Case Presentation: A 36 y/o African American female with a history of hypertension, possible congenital right renal atrophy, and endometriosis, presented with a two-day history of severe left flank and abdominal pain similar to her prior endometriosis flares. She noted no personal or family history of thromboembolic disorders. On physical exam, vitals were significant for a systolic blood pressure of 160mmHg but was otherwise within normal limit. Patient was in severe distress, but abdominal exam was negative for peritoneal signs. There was no CVA tenderness. Initial lab and urinalysis work up was unremarkable. Urine pregnancy test was negative. EKG revealed normal sinus rhythm. Her symptoms did not improve with analgesia and anti-emetics, prompting further imaging work up. CT abdomen/pelvis without IV contrast was negative for obstructive uropathy but revealed an asymmetrically enlarged left kidney and an atrophic right kidney. MRA of the abdomen/pelvis revealed a previously unknown lower pole infarct in the left kidney without any significant infrarenal atherosclerosis, or aneurysms. Renal ultrasound was significant for an atrophic right kidney (3.3 cm) and a slightly enlarged left kidney (13.5 cm) with decreased echogenicity of the lower pole consistent with known infarction. Left renal artery duplex scan showed no evidence of significant renal artery stenosis. Hypercoagulable work up (Protein C and S, anti thrombin III, factor V Leiden, homocysteine, SPEP) was negative. Transthoracic echocardiography revealed no vegetations, valvular abnormalities, or septal defects. Bilateral lower extremity venous duplex scan was negative for superficial or deep venous thrombosis. Patient was medically managed and discharged home without chronic anticoagulation after symptomatic improvement.
Discussion: Spontaneous renal infarction is a rare cause of abdominal pain, especially in young patients with significant underlying cardiac risk factors. The most common etiology of renal infarct is thromboembolism secondary to atrial fibrillation. Other potential causes include hypercoagulable states, infective endocarditis, previous endovascular intervention, renal artery dissection, and oral contraceptive use. In the absence of these, spontaneous renal infarction is rare.
Conclusions: Spontaneous renal infarction is rare in the absence of predisposing risk factors. Our case is unique in that extensive work up for thromboembolic disorders and hypercoagulable states were negative. Due to non-specific clinical manifestations, diagnosing renal infarction is a challenge and may lead to delayed diagnosis and intervention. Physicians must maintain a high index of suspicion so that timely interventions can be performed to properly assess and maintain kidney function.