the urinary tract of the allograft (B): coronal image, (C): sagittal image, red arrow: hematoma with air. Abbreviations: CT, computed tomography; RI, resistive index; US, ultrasonography; PS, peak systolic; ED, end-diastolic; MD, mean diastolic; TAMAX, time averaged maximum; PI, pulsatility index; RI, resistance index; AT, acceleration time.
Figure 2
Figure 2
Representative allograft image and schematic for surgical exploration. Notes: Representative image of the allograft during surgical exploration. Arterial anastomotic stenosis was not observed. The proximal renal vein was branched into two, and one branch was compressed by the surrounding tissues, including the allograft, renal artery, and abdominal wall, resulting in TRVT. In addition, the upper urinary tract of the allograft was occupied by a hematoma with clots and air (A), red arrow: renal artery, blue arrow: renal vein, green arrow: allograft, and yellow arrow: ureter. A schematic of the intraoperative allograft is shown. The trunk of the renal vein had no evidence of thrombosis, and a thrombectomy was performed. In addition, a hematoma with a clot of the upper urinary tract was evacuated (B). Doppler US showed improved end-diastolic blood velocity (11.7 cm/s) and RI (0.56) (C). Abbreviations: RI, resistive index; TRVT, transplant renal vein thrombosis; US, ultrasonography; PS, peak systolic; ED, end-diastolic; MD, mean diastolic; TAMAX, time averaged maximum; PI, pulsatility index; RI, resistance index; AT, acceleration time.
Figure 3
Figure 3
Representative allograft images of CT after surgical exploration. Notes: CT revealed a loss of the hematoma with air in the upper urinary tract of the allograft. (A): coronal image, (B): sagittal image, red arrow: allograft. Abbreviation: CT, computed tomography.
Figure 4
Figure 4
Clinical course of serum creatinine levels and urine output and the immunosuppression regimen. Notes: On POD 4, the serum creatinine level was 7.0 mg/dL, and urine output decreased; thus, surgical exploration was performed. After evacuation of the transplant renal vein thrombosis and hematoma of the upper urinary tract of the allograft, serum creatinine levels decreased to 1.8 mg/dL, and urine output increased. The immunosuppression regimen was as follows: tacrolimus, MMF, PSL, and BXM. At discharge, the doses of each immunosuppressive agent were as follows: 10 mg/day tacrolimus, 1,000 mg/day MMF, and 5 mg/day PSL. Abbreviations: BXM, basiliximab; MMF, mycophenolate mofetil; POD, postoperative day; PSL, prednisone; Tac, tacrolimus.

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