Anuria as a Chief Presentation of Takayasu Arteritis, a Case Report

Case Report

Austin J Clin Case Rep. 2021; 8(1): 1189.

Anuria as a Chief Presentation of Takayasu Arteritis, a Case Report

Sara K Alrasheed¹*, Basel Alheijani¹, Rahmah Alzahrani¹ and Shaker Alshehri²

¹Department of Medicine, King Abdulaziz Medical City, Ministry of National Guard-Health Affairs, Saudi Arabia

²Department of Radiology, King Abdulaziz Medical City, Ministry of National Guard-Health Affairs, Saudi Arabia

*Corresponding author: Sara K Alrasheed, Department of Medicine, King Abdulaziz Medical City, Ministry of National Guard-Health Affairs, Saudi Arabia

Received: December 10, 2020; Accepted: January 04, 2021; Published: January 11, 2021


Takayasu vasculitis is a rare type of large vessel vasculitis that primarily affects the aorta and its main branches; signs and symptoms are usually due to systemic inflammation or ischemia of an organ or limb, depending on the group of blood vessels involved. In addition, Takayasu arteritis is associated with increased platelet and coagulation activity, leading to a hypercoagulable state and thrombus formation. We report a case of a 47-year-old male who presented with a history of complete anuria for 3 days and was found to have progressively worsening kidney function. Renal Doppler ultrasound confirmed the presence of bilateral renal artery thrombosis, while Contrast- Enhanced Computed Tomography (CECT) of the abdomen and pelvis showed extensive abdominal aortic thrombosis with radiological findings consistent with large vessel vacuities. After catheter-directed thrombolytic therapy of the renal arteries, the patient started producing urine and his kidney function significantly improved. Later, Positron Emission Tomography scan (PET) confirmed large vessel Takayasu arteritis. Echocardiography showed no intracardiac thrombus, along with an extensive work up for thrombophilia, as autoimmune and vasculitis serology came back negative. This is an extremely rare presentation of Takayasu arteritis, with an unusual recovery of acute renal failure after delayed anuria due to bilateral renal artery thrombosis.


Bilateral renal artery thrombosis, secondary to aortic thrombosis is infrequent, often associated with atherosclerotic and/or aneurysmal changes, rarely caused by other conditions. Takayasu large vessel vasculitis (nonspecific) is one of the rare causes of aortic thrombosis [1], and is often missed, although it is a reversible and treatable condition.

Case Presentation

A 47-year-old male presented with an abrupt onset of anuria for 3 days. There was no history of flank pain, dysuria, hematuria, fever, vomiting, or diarrhea. Ten days prior to his presentation, he was complaining of abdominal pain, mainly around the umbilicus, associated with bloating and constipation. He went to another hospital and was managed with: bisacodyl, oral lactulose, and fleet enema, and was discharged. Review of other systems revealed a history of general fatigue and lower limb claudication after a walking distance of 20 to 30 meters. There was no history of skin rashes, joint pain or swelling, cough, chest pain, palpitation, or shortness of breath. Moreover, there was no history of headache, or any neurological symptoms. His past medical history was significant for hypertension and lumbar spine disk prolapse.

Past medical history was significant for a hospitalization 5 years ago, for unprovoked massive bilateral pulmonary embolism. Investigations at that admission included: thrombophilia workup, which was non-revealing, an echocardiography which showed reduced left ventricular Ejection Fraction (EF) of 45%. Follow-up Computerized Tomography (CT) of the coronary arteries revealed a zero calcium score and a mild non obstructive Coronary Artery Disease (CAD) in the proximal Left Anterior Descending Coronary Artery (LAD). Cardiac MRI showed an old infarction in the apical segment, with no Left Ventricular (LV) cavity thrombus. At the time, there was no history of thrombosis (before that presentation), abdominal aortic aneurysm, or renal stones in the patient’s history or family. His medications included aspirin, valsartan, metoprolol, and atorvastatin. He did not smoke, use alcohol, or illicit drugs.

Physical exam at presentation: Patient was conscious, oriented, not in pain or distress, body temperature of 36.3°C, blood pressure: left arm 127/80, right arm 121/78, left leg 57/30, right leg 62/31, heart rate of 79 beats per minute, regular with absent left radial pulse, lower limb pulse was palpable but weak bilaterally, respiratory rate of 21 breaths per minute and pulsoximetry of 98% on room air. Cardiovascular examinations revealed normal heart sounds, no murmurs, normal JV, no carotid bruit, and no pedal edema. His abdominal exam revealed mild tenderness to palpation, more on the right flank compared to the left: no rebound, guarding, distention, or organomegaly. The rest of the exam was normal.


The initial emergency department evaluation included an Electrocardiogram (EKG), which was unremarkable, a White Blood Cell (WBC) of 7.10 k/uL (normal range 4-11), a hemoglobin of 136 g/dL (normal range 135-180 gm/L), a platelet count 302 K/uL (normal range 150-400). Other laboratory investigations revealed a creatinine of 500 umol/L (normal range 64-110 umol/L), with his last documented baseline was 70 umol/L, a Blood Urea Nitrogen (BUN) of 8 (normal range 7.4-3.2 mmol/L), a potassium of 3.4 (normal range 3.5-5.1 mmol/L), a bicarbonate level of 19 (normal range 22-29 mmol/L). Furthermore, his Lactate Dehydrogenase (LDH) level was 840 (normal range 125-220), and Erythrocyte Sedimentation Rate (ESR) was 49 mm/H (normal range 0-15 mm/hr). Other laboratory work-up included liver profile, lactic acid level, and coagulation profile which were within normal limits. Patient was not able to produce urine even after Foley’s catheter insertion. Non-enhanced CT of the abdomen and pelvis showed no overt obstructive uropathy or renal stones. On admission, his creatinine level increased to 900 umol/L. Renal Doppler ultrasound was done and showed findings suggestive of evolving bilateral main renal artery thrombosis versus stenosis (Figure 1).