A new patient pops up on the board.
40-year-old female history of hypertension presenting with sudden-onset right flank pain with nausea and vomiting. Vital signs are significant for elevated blood pressure to 205/115. The patient states she has been intermittently compliant with her medication.
Bread and Butter. You are a good PGY-2, so you start going through your usual list of suspects.
- 1. Pyelonephritis – check.
- 2. Ureterolithiasis – check.
- 3. Cholelithiasis – less likely, but possible.
- 4. Abdominal Aortic Dissection – always possible
On history, there are no reported symptoms consistent with prior renal or biliary colic, nor are there any diagnoses of aneurysms or liver disease. The review of systems is negative for fevers, dysuria, abnormal bowel movements, vaginal discharge, and bleeding. There are regular cardiac rhythm and right costovertebral tenderness. Bedside ultrasound of kidneys and biliary tree are both unremarkable. WBC, BUN, and creatinine are within normal limits. Urinalysis is negative for hematuria, bacteria, or nitrites. Urine pregnancy is negative.
Despite repeated doses of pain medication, your patient continues to describe 10/10 pain as she lies curled up, clutching her right side. You discuss with your attending and decide to order a CT abdomen/pelvis with contrast to explore other etiologies of her discomfort.
Computed tomography of the abdomen and pelvis with contrast revealing wedge-shaped non-enhancing areas within the right kidney suspicious for renal artery infarcts
On rare occasions, when you hear hoofbeats behind you, it actually is a zebra.
Presentation Patients with acute renal artery infarction most often present with flank pain, nausea, and vomiting.1 Elevated blood pressure at the time of presentation may also be present.2 Increased renin secretion from juxtaglomerular kidney cells, secondary to decreased renal perfusion, may cause an abrupt increase in blood pressure.
Causes Renal infarction is rare, especially in patients who do not have typical risk factors. The overall incidence has been estimated between 0.004% to 0.007%.3 Atrial fibrillation is estimated to be present in 25% to 65% of cases.4 Other causes include renal artery injury or an underlying hypercoagulable state, whether autoimmune or malignancy-related, predisposing to thromboembolism. Emboli usually originate from the heart, but the aorta may also serve as a source. Renal infarctions have also been recently observed in COVID-19 patients, although studies are limited.5
Lab Findings Markers for kidney function, such as creatinine and GFR, may not be helpful in diagnosis and can be normal in cases of unilateral renal artery infarction due to compensation by the contralateral kidney. Elevated lactate dehydrogenase and leukocytosis may be present but are non-specific.6
Imaging CT abdomen/pelvis with IV contrast is the preferred imaging modality. Renal doppler ultrasound is not sensitive enough to detect segmental infarcts.7 In one study (n=44), ultrasound was only positive in 11% of cases or renal infarction.8 CT Angiogram (CTA) may be useful to evaluate for an intra-aortic thrombus or to determine the extent of the occlusion. An acute aortic dissection or mesenteric ischemia can also present similarly, and a CTA can help further distinguish between them. Surgical repair is necessary for dissections extending into the renal artery, and mesenteric ischemia may require anticoagulation. An echocardiogram may rule out thrombus or patent foramen ovale that may predispose to paradoxical emboli.
Management Treatment is based on etiology. For non-traumatic renal artery infarction, there are two options. Percutaneous endovascular therapy with early balloon-catheter thrombolysis/stenting has demonstrated successful return of renal perfusion.9,10 Vascular surgery or interventional radiology consultation should be obtained for patients that are candidates for thrombolysis, thrombectomy, or stenting. Patients with complete renal artery occlusion < 6 hours or partial occlusion < 24 hours might benefit from early endovascular intervention.11 For all other patients, IV Heparin is the mainstay of therapy to prevent further thromboembolism. Patients without an underlying cause should be bridged to oral anticoagulation paired with antiplatelet therapy and remain on therapy for at least 6 months. In one retrospective study (n=438) of patients with acute renal infarction who received anticoagulation and antiplatelet therapy, 2.8% had recurrent infarction within 20 months without statistically significant differences between subgroups of underlying etiology (i.e. cardiogenic vs hypercoagulable state vs renal artery injury vs idiopathic).12 Patients with renal infarction and atrial fibrillation may benefit from anticoagulation.13 However, in cases of idiopathic renal infarction, there are no studies demonstrating the benefit of long-term anticoagulation.
ED Course This patient underwent CTA which was significant for a thrombus in the descending aorta. Imaging was also significant for multifocal liver lesions and a right hilar lymph node with multiple pulmonary nodules, concerning for neoplastic disease. Transthoracic echocardiogram revealed mild concentric left ventricular hypertrophy without evidence of thrombus. The patient was heparinized and vascular surgery recommended transfer to a nearby hospital for further management and possible stenting.
Conclusion Acute renal artery infarction should be considered in patients who present to the ED with acute flank pain, nausea, and vomiting. The presentation can mimic common diagnoses such as ureterolithiasis or pyelonephritis, but also life-threatening ones such as aortic dissection. Patients with elevated blood pressure and pain that is refractory to adequate analgesia should raise suspicion for renal infarction. Patients with atrial fibrillation and hypercoagulability are at higher risk and imaging should be obtained to expedite early endovascular intervention.
Take Away Points
References
Acknowledgements: Dr. Roderick Alfonso, Dr. Markus Little, Dr. Ian deSouza, Dr. Robby Allen
Marie J Murphy, MD MPH
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1 Comment
J Edward Murphy · March 23, 2021 at 3:01 pm
Thanks for the detailed assessment and navigation of this interesting case.