Renal infarction is a serious condition due to renal artery occlusion that needs rapid diagnosis, as it may lead to irreversible kidney damage. The diagnosis may be difficult to make, as patients present with nonspecific symptoms.
Renal infarction usually occurs in patients with cardiovascular risk factors, such as arterial hypertension, atrial fibrillation, ischemic heart disease or valvulopathy, previous infarction or thromboembolism [1]. However, this condition can also be associated with malignancies, trauma, clotting disorders, kidney transplantation, fibromuscular dysplasia, Marfan and Ehlers-Danlos syndromes [2] or cocaine use [3].
Symptoms start abruptly and consist of abdominal, flank, costovertebral or lower back pain, nausea, vomiting, fever and sometimes oliguria [4] and hematuria [5]. Blood pressure may be high during the acute episode [6]. Small renal infarction may only cause fatigue [7].
On examination, the affected kidney may be palpable or tender. Symptoms due to shock such as hypotension, tachycardia and prolonged capillary refill time may be present.
If the disease occurs in pregnant women, symptoms include vaginal bleeding, lower abdominal pain and uterus contractions.
Blood workup in suspected renal infarction patients should include a complete blood cell count that may show leukocytosis [8], elevated levels of lactate dehydrogenase, [9], creatinine, blood urea nitrogen, as well as, C-reactive protein and aminotransferases [2]. Fibrinogen level will be low and fibrin-degradation product levels will be high. Metabolic acidosis, hyperkalemia, and hypocalcemia may be encountered. Other causes of lactate dehydrogenase elevation, such as myocardial infarction, hemolysis or malignancy should be excluded. Urinary analysis will show macroscopic or microscopic hematuria [6] and proteinuria [2].
An electrocardiogram is useful in order to determine if atrial fibrillation, a risk factor for renal infarction, is present. Other imaging studies include spiral computer tomography, renal ultrasound, computer tomography or classical angiography and dimercaptosuccinic acid or diethylenetriamine penta-acetic acid radioisotope scan. Computer tomography is used to exclude nephrolithiasis [5] and other lesions. It shows a typical wedge-shaped parenchymal opacification defect, while angiograms are capable of highlighting the occluded vessel [10]. Seldom, the renal vein may also be occluded. If contrast agents are used, the physician should consider their toxicity on an already compromised kidney and even order hemodialysis, if needed.
The infarction usually involves both the cortical and medullary areas and extends into the renal capsule. Hematoma, if present, indicates kidney trauma or transection. If contrast enhanced computer tomography is performed eight to seventy-two hours after the infarction developed, the cortical rim sign appears: a thin rim of cortex is visualized, due to collateral perfusion. Ultrasound and contrast-enhanced ultrasound, although less precise, may show the absence of flow on color Doppler evaluation [11]. These methods are also capable of detecting preexisting infarctions, that appear as hyperechoic scar tissue. Scintigraphic imaging will show diminished or absent renal perfusion and function.
As a last resort, a kidney biopsy may be performed in order to establish the diagnosis and exclude malignancy, if the patient has no contraindications.