Case Presentation: A previously healthy 42 year-old man was admitted with acute abdominal pain. He described onset of periumbilical pain on the morning of admission, resolving after an episode of non-bloody, non-bilious emesis. Later that day, he developed a severe, sharp, constant and non-radiating left lower quadrant pain associated with emesis. He denied fevers, chills, diarrhea, dysuria, travel, trauma, or IV drug use. He had mild tenderness to palpation in the left lower abdomen on exam. Except for a serum LDH of 328 U/L (110-210 U/L), routine laboratory tests including CBC, CMP and urinalysis were normal. CT of abdomen and pelvis with IV contrast showed left lower pole renal infarction, a 1.4 cm thrombus in the distal left renal artery without any evidence of vascular irregularity. CT angiogram showed dissection of the left distal main renal, celiac and splenic arteries, and ectasia and tortuosity of other visceral vessels, consistent with fibromuscular dysplasia. Following consultation with vascular surgery, IV heparin infusion was initiated. Endovascular intervention was not performed given normal blood pressure and renal function. Electrocardiogram, echocardiogram and routine hypercoagulability studies were unremarkable. He was discharged on apixaban.
Discussion: Hospitalists commonly encounter patients with acute abdominal pain and vomiting. Differential diagnosis in this setting may overlook renal infarction as the signs are nonspecific; they may variably include fever, nausea, microscopic hematuria, elevated WBC count, CRP or creatinine. Elevated LDH with normal liver function is strongly suggestive of renal infarction. As our case illustrates, the absence of hematuria should not rule out renal infarct as a cause of abdominal pain. In a large case series of 438 patients with renal infarction hematuria was only present in 32 percent. Cardiac thromboembolic, in-situ thrombosis and renal artery injury are the major causes of renal infarction. CT with IV contrast is the diagnostic modality of choice but can miss vascular lumen irregularities. CT angiogram is the gold standard for delineating the etiology of renal infarction. The presence of an intralumenal thrombus should not rule out arterial injury, as seen in our patient. Workup should include evaluation for atrial fibrillation, intracardiac shunt or thrombus and hypercoagulability states. No evidence-based guidelines exist for treatment of renal infarction. Anticoagulation is routinely used, either for direct treatment of thrombi or prevention of thrombi after vascular injury. Unfortunately, guidelines for optimal utilization of endovascular therapy are currently lacking.
Conclusions: A case of renal infarction as a rare complication of fibromuscular dysplasia is presented. This case highlights the importance of considering renal infarction in the differential diagnosis for abdominal pain, even in the absence of microscopic hematuria. Clinicians should have a low threshold to image, especially with the presence of high LDH with normal LFTs. Common approaches to delineating the cause of renal infarction and its management are briefly reviewed. Although randomized-controlled studies are lacking, stable patients seem to have favorable outcomes when treated conservatively with anticoagulation alone.