After a Wild Party, a 24-Year-Old Has Intense Abdominal Pain

Marie-Lee Simard, MD; Alexandre Lafleur, MD, MSc

Disclosures

July 08, 2021

Discussion

This patient with acute flank pain and mildly impaired kidney function underwent an investigation for renal colic, on the basis of the history and the initial laboratory results. A noncontrast CT scan did not show nephrolithiasis, and the kidneys appeared normal. Extensive laboratory testing revealed a remarkably high LDH level, with a mild increase in the serum aminotransferase values. Given the patient's recent cocaine consumption, an acute renal thrombosis was suspected. A thoracoabdominal CT angiogram (CTA) was ordered. It revealed renal ischemia with hypodensities that affected 50% of the right kidney and an underlying thrombus that occluded 90% of the middle portion of the right main renal artery (Figure).

Figure.

Symptomatic kidney stones can result in flank pain, nausea, vomiting, hematuria, and dysuria, but they would not be associated with a high LDH level. Intestinal ischemia often presents with acute abdominal pain out of proportion to the physical examination findings. The absence of radiologic signs (eg, bowel wall edema) or lactic acidosis made this diagnosis less likely. Moreover, it would not explain the high LDH level. Acute hepatitis with hepatocellular injury could cause right upper quadrant pain but usually results in higher levels of serum aminotransferases than of LDH. It would not be associated with proteinuria. Pyelonephritis can also produce acute flank pain, nausea, vomiting, and abnormal urinalysis findings, but not abnormal liver function test results. In this case, the urinalysis did not show an elevation in leukocytes or nitrites. The results of a urine culture were negative.

Renal infarction is a challenging diagnosis. The time to diagnosis ranges from 24 hours to 7 days,[1] and 22% of renal infarcts are missed upon initial presentation.[2] The true incidence of renal infarction is probably underestimated. The estimated prevalence is 0.48%–1.4% in necropsy studies.[3,4] More recent case series in the ED report incidences that range from 0.002% to 0.007%.[1,5,6,7] In a large case series, the patients were mostly men (58%), with a mean age of 60 years.[8]

Renal infarction can be classified in four main groups depending on the underlying cause[8,9]:

  • Cardiogenic (56%)

  • Renal artery injury (8%)

  • Hypercoagulable state (7%)

  • Idiopathic (30%)

A cardioembolic source, usually associated with atrial fibrillation, is by far the most important cause of renal infarction[7,8,9] and is responsible for more than half of cases.[8] Other cardioembolic disorders associated with renal infarction include valvular heart disease, cardiomyopathy with cardiac thrombus, and endocarditis. Patients affected by cardiogenic causes are significantly older and have cardiovascular risk factors.[10]

Rare causes of renal infarction include hypercoagulable states (eg, malignancy, antiphospholipid syndrome, hyperhomocysteinemia, and paroxysmal nocturnal hemoglobinuria) and renal artery injury with or without an underlying disease (eg, renal artery dissection, trauma, Marfan syndrome, polyarteritis nodosa, and fibromuscular dysplasia).[9] In 30% of patients, no identifiable cause is found despite extensive workup.[8,11]

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