Case Presentation: A 45 year-old male with a history of nephrolithiasis and hypertension presented with acute onset of right-sided flank pain and hematuria. He presented to an outside hospital and underwent workup for suspected nephrolithiasis. Urinalysis was negative for pyuria or leukocyte esterase. Non-contrast CT scan of his abdomen and pelvis was performed and was negative for nephrolithiasis. He was given pain medication and then discharged home. He experienced worsening nausea and renal colic and presented to our hospital for further evaluation. Vitals and physical exam on arrival were notable for blood pressure of 170/100 and costovertebral tenderness along the right flank. Laboratory evaluation showed normal kidney function and white blood cell count. C-reactive protein and lactate dehydrogenase were elevated to 4.70 and 322, respectively. Contrast-enhanced abdominal CT scan revealed a prominent right renal infarct. Selective angiography disclosed a subintimal dissection of the anterior inferior branch of the right renal artery. Vascular surgery was consulted and recommended aggressive medical management. Patient was started on blood pressure medications, dual-anti platelet therapy and a statin. Anti-nuclear antibody, rheumatoid factor and anti-neutrophil cytoplasmic antibody were all within normal limits. He underwent repeat angiography, which did not show any further extension of the dissection and he was continued on conservative management. Patient was discharged home within seventy-two hours of admission with resolution of symptoms.
Discussion: The rarity and nonspecific presentation of SRAD leads to diagnostic delays and can result in renal parenchymal injury. As in our patient – it is often seen as a sequelae of uncontrolled hypertension, as sustained elevations in blood pressure can contribute to the development of arterial dissection. Other risk factors include direct vessel injury from endovascular intervention, atherosclerosis, fibromuscular dysplasia or connective tissue disease. Renal ultrasound and/or doppler have poor diagnostic sensitivity. Contrast-enhanced CT scan can suggest the diagnosis but may miss dissections of smaller branches. The gold standard remains renal angiography, as it shows the extent of vascular involvement and may help guide management. Given the rarity of SRAD, there lacks consensus on treatment or management. Options include observation, blood pressure control, anticoagulation, endovascular intervention or surgical revascularization.
Conclusions: Spontaneous renal artery dissection (SRAD) is an uncommon cause of flank pain that poses a diagnostic challenge. Its clinical presentation is nonspecific and diagnosis is often missed or delayed. Our case demonstrates the difficulty in establishing the diagnosis of SRAD. Early recognition is essential in avoiding renal complications and improving outcomes.