RECURRENT TRANSPLANT RENAL ARTERY STENOSIS

RECURRENT TRANSPLANT RENAL ARTERY STENOSIS

Miss Stephanie Lam1, Dr Mathew Mathew1, A/Prof Rajesh Raj1

1Launceston General Hospital, Launceston, Australia

Background: Transplant renal artery stenosis (TRAS) is a known complication of renal transplantation and a cause for graft failure, typically managed with percutaneous intervention. Restenosis of an intervened site can occur, with repeated percutaneous intervention as management.

Case report: A 51-year-old man with end-stage renal disease secondary to diabetic nephropathy underwent deceased-donor kidney transplant, with creatinine plateauing at 150µmol/L post transplantation. Complications of acute T-cell mediated rejection transpired 4 months post transplantation and renal arterial doppler ultrasound at that time demonstrated normal transplant renal artery. 8 months post transplantation there was further graft dysfunction with creatinine rise to 478µmol/L. A biopsy was unremarkable but repeat transplant doppler ultrasound showed elevated peak systolic velocities of 450cm/sec in the proximal portion of the transplant renal artery. Angiogram identified stenosis at the lower pole branch of the dominant lower renal artery, which was balloon angioplastied with subsequent improvement of creatinine to 205µmol/L. At 1 week post angioplasty, candesartan was commenced for hypertension management, however creatinine rose to 334µmol/L and candesartan was ceased. Despite this, creatinine continued to rise to 399µmol/L. A repeat ultrasound showed restenosis of the proximal lower pole renal artery and another angiogram was conducted. Repeat angiogram again showed stenosis, but now at the upper and mid branches of the lower pole renal artery. Balloon angioplasty was successfully conducted, and creatinine improved to 205µmol/L.

Conclusion: We report an unusual occurrence of TRAS at two differing regions of renal artery branches, which could be related to surgical technique at time of transplantation. This case highlights the importance of always considering TRAS as a cause for graft dysfunction even in patients with recent percutaneous intervention.

Biography:

Stephanie is a first year nephrology advanced trainee at Launceston General Hospital.

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