Korean J Transplant.  2020 Dec;34(4):272-278. 10.4285/kjt.20.0034.

Acute allograft dysfunction mimicking thrombotic microangiopathy in kidney transplant recipient with renal infarction: case report and review of literatures

Affiliations
  • 1Division of Nephrology, Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea
  • 2Department of Medicine and Geriatrics, Kwong Wah Hospital, Hong Kong, China
  • 3Transplant Research Center, Department of Internal Medicine, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea
  • 4Division of Nephrology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea
  • 5Division of Vascular and Transplant Surgery, Department of Surgery, College of Medicine, The Catholic University of Korea, Seoul, Korea

Abstract

Acute allograft dysfunction is rarely observed in kidney transplantation (KT). We report an unusual case of acute allograft dysfunction mimicking thrombotic microangiopa- thy (TMA) in recipient with renal infarction. A 65-year-old man underwent KT from his 39-year-old son. Pre-transplant donor evaluation was normal except for the branches of the upper and lower pole renal arteries originating from the aorta in renal computed topographic angiography, respectively. The immediate post-transplant clinical course was uneventful, but serum creatinine (SCr) increased from 2.2 to 4.5 mg/dL, anemia and throm-bocytopenia were shown, and serum lactate dehydrogenase increased to 919 U/L on the third day after transplantation. We suspected TMA, because of no evidence of acute bleeding. The laboratory parameters associated with TMA were within normal ranges. Renal magnetic resonance angiography revealed a focal wedge-shaped perfusion defect in the upper pole of the graft and renal Doppler ultrasonography showed decreased per- fusion of the lower pole of the graft. Graft function improved with conservative therapy. The patient was discharged with SCr of 1.21 mg/dL. Graft function has been stable after discharge. Acute allograft infarction should be considered in the differential diagnosis of acute allograft dysfunction mimicking TMA in recipients with grafts supplied by multiple renal arteries.

Keyword

Kidney transplantation; Primary graft dysfunction; Thrombotic microangiopathy

Figure

  • Fig. 1 Renal computed tomography angiogram of the donor. A small lower polar branch arises from the aorta (arrow), supplying the lower pole (A) and a tiny upper polar branch arises from the aorta (arrow), supplying the upper pole of the left kidney (B).

  • Fig. 2 Radiologic findings of the recipient. Focal wedge shaped perfusion defect in the upper pole of the transplanted kidney on flair images (arrow), coronal view of renal magnetic resonance angiography (A) and slightly decreased vascularity and perfusion in inferior pole of graft kidney on kidney Doppler ultrasonography (B). Peak systolic velocity of lower inter-lobar artery reduced to 14.3 cm/sec.

  • Fig. 3 Change of laboratory findings after kidney transplantation. (A) On the 1st day after transplantation, serum creatinine (SCr) decreased to 2.19 mg/dL. However, on the 2nd day after transplantation, SCr began to increase and reached to 5.59 mg/dL on the 4th day after transplantation. At the same time, serum lactate dehydrogenase (LDH) also increased to 919 U/L. SCr recovered to 1.21 mg/dL on the day of discharge. (B) Serum hemoglobin (Hb) decreased from 10.9 g/dL to 7 g/dL for 3 days after transplantation. At the same time, serum platelet (PLT) count decreased from 159×103/µL to 65×103/µL. Serum Hb and PLT count recovered to normal with allograft renal function. OD, operative day; POD, postoperative day.


Reference

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