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Case Report

are Renal Pseudotumor Associated withhronic Glomerulonephritis Mimickingenal Cell Carcinoma

inoru Kobayashi, Kazuhiko Nakano, Akinori Nukui, Masayuki Yuzawa,nd Tatsuo Morita

e describe a unique case of chronic glomerulonephritis that simulated a renal neoplasm observed on abnormalmaging. Histologic examination of the resected specimen supported the assumption that the observed mass lesionesulted from regional sparing in the development of chronic glomerulonephritis. We believe this case is the first tohow the etiology of pseudotumor as an extremely uncommon manifestation of chronic glomerulonephritis by

istologic examination. UROLOGY 72: 461.e15–461.e17, 2008. © 2008 Elsevier Inc.

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any renal lesions that mimic renal neoplasmson imaging are observed at subsequent surgeryand histopathologic evaluation to have been

ncorrectly diagnosed. These masses may be composed oformal or benign renal tissue and are referred to as renalseudotumors. These lesions arise from many conditionshat are developmental, infectious, granulomatous, andascular in nature.1 Especially noteworthy, some renalesions that are composed of normal parenchyma, theause of which is assumed to be compensatory hypertro-hy, mimic renal tumors on imaging.2 We describe a rarease of renal pseudotumor, which was assumed to haveesulted from regional sparing in the development ofhronic glomerulonephritis.

ASE REPORT17-year-old, previously healthy male student presented

o a local hospital with the reports of abdominal pain andiarrhea. Two days later, he developed anuria with sys-emic edema. Initial laboratory investigations showed theollowing: serum creatinine 29.8 mg/dL, blood urea ni-rogen 239 mg/dL, aspartase aminotransferase 1193 IU/L,lanine aminotransferase 1114 IU/L, white blood count1,900/�L, red blood count 238/�L, and platelet 17.3/L. With signs of multi-organ failure, he was transferred

o our hospital the same day. Coagulo-fibrinolytic testinghowed moderately prolonged prothrombin time (25.1econds) and activated partial thromboplastin time (43.7econds) and increased levels of fibrinogen degradationroduct (88.4 �g/mL) and fibrinogen (359 mg/dL). Uri-alysis showed 3� proteinuria, with a normal range of

rom the Department of Urology, Jichi Medical University, Tochigi, JapanReprint requests: Minoru Kobayashi, M.D., Department of Urology, Jichi Medicalniversity, 3311-1, Yakushiji, Shimotsuke-shi, Tochigi, 329-0498, Japan. E-mail:

ainoruk@jichi.ac.jpSubmitted: September 22, 2007, accepted (with revisions): December 3, 2007

2008 Elsevier Inc.ll Rights Reserved

icroscopic hematuria. Chest radiography showed annlarged cardiac shadow with an enlarged vascularhadow in the lung field, suggesting cardiopulmonaryongestion, which resulted in congestive liver damage.hus, the clinical manifestations and laboratory dataere compatible with coincident acute renal failure withisseminated intravascular coagulation (DIC). The pa-ient was treated with continuous intravenous infusion ofafamostat mesylate (80 mg/day) for DIC. Because bothidneys were atrophic on ultrasonography, no medicalreatment for acute renal failure was administered andnly hemodialysis was performed. Abdominal computedomography further revealed the presence of a roundsodense mass in the middle of the right kidney. Magneticesonance image confirmed a well-defined mass 3.5 � 5m in size, which had slightly higher signal intensity on1 and T2-weighted images and identical enhancement

o that of the renal parenchyma (Fig. 1A). Based on thelinical background of anuria of unknown etiology andadiologic findings suggestive of renal cell carcinoma, weerformed a right nephrectomy 11 weeks after the onsetf acute renal failure. The postoperative course was un-ventful, although the patient required permanent he-odialysis.

ISTOPATHOLOGIC EXAMINATIONross examination disclosed the absence of a tumor,

lthough we observed an area with a thickened cortex inhe middle kidney in accordance with the imaging find-ngs. Microscopic examination of what appeared to be aumorous lesion on imaging revealed that the nephronsere relatively preserved in contrast with intensive scle-

otic changes in the surrounding parenchyma (Fig. 1Bnd C). This lesion involved glomeruli by cellular orbrous crescent changes. Tubular epithelium showed hy-

line droplet degeneration. In the surrounding atrophic

0090-4295/08/$34.00 461.e15doi:10.1016/j.urology.2007.12.006

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enal parenchyma, we observed chronic inflammatoryell infiltration. Furthermore, periodic acid-methena-ine-silver staining combined with Masson trichrome

taining showed that immune depots were scattered inhe mesangium and partly present along the capillaryalls. Collectively, we suspected membranoproliferativelomerulonephritis that developed into nephrosclerosis.ccordingly, we considered that the tumorous lesion

hared a fundamental pathogenesis with the surroundingrea, despite the different degrees of histologic change.

