Two Cases of Acute Renal Infarction in the Setting of Atrial Fibrillation

INTRODUCTION

Renal infarction is defined as the interruption of blood supply to a portion of the kidney or the entire kidney. This condition typically involves older patients who have a higher incidence of atherosclerosis or thromboembolic phenomenon than the general population.¹ Often, patients have small renal infarcts that cause no symptoms. Even in patients with larger infarctions, acute renal infarction (ARI) is commonly underdiagnosed because the symptoms at the time of presentation are predominantly nonspecific. In a 2006 study, Bolderman et al found that of 27 patients ultimately diagnosed with renal infarction, 74% presented with abdominal pain, 63% presented with lumbar pain, 63% presented with nausea, 33% presented with vomiting, and 15% presented with urinary concerns.² These nonspecific symptoms delay the diagnostic workup for ARI. Many patients with ARI also present with elevation of low-density lipoprotein, transaminitis, and hematuria.

The physiology underlying atrial fibrillation that causes the heart to quiver is a common cause of renal thromboembolism. Consequently, clinicians should consider the possibility of ARI in the differential diagnosis for patients at high risk of thromboembolism who present with acute kidney injury. Our cases highlight the clinical diagnosis of ARI.

CASE 1

A 55-year-old male presented to the emergency department with a 2-day history of left-sided severe flank pain. His medical history included coronary artery disease status post stent placement, abdominal aortic aneurysm status post repair, and atrial fibrillation treated with warfarin. The patient reported dysuria, increased urinary frequency, and tea-colored urine. Associated symptoms included sweating, nausea, vomiting tinged with bile and blood, chills, subjective fever, and anorexia lasting 3 days.

During physical examination, the patient was hemodynamically stable but appeared to be in moderate distress. Apart from localized tenderness over the right lower quadrant of the abdomen, the examination was unremarkable. Pertinent laboratory results at the time of presentation are listed in the Table. Urinalysis was essentially unremarkable except for pyuria (6-10 leukocytes).

Computed tomography (CT) scan of the abdomen with intravenous contrast revealed areas of decreased perfusion involving the lower pole of the right kidney, occlusion of the left internal iliac artery, and aneurysms involving the right common iliac artery and both common femoral arteries (Figure).

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Figure.

Computed tomography scan of the abdomen with intravenous contrast reveals areas of decreased perfusion involving the lower pole of the right kidney (patient 1).

The initial diagnosis was pyelonephritis, for which intravenous ceftriaxone was empirically administered. Given the results of the CT scan and subtherapeutic international normalized ratio, anticoagulation was instituted with warfarin and enoxaparin throughout the patient's hospital course. His clinical course improved minimally, and his symptoms were less suggestive of infection.

Given the character of the pain, the etiology of left-sided flank pain was considered more likely secondary to renal infarct than infection, and hence antibiotics were discontinued. Bilateral renal duplex ultrasound was remarkable for increased velocity in the right proximal third of the renal artery, suggesting stenosis. Transthoracic 2-dimensional and transesophageal echocardiographic studies were negative for the presence of a thrombus. During a 5-day hospital stay, the patient's pain significantly improved with supportive measures including fluids, pain medications, and avoidance of nephrotoxic agents.

CASE 2

A 53-year-old male presented to the emergency department with acute, left-sided flank pain associated with nausea and vomiting and a noticeable decline in urine output. The patient's medical history included chronic kidney disease, hypertension, and atrial fibrillation treated with warfarin.

During presentation, he appeared uncomfortable and was in moderate distress. Pertinent findings during physical examination included an irregular pulse and left costovertebral angle tenderness without rebound tenderness. Laboratory results at the time of presentation are listed in the Table.

Unenhanced CT scan of the abdomen revealed the absence of the right kidney. A mercaptoacetyltriglycine nuclear medicine scan showed diminished flow to the left kidney. CT angiogram demonstrated evidence of a thrombus in the left renal artery. The patient was administered heparin for anticoagulation and underwent a wire-guided thrombolysis with thrombectomy. Subsequently, the patient required initiation of hemodialysis.

