ORIGINAL PAPER

Gallbladder wall thickening in a patientwith acute poststrepotcoccal glomerulonephritis

Toru Watanabe & Yumi Baba

Received: 13 August 2008 /Accepted: 2 September 2008 /Published online: 18 September 2008# Springer-Verlag 2008

Abstract Although thickening of the gallbladder wall is arelatively frequent finding on diagnostic imaging studies,the condition has never been reported in patients with acutepoststreptococcal glomerulonephritis (APSGN). We de-scribe a patient with APSGN who presented with transientthickening of the gallbladder wall. While the precisepathogenic mechanism underlying this change in ourpatient was unclear, elevated systemic venous pressure orsubclinical vasculitis may have caused edema of thegallbladder wall.

Keywords Thickening of the gallbladder wall .

Ultrasonography . Abdominal imaging . Kidney disease .

Secondary gallbladder involvement

Introduction

Although thickening of the gallbladder wall is the mostcommon finding in acute cholecystitits, it is also anonspecific change found in various conditions unrelatedto intrinsic gallbladder disease, such as liver dysfunction,heart failure, hypoproteinemia, and pancreatitis [8]. Thick-ening of the gallbladder wall has also been reported inpatients with kidney disease including pyelonephritis [7,10] and chronic kidney failure [5, 8, 9]. However, thecondition has never been reported in patients with acutepoststreptococcal glomerulonephritis (APSGN). In thispaper we describe a patient with APSGN who developed

gallbladder wall thickening, detected during the acute phaseof the disease by abdominal ultrasonography.

Case report

A previously healthy 11-year-old girl was seen by herfamily physician because of edema of the eyelid and righthypochondrial pain. She had presented with a history of asore throat and 2-day fever 3 weeks prior to this referral.The patient was suspected of having renal disease as shewas hypertensive with microscopic hematuria and protein-uria and was therefore transferred to our hospital.

Physical examination of the patient was as follows: bodytemperature 36.8°C, body weight 55.7 kg (+5.7 kg beforethe present illness), blood pressure 134/95 mmHg, mildeyelid and pretibial edema, and right hypochondrial painand tenderness. Murphy sign was negative and the patientdid not exhibit any skin lesions or central nervous systeminvolvement.

Laboratory studies revealed proteinuria (0.6 g/day), micro-scopic hematuria (urinary red blood cell, 30–49 cells/high-power-field), hypocomplementemia (C3, 33 mg/dl [normal77–146 mg/dl], C4, 13 mg/dl [normal 13–34 mg/dl] andCH50, 19.4 CH50/ml [normal 25–48 CH50/ml]), an elevatedanti-streptolysin O titer (1496.99 U/ml [normal 6.09–211.46 U/ml]), and mild azotemia (blood urea nitrogen28.1 mg/dl). The serum levels of C-reactive protein(0.26 mg/dl), total protein (6.6 g/dl), albumin (4.0 g/dl),creatinine (0.76 mg/dl), IgG (1575 mg/dl), IgA (162 mg/dl),and IgM (92 mg/dl), as well as liver function indices includingaspartate aminotransferase, alanine aminotransferase, lactatedehydrogenase, and total bilirubin concentrations were allwithin normal ranges. Hepatitis B surface antigen, hepatitis Cantibody, and antinuclear antibody screens were negative. The

Eur J Pediatr (2009) 168:717–719DOI 10.1007/s00431-008-0830-y

T. Watanabe (*) :Y. BabaDepartment of Pediatrics, Niigata City General Hospital,463-7 Shumoku, Chuo-ku,Niigata City 950-1197, Japane-mail: twata@hosp.niigata.niigata.jp

serum pattern of Epstein-Barr virus antibodies indicated a pasthistory of Epstein-Barr virus infection. A throat swab culturegrew group-A beta-hemolytic Streptococcus pyogenes, whilea urine bacterial culture grew no pathogens. An abdominalultrasonography, performed the morning after an overnightfast, demonstrated thickening of the gallbladder wall(11 mm), without gallstones or a biliary tract obstruction(Fig. 1a). The gallbladder was not distended.

The patient was diagnosed with APSGN and thickeningof the gallbladder wall. Eyelid and pretibial edema,hypertension, and right hypochondrial pain improved1 week after admission, following dietary restriction ofwater and sodium chloride. Two weeks after admission, thegallbladder wall thickening had completely resolved(Fig. 1b) and proteinuria had returned to normal levels.Four weeks after admission, the patient’s serum comple-ment levels had also returned to within the normal range.