ISCUSSIONnumber of masses composed of normal or benign renal

issue can mimic renal neoplasm. For example, renal cystsnd some renal abscesses may be confidently diagnosedadiologically and managed conservatively. Unfortu-ately, not a few uncommon lesions mimic neoplasia solosely that they are inevitably resected because of diag-ostic uncertainty and concern about potential malig-ancy.We report a case of chronic glomerulonephritis with

emarcated enlargement mimicking a renal tumor. Fromhe histologic findings in the entire resected specimen,e assumed that a regional parenchyma with nephrons

hat were comparatively spared relative to the observedclerotic changes had exaggerated perfusion and simu-ated a tumor. This is an extremely uncommon manifes-ation of chronic glomerulonephritis. To our knowledge,

igure 1. (A) Gadolinium-enhanced magnetic resonance imhe tumorous area to that of the renal parenchyma. (B) Hisith a tumorous appearance on imaging are relatively prese100). (C) Sclerotic changes with inflammatory cells are ou

nly Depner et al. have reported a similar case,2 which d

61.e16

epresented a variant of unilateral glomerulonephritisith sparing of a segment of one kidney and subsequentompensatory hypertrophy in the remaining parenchy-al atrophy, which showed tumor-like expansion on

enal arteriography. However, because a biopsy sampleas obtained only from the contralateral kidney showinglomerulonephritis, the contention that the observedass lesion resulted from segmental compensatory hyper-

rophy was not supported histologically. Therefore, weelieve that the current case is the first to show thetiology of a unique case of chronic glomerulonephritis aspseudotumor by meticulous histologic examination of

he entire resected specimen.Taken together, segmental or regional sparing and

ubsequent hypertrophy in non-uniform parenchymal at-ophy could be another manifestation of renal pseudotu-ors. This type of morbidity can result from several

nderlying pathologies. First, chronic pyelonephritis in-olves the kidney in a patchy distribution often resultingn irregular cortical outlines with skip areas and focalcarring and simulating renal tumor.3 Second, severeypertension can lead to uneven attenuation in sizeesulting from arteriolar nephrosclerosis.4 Third, corticalecrosis resulting from severe ischemia or intravascularoagulation is also a patchy process. Finally, diffuse cor-ical atrophy is caused most commonly by uniformhronic glomerulonephritis involving both kidneys,hich thereby leads to smooth cortical outlines. How-ver, unilateral glomerulonephritis, which might be in-

shows a well-defined mass with identical enhancement inthology of the resected specimen. Nephrons in the lesioncompared with the surrounding area (original magnificationding in the surrounding area (original magnification �200).

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uced by some protective mechanism sparing a segment

UROLOGY 72 (2), 2008

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f the kidney, would result in a non-uniform image as inhe current case.5,6

In conclusion, the current case is a striking example ofhe development of regional sparing that simulated aumor on imaging in the rapid process of chronic glomer-lonephritis. Surgeons should be aware of this rare entityf renal pseudotumor to avoid unnecessary surgery.

eferences. Bhatt S, MacLennan G, and Dogra V: Renal pseudotumors. AJR

188: 1380-1387, 2007.

ROLOGY 72 (2), 2008

. Depner TA, Ryan KG, and Yamauchi H: Pseudotumor of the kid-ney: a sequel to regional glomerulonephritis. AJR 126: 1197-1202,1976.

. Kitamura M, Miyanaga T, Sato Y, et al: A case of renal pseudotumorcaused by pyelonephritis. Hinyokika Kiyo 40: 241-243, 1994. (Jap-anese).

. Mena E, Bookstein JJ, and Gikas PW: Angiographic diagnosis ofrenal parenchymal disease: chronic glomerulonephritis, chronic py-elonephritis, and arteriolonephrosclerosis. Radiology 108: 523-532,1973.

. Dikman SH, Strauss L, Berman LJ, et al: Unilateral glomerulone-phritis. Arch Pathol Lab Med 100: 480-483, 1976.

. Salyer WR, and Salyer DC: Unilateral glomerulonephritis. J Pathol

113: 247-251, 1974.

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