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Abstract: SA-PO874

Transplant Renal Artery Stenosis: An Overlooked Cause of Acute Kidney Allograft Injury

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Aloor, Rohit, University of California Irvine School of Medicine, Irvine, California, United States
  • Tantisattamo, Ekamol, University of California Irvine School of Medicine, Irvine, California, United States
Introduction

While recognized as an etiology of kidney dysfunction, transplant renal artery stenosis (TRAS) remains underdiagnosed and can exist with other causes of acute kidney injury (AKI), leading to a delay in diagnosis and treatment. We report a case of kidney transplant recipient that presented with biopsy-proven acute kidney allograft rejection that did not improve despite adequate therapy. Pathology revealed areas of allograft ischemia, leading to treatment for TRAS with balloon angioplasty and subsequent kidney recovery.

Case Description

A 74 year old woman with end stage kidney disease secondary to diabetes mellitus status post deceased donor kidney transplant five months prior to admission presented with sepsis from urinary tract infection and pneumonia complicated by oliguric AKI. Serum creatinine (SCr) was 3.7 mg/dL from the baseline creatinine of 2.7-3.1 mg/dL, peaking at 8.8 mg/dL on hospital day 15. Given persistently elevated SCr despite resolved sepsis, transplant allograft biopsy was performed with concerns for acute rejection. Pathology revealed severe tubulitis and acute T-cell mediated rejection (TCMR). Kidney function did not improve with pulse steroids and anti-thymocyte globulin. Further review of the pathology showed multiple areas of ischemia, suspected from compromised renal artery. Blood pressure (BP) was persistently elevated and no bruit noted at the allograft site. Cytomegalovirus PCR was not detected. Transplant ultrasound revealed peak systolic velocity of 310 cm/second at the anastomosis. Carbon dioxide angiography was consistent with severe transplant renal artery stenosis. Balloon angioplasty resulted in allograft recovery and SCr improved to a nadir of 1.0 mg/dL along with blood pressure normalization.

Discussion

Although AKI in our patient could be possibly explained by TCMR, persistent allograft dysfunction despite therapy for rejection raised suspicion for other causes. Scattered renal ischemic changes in the setting of ongoing AKI and hypertension within the first 6 months posttransplant led to TRAS evaluation. TRAS is a common complication but rarely occurs concomitantly with acute allograft rejection. Clinical presentation that includes allograft dysfunction and uncontrolled BP, particularly with evidence of allograft ischemia during early post-transplant period, should raise suspicion for this treatable cause of kidney allograft injury.