DISCUSSION

A 1940 autopsy study of 14,411 patients documented the incidence of ARI at 1.4%.¹ However, a 2006 study found the incidence rate of ARI to be even lower at 0.3% after identifying 55 patients with kidney infarction among 18,287 patients.³

ARI is an important yet significantly underdiagnosed condition. The symptoms of ARI commonly mimic other diagnoses such as urinary tract infection, nephrolithiasis, biliary pathologies, appendicitis, and mesenteric ischemia.⁴ Clinicians should have a low threshold for suspicion of ARI because of the difference in the way it is treated compared to other diagnoses for these nonspecific symptoms.

Patients with ARI should demonstrate leukocytosis, elevated low-density lipoprotein, and elevated liver function tests (alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase). Urinalysis should reveal variable presence of hematuria and proteinuria.⁴ The absence of hematuria points to more serious loss of kidney function because it correlates with marked reduction in blood flow to the infarcted area that results in local cessation of glomerular filtration and urine flow.⁵ Elevation of lactate dehydrogenase is believed to be the hallmark feature of ARI.⁶

Most patients ultimately diagnosed with ARI have predisposing risk factors for thromboembolism, with atrial fibrillation being the underlying etiology in most cases. Some of the risk factors for ARI include mitral stenosis, hypertension, and ischemic heart disease.^5,8 Less common risk factors include trauma, hereditary or acquired clotting disorders, vessel anomalies (such as fibromuscular dysplasia), sickle cell disease, and Marfan syndrome.⁹

As demonstrated in our 2 cases, several modalities can be used to diagnose ARI. Renal arteriography is considered the gold standard for diagnosis because it allows x-ray imaging of the kidney's blood vessels as contrast dye is simultaneously administered, resulting in complete visualization of the renal vessels. Contrast-enhanced CT scan is a widely accepted noninvasive test and is the diagnostic modality of choice.⁷

ARI can also be diagnosed by an intravenous pyelogram. A kidney that does not adequately opacify, despite having a healthy pelvicalyceal system revealed by a retrograde urography, is considered diagnostic for renal artery occlusion by an embolus or thrombus. The demonstration of a nonobstructed, nonfunctioning kidney points to the diagnosis of a renal embolism.⁴ However, intravenous pyelogram is rarely used to diagnose ARI because of the advent of contrast-enhanced CT. Another inexpensive diagnostic tool is color Doppler ultrasound. Acute infarction appears as an absence of perfusion in a color Doppler ultrasound.

The generally accepted treatment for ARI is systemic anticoagulation with intravenous heparin followed by warfarin.⁴ The goal international normalized ratio may vary with the cause of the ARI.^5,6 The usual goal is 2.0-3.0, but a goal of 2.5-3.5 is reasonable if ARI occurs in patients with atrial fibrillation who are on adequate warfarin therapy or if patients are at a particularly high risk of ARI such as patients with rheumatic heart disease and a prosthetic heart valve.²

Thrombolytic therapy is typically reserved for patients who are diagnosed early in the course of the disease. The ideal door-to-treatment time is 90-180 minutes.^8,11 Surgical embolectomy is reserved for patients with complete renal parenchymal compromise caused by emboli that do not respond to less-invasive treatment.¹²

No studies have compared the outcomes of different treatment modalities because of the difficulty of diagnosing ARI. Nonetheless, most published case series have favored the use of anticoagulation. The prognosis for patients with ARI is favorable. Most patients recover and display normal renal function or return to baseline.⁴

CONCLUSION

ARI is a unique and challenging cause of acute kidney injury. It is a commonly overlooked phenomenon but should remain high in the differential diagnosis of a patient presenting with acute kidney injury associated with abdominal pain, particularly in the presence of known predisposing risk factors for thromboembolism. We highly recommend a retrospective review of all documented cases of ARI to establish a uniform protocol to aid in diagnosis and assess the best treatment modality.