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Abstract: TH-PO1043

Bilateral Multiple Renal Arteries as a Cause for Renal Infarction

Session Information

Category: CKD (Non-Dialysis)

  • 2302 CKD (Non-Dialysis): Clinical, Outcomes, and Trials


  • Chauhan, Mit A., Saint Michael's Medical Center, Newark, New Jersey, United States
  • Bhatt, Heli, Texoma Medical Center, Denison, Texas, United States
  • Malhotra, Pooja, Saint Michael's Medical Center, Newark, New Jersey, United States

Atrial fibrillation is the most common cause of renal infarction followed by valvular or ischemic heart disease, and coagulopathy. However, when all tests are unremarkable, renovascular abnormalities must be kept in the differential. We present one such case of bilateral double renal artery as a likely cause of renal infarction.

Case Description

Forty-six-year-old male with no known past medical history presents to the emergency department for sudden onset left lower quadrant pain radiating to left flank and thigh, severe, 10/10, constant and progressively worsening. Patient denies any dysuria, hematuria, or change in urine output. Patient is hemodynamically stable. The physical exam elicited left sided flank tenderness, left testicular tenderness without swelling or evidence of varicose veins. Lab results showed elevated white blood cell count of 16.5, normal BUN and creatinine. The erythrocyte sedimentation rate was normal. ECG showed normal sinus rhythm with early repolarization pattern. CT abdomen pelvis with IV contrast showed multiple medium sized wedge-shaped parenchymal hypodensities in the left kidney. Complete renal ultrasound denoted occult findings of renal infarction. MRI angiogram of the abdomen with contrast showed two renal arteries bilaterally and reaffirmed renal infarctions in the left upper, middle, and lower kidney. Transthoracic and transesophageal echocardiograms were unremarkable for cardiac thrombosis. Pharmacological nuclear stress test was normal.
The patient was started on therapeutic anticoagulation, initially on heparin drip and subsequently discharged on Rivaroxaban. C3 complement was 232 and C4 Complement was 54. Anti-nuclear antibody, lupus anticoagulant, Protein C & S, beta-2 glycoprotein antibodies, Anticardiolipin antibody, and rheumatoid factor were unremarkable.


This case is unique because this patient has double bilateral renal arteries which is anatomically rare. Predominantly, there are two renal arteries, originating from the aorta. Few are seen to have double renal arteries and rarely bilaterally. To the best of our knowledge, multiple renal arteries have not been reported as a cause of renal infarction. Therefore, we emphasize renal anatomical abnormalities as an etiology of renal infarction, given all other hypercoagulable work up and cardiac work up is unremarkable.