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Case Report |
1 Department of Radiology, St. Francis Medical Center, 400 45th St., Pittsburgh, PA 15201.
Received April 20, 1999;
accepted after revision June 21, 1999.
Presented at the annual scientific assembly of the Society of Uroradiology,
New Orleans, May 1999.
Introduction
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We describe a patient who arrived at the emergency department with noncalculus-related acute flank pain. We used contrast-enhanced CT to arrive at the final diagnosis.
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Unenhanced CT of the abdomen and pelvis showed an ectopic right kidney located at the level of the iliac crest (Fig. 1A). There was no evidence of calculus or hydronephrosis. Sonography of the abdomen and pelvis failed to show abnormalities involving the right kidney. Excretory urography showed faint opacification of the right kidney. No calculi were identified. Four hours after excretory urography the patient voided a 3-mm calculus; however, she continued to be symptomatic, requiring right retrograde pyelography and right ureteric stent placement. Retrograde pyelography showed the ectopic right kidney but no obstruction. After 36 hr of hospitalization without a definite diagnosis, the patient continued to be symptomatic. Contrast-enhanced CT of the abdomen and pelvis was performed. CT showed an acutely swollen right kidney with surrounding perinephric inflammatory changes (Fig. 1B). CT also showed abnormal enhancement of the ectopic right kidney. Most of the kidney was nonenhancing and a portion of the lateral aspect was enhancing in a patchy fashion, signs consistent with acute subtotal infarction of the right kidney. The patient refused any surgical or angiographic intervention. She was treated with IV heparin and discharged from the hospital on Coumadin.
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Acute renovascular occlusion is often difficult to diagnose and requires a high degree of suspicion. Acute renovascular occlusion should be suspected in patients with acute flank pain and a history of valvular heart disease, atrial fibrillation, endocarditis, or previous embolic episodes. Acute renal infarction may be asymptomatic or manifest as a sudden onset of severe abdominal or flank pain, with nausea, vomiting, hematuria, and albuminuria. Hematuria may be gross or microscopic. Fever and leucocytosis may also be present. Urinalysis may be completely normal when damage to the kidney is severe enough to prevent urine formation. After infarction, levels of renal enzymes such as aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase may be elevated. The most sensitive marker for renal infarction is lactate dehydrogenase [4]. In the review by Lessman et al. [2], lactate dehydrogenase was elevated in 14 patients.
In major renal artery embolic occlusion, excretory urography will show a normal or enlarged kidney with poor or no opacification. A nephrogram phase is typically absent, even on delayed films, except in situations of severe or long-standing renal obstruction, renal vein thrombosis, chronic renal failure, renal transplant rejection, or acute pyelonephritis [5]. A nonopacified kidney of normal or increased size with a healthy pelvicaliceal system revealed by retrograde pyelography is considered diagnostic of renal artery occlusion caused by embolus or thrombus [6]. This combination of signs was present in our patient. Voiding of a stone after excretory urography and subsequent normal retrograde pyelography misled interpreters to a calculus-related obstruction rather than renal artery occlusion. A cortical rim nephrogram sign occurs in nearly half of the patients with global renal infarction. That sign represents opacification of a rim of functioning nephrons, supplied via capsular collaterals, surrounding an otherwise nonfunctioning kidney. A cortical rim sign is best identified by contrast-enhanced CT but can also be identified using high-dose nephrotomography. Although the cortical rim nephrogram sign is suggestive of renal artery occlusion, it is also seen in longstanding hydronephrosis, renal vein obstruction, and acute renal failure [7].
Recent publications have indicated that unenhanced helical CT may be the ideal diagnostic test for patients with acute flank pain [8, 9]. Compared with excretory urography, unenhanced helical CT can be completed in less than 5 min without the discomfort, inconvenience, and risks associated with contrast material. Unenhanced helical CT can detect almost all types of urinary tract calculi. In addition, helical CT can be used in place of excretory urography to plan treatment regimens for patients with flank pain caused by obstructing ureteral stones. When a patient complains of acute flank pain, ureteral obstruction caused by stone disease should be considered, and most testing is initially aimed at making or excluding this diagnosis. However, flank pain is a nonspecific symptom associated with a wide array of disease processes, both renal and extrarenal. Unenhanced helical CT can diagnose many extrarenal causes of abdominal pain including appendicitis, diverticulitis, biliary tract disease, leaking aortic aneurysm, and gynecologic disease. However, unenhanced helical CT cannot diagnose some of the noncalculus-related renal disease processes that produce flank pain, including pyelonephritis, and less commonly, renal vein thrombosis and renal artery thromboembolism. In these situations, contrast-enhanced CT plays a vital role in early diagnosis.
Contrast-enhanced CT should be used to diagnose patients who are at risk for thromboembolic occlusion of the renal artery. Contrast-enhanced CT may also be used for patients with atrial fibrillation, vavular heart disease, prosthetic valves, and elevated levels of serum lactate dehydrogenase. Elevated levels of serum lactate dehydrogenase are a consistent marker for renal infarction.
Acknowledgments
We thank Gerald J. Ross for his careful review of the manuscript and Ronald
A. D'Altorio, Darcell Saunders, and Brad Long for their invaluable
assistance.
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This article has been cited by other articles:
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R. Zissin, V. Amilineni, D. F. Lackner, W. S. Morse, and N. Srinivas Nonopacification of an Existing Kidney on Excretory Urography Am. J. Roentgenol., October 1, 2000; 175(4): 1187 - 1188. [Full Text] [PDF] |
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