Case Report

Considerations in the diagnosis and therapy for acute loin pain

Abstract

The clinical presentation of acute onset of nausea, vomiting, and flank pain in combination with acute elevation of blood pressure should raise high suspicion of Renal infarction. However, because of its nonspecific presentation, diagnosis may be delayed. We report the case of a 63-year-old man who presented with a 2-day history of Right flank pain that was treated initially as a renal stone. He had a background history of atrial fibrillation. Further investigations confirmed this as a case of renal infarction. Renal infarction is underdiagnosed because of the similarity of its presentation to other renal pathology. Renal infarction should be considered in the differential diagnosis of loin pain, particularly in a patient with atrial fibrillation.

Acute embolic renal infarction is uncommon and is infrequently recognized at presentation. This delays treat- ment and significantly lessens the prospect of renal salvage [1]. It is frequently confused with other, more common diagnoses because of similarity of presenting symptoms.

We report the case of a 63-year-old man with a 2-day history of right flank pain with associated nausea and vomiting. History was positive for atrial fibrillation, and he was noncompliant regarding his anticoagulation therapy. The pain was continuous, and there was no hematuria, frequency, fever, dysuria, or rigors. He had no history of trauma or previous renal stones. He was afebrile with a blood pressure of 155/85 mm Hg, and electrocardiogram showed atrial fibrillation (63/min) with Right ventricular hypertrophy pattern. Abdominal exam- ination revealed right loin tenderness. Urinalysis showed +++ Red blood cell count, white blood cell 2 to 5 per high-power field, and ++ protein. Blood urea nitrogen, creatinine, electrolytes, and liver function tests were all normal. White blood cell count was 12.78 x 10 ⁹/L, hemoglobin level 11.9 g/ dL, platelets 396 x 10 ⁹/L, and international normalized ratio

1.1. He was treated with analgesics for 12 hours while awaiting a noncontrast helical computed tomography (CT) of the abdomen. It demonstrated a large attenuated area in the right kidney suspicious for an infarct, and arterial contrast enhance- ment confirmed diagnosis by showing characteristic capsular enhancement (Figs. 1 and 2). Thrombolytic therapy was not

considered because of the late diagnosis, and treatment with analgesics and anticoagulants was started.

Renal artery embolism is an infrequent but important cause of renal infarction. Acute embolic renal infarction’s presentation is nonspecific and thus is frequently mistaken for the more commonly encountered ureterolithiasis, pyelonephritis, appendicitis, diverticulitis, biliary obstruc- tion, and torsion of pelvic masses. This leads to a delay in treatment and thus to increased morbidity.

Two major causes of renal embolic disease are throm- boemboli and atheroemboli. The former usually originate from a thrombus in the heart or aorta, whereas the latter occurs with erosive atheromatous disease, most often after aortic manipulation [2,3]. In situ thrombosis of a stenotic renal artery is a less common source of renal infarction. The major sources of clot embolism include the left atrium or left atrial appendage in atrial fibrillation, a left ventricular thrombus in patients with a myocardial infarction, and thromboemboli originating from complex plaque in the aorta [3-5]. The incidence of renal thromboembolism in atrial fibrillation patients was 2% in a series of almost 30 000

Fig. 1 Axial CTshowing right main renal artery with large thrombus extending from 3 cm beyond the origin into parenchymal vessels.

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254.e4 Case Report

Fig. 2 Computed tomography showing 70% to 80% infarction of kidney. Upper pole and lower pole show some normal parenchyma as a renal branch comes off proximal to the thrombus to supply the upper and an accessory renal supplies the lower pole.

patients followed for up to 13 years [6]. Other potential Embolic sources include valvular vegetations in Infective endocarditis, and rarely tumor and Fat emboli and paradoxical embolism through a patent foramen ovale.

Common clinical presentations include abrupt persistent flank pain, abdominal pain or low back pain, accompanied by fever, headache, nausea, and vomiting. In addition, they may complain of lumbar pain on the side of the renal infarction, hypertension, and renal dysfunction. However, these symp- toms are nonspecific. Physical examination reveals costover- tebral angle tenderness, a characteristic sign. Kidney infarction induces acute hypertension, which in many instances is of a temporary nature: some patients present hypertension alone without any symptoms referable to renal infarction [7]. The prevalence of spontaneous kidney infarction in patients referred for hypertension is 3? and the incidence is 0.18? per year [7]. A rapid deterioration in renal function with anuria or oliguria usually develops in patients with bilateral renal Artery thrombosis or infarction in a solitary kidney.

Acute renal infarction is often a diagnosis made by exclusion. The common laboratory tests are either nonspecific or lacking in sensitivity. Renal scintigraphy, ultrasonography, and enhanced CT may be useful in its diagnosis. Although ultrasonography still has its role in excluding obstructive uropathy, it lacks sensitivity to detect early renal infarction. contrast-enhanced CT is the noninvasive standard for imaging acute renal infarction. Selective renal artery angiography is an invasive diagnostic method that is not without morbidity.

Prompt recognition of acute renal infarction is important as ischemia can cause irreversible kidney damage in a few hours [8]. The limit of warm Ischemic time for the kidney is

60 to 90 minutes. The recommended therapy has changed drastically during the past 30 years. Previous studies demonstrated that anticoagulation is as effective as surgical therapy, and Conservative therapy is recommended except in the case that bilateral emboli or infarctions of a solitary kidney have occurred [9]. Thrombectomy may be appro- priate in these cases. Currently selective intraarterial thrombolytic therapy is considered as an effective treatment of unilateral renal infarction [10]. If nephronecrosis devel- ops, a nephrectomy should be performed.

In conclusion, the occurrence of renal infarction second- ary to atrial fibrillation remains rare. Physicians should consider the possibility of acute renal infarction in any patient presenting with acute onset of flank pain with a history of cardiovascular disease. Awareness of presentation, Predisposing factors, as well as appropriate use of Imaging techniques, is crucial to the timely establishment of this diagnosis and early institution of appropriate therapy.

Graham Roche-Nagle

Bary B. Rubin

Department of Vascular and Endovascular Surgery

Toronto General Hospital Toronto, ON, Canada M5G 2C4 E-mail address: [email protected]

doi:10.1016/j.ajem.2008.06.030

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