Transplant renal artery stenosis (TRAS),R enal transplantation is the definitive therapy for end-stage kidney disease and provides substantial lifesaving and quality-of-life benefits for patients who would otherwise undergo dialysis.1 Posttransplantation stenosis of the renal artery-more commonly called TRAS, or transplant renal artery stenosis-is the most frequent vascular complication of kidney transplantation.2 It is implicated in graft dysfunction, concomitant congestive heart failure, and refractory hypertension. Transplant renal artery stenosis is often detected during routine Doppler-ultrasonographic screening of the transplanted kidney or during the clinical evaluation that occurs when graft function deteriorates.3 Percutaneous revascularization of TRAS is indicated to treat graft dysfunction; however, the conventional use of angiography to guide the intervention can put the graft at substantial risk of contrast nephropathy. 4,5 We present a case of TRAS that was discovered during the evaluation for causes of a patient's failing transplanted kidney.
Case ReportIn January 2013, a 70-year-old man with end-stage polycystic kidney disease underwent cadaveric kidney transplantation. He had a history of hypertension, transient ischemic attack, and coronary artery disease. In the 4 months after his kidney transplantation, he had hospital admissions for heart failure, gastrointestinal bleeding, and acute coronary syndrome requiring percutaneous coronary intervention. The patient's serum creatinine levels increased steadily during this time, from 1.47 mg/ dL at the time of transplantation to 6.99 mg/dL 5 months after transplantation. The rise in creatinine was attributed to cumulative kidney damage from intra-arterial contrast medium administered during the above-mentioned percutaneous coronary intervention, to acute tubular necrosis from hypotension, and possibly to cardiorenal syndrome. Five months after the transplantation, he presented with refractory pulmonary edema and acute-on-chronic renal failure (serum creatinine level, 6.05 mg/ dL). He was treated with diuresis, which further elevated the creatinine to a peak of 7.31 mg/dL. Hemodialysis was initiated to treat azotemia and volume overload. Biopsy specimens of the transplanted kidney did not reveal any specific cause for his Case Reports