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

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

Disclosures

July 08, 2021

At presentation, patients with renal infarction typically report flank or abdominal pain (50%) that may be associated with nausea (17%), vomiting (13%), and mild fever (10%).[8] Possible physical examination findings include renin-mediated hypertension, apparent distress as a result of uncontrolled pain, and tenderness on palpation or percussion of the flank.[8] Stroke, mesenteric ischemia, or limb ischemia may be additional features that suggest an underlying embolic process.

The initial workup usually shows mild leukocytosis, an elevated C-reactive protein level, abnormal liver function test results, and remarkably high LDH levels. Mildly impaired renal function, microscopic hematuria, and proteinuria are other nonspecific findings of renal infarction.[9,10]

In view of such findings, the initial differential diagnosis includes frequent pathologies such as renal colic, pyelonephritis, acute abdomen, and even myocardial infarction. Renal infarction is often overlooked.[2]

Renal infarction should be included in the differential diagnosis for patients who present with a triad of acute flank pain, mild acute renal injury, and abnormal urinalysis results, especially if they have cardioembolic risk factors such as atrial fibrillation. In this setting, high LDH levels with little or no rise in serum aminotransferase levels are even more suggestive of renal infarction.[1,7,9,12] Case series report mean LDH levels of 656 U/L (range, 152-7660 U/L).[2,6,13,14] The sensitivity of LDH for renal infarction varies from 70% to 100%; most series report sensitivities of 95%–100%.[1,7,9,12] An increase in LDH occurs within 24 hours of symptom onset, and the level may remain elevated for up to 15 days.[9] Although this cell necrosis marker may be elevated in other conditions (eg, hepatitis, myocardial infarction, rhabdomyolysis, hemolysis, and malignancies), levels should be normal in other diagnoses in the differential, such as nephrolithiasis, pyelonephritis, pancreatitis, and appendicitis.

A CT scan of the abdomen and pelvis without contrast is commonly ordered in the initial investigation of acute flank pain to rule out nephrolithiasis. However, a negative noncontrast CT scan does not exclude other differential diagnoses of acute abdominal pain (eg, intestinal ischemia, splanchnic vein thrombosis, small abscess, and renal infarction). A contrast-enhanced CT is the recommended initial imaging study to confirm renal infarction.[6,15] Classic findings are wedge-shaped hypodensities. Perirenal fat stranding may also be observed but is less common.[7] A CTA can be ordered if an acute renal artery thrombosis or dissection is suspected.[16] MRI with gadolinium is an alternative imaging modality.

Renal impairment due to renal infarction is typically mild and does not preclude contrast-enhanced imaging. A case series of 438 patients with renal infarcts reported a mean creatinine level of 84 µmol/L.[8] The presence of moderate or severe renal insufficiency suggests other diagnoses. Contrast-enhanced CT should not be ordered without careful consideration of the risks of contrast-induced nephropathy.

To determine the cause of renal infarction, investigations encompass extensive cardiac workup (echocardiography, prolonged cardiac monitoring, and blood cultures), investigations for hypercoagulable states (antiphospholipid syndrome, hyperhomocysteinemia, paroxysmal nocturnal hemoglobinuria, and myeloproliferative disorders), appropriate malignancy screening for the age of the patient, and collagen disorder testing.[8]

The appropriate treatment for renal infarction remains debated, because no comparative studies are available to support clear recommendations. Therapeutic options include medical treatments (anticoagulation, pain management, and control of hypertension), endovascular approaches (thrombolysis, thrombectomy, and angioplasty) and open surgery.[16,17,18,19] The choice of treatment should be tailored to the underlying mechanism of ischemia and the patient's clinical state and comorbidities.

Acute renal infarction should be discussed urgently with specialized teams to assess the indication and eligibility for an invasive revascularization procedure. Only a minority of patients undergo such procedures. In one case series of 42 patients who presented with renal artery occlusion, the median time from presentation to diagnosis was 42 hours. Of these patients, 69% were treated conservatively.[17] Loss of renal function and secondary renovascular hypertension have been described after renal infarction.[20] The benefit of revascularization for these two outcomes is unclear.[17,18]

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