Discussion

Thickening of the gallbladder wall is a relatively frequentfinding on diagnostic imaging studies and results fromprimary gallbladder disease or secondary gallbladderinvolvement [8]. Although surgical interventions such ascholecystectomy and cholecystostomy are often required inpatients with diffuse gallbladder wall thickening due toprimary gallbladder diseases such as cholecystitis, theseprocedures are unwarranted in patients with secondarygallbladder involvement, given that wall thickness usuallyreturns to normal in these patients after correction of theextrinsic factor causing the change [8].

Our patient with APSGN exhibited transient thickeningof the gallbladder wall. As our patient did not have apositive Murphy sign or serum inflammatory findings,cholecystitis was considered an unlikely cause of thegallbladder wall thickening we observed.

Kidney diseases such as acute pyelonephritis [7, 10] andchronic kidney failure [5, 8, 9] have been reported to cause

diffuse thickening of the gallbladder wall. Renal inflamma-tion with secondary involvement of the gallbladder wall hasbeen suggested as the pathogenic mechanism for gallblad-der wall thickening in pyelonephritis [7, 8]. On the otherhand, elevated systemic venous pressure is also thought tocause edema of the gallbladder wall in chronic kidneyfailure [8, 9]. As our patient with APSGN had mildsystemic edema and hypertension without any signs ofrenal failure, pyelonephritis or hypoproteinemia, elevatedsystemic venous pressure may have been the cause ofgallbladder wall thickening in this case. Systemic edemaand vascular congestion, resulting from sodium and waterretention, are common in APSGN [6]. However, diffusethickening of the gallbladder wall has never been reportedin such patients. Although the reason for the rarity ofgallbladder wall thickening in APSGN is unclear, it ispossible that an elevation in systemic venous pressure ofsufficient duration, as occurs in chronic renal failure, maybe necessary to induce this change.

Another possible cause of gallbladder wall thickening inour patient was vasculitis associated with APSGN. Cerebralvasculitis [2] and Henoch-Schönlein purpura (HSP) [3]have been reported previously in patients with APSGN.Furthermore, gallbladder wall thickening has also beenreported in patients with HSP [1, 4]. Although our patientdid not exhibit any apparent symptoms or signs of systemicvasculitis, it is possible that local or subclinical vasculitismay have caused gallbladder wall thickening.

References

1. Amemoto K, Nagita A, Aoki S, Azumagawa K, Hirano K, MinoM (1994) Ultrasonographic gallbladder wall thickening inchildren with Henoch-Schonlein purpura. J Pediatr GastroenterolNutr 19:126–128 doi:10.1097/00005176-199407000-00024

2. Kaplan RA, Zwick DL, Hellerstein S, Warady BA, Alon U (1993)Cerebral vasculitis in acute post-streptococcal glomerulonephritis.Pediatr Nephrol 7:194–195 doi:10.1007/BF00864396

BA

Fig. 1 a Abdominal ultrasonog-raphy during the acute phase ofAPSGN showing a diffusethickened gallbladder wall mea-suring 11 mm in diameter. b Thethickening of the gallbladderwall resolved completely in theconvalescent phase of thedisease

718 Eur J Pediatr (2009) 168:717–719

3. Kikuchi Y, Yoshizawa N, Oda T, Imakiire T, Suzuki S, Miura S(2006) Streptococcal origin of a case of Henoch-Schoenleinpurpura nephritis. Clin Nephrol 65:124–128

4. Kumon Y, Hisatake K, Chikamori M, Hara H, Numata Y, YamanoT et al (1988) A case of vasculitic cholecystitis associated withSchönlein-Henoch purpura in an adult. Gastroenterol Jpn 23:68–72 doi:10.1007/BF02918859

5. Shlaer WJ, Leopold GR, Scheible FW (1981) Sonography of thethickened gallbladder wall: a nonspecific finding. Am J Rent-ogenol 136:337–339

6. Sulyok E (2004) Acute proliferative glomerulonephritis. In: AvnerED, Harmon WE, Niaudit P (eds) Pediatric Nephrology, 5th edn.Lippincott Williams and Willkins, Philadelphia, pp 601–613

7. Talarico HP, Rubens D (1990) Gallbladder wall thickening inacute pyelonephritis. J Clin Ultrasound 18:653–657

8. van Breda Vriesman AC, Engelbrecht MR, Smithuis RHM,Puylaert JBCM (2007) Diffuse gallbladder wall thickening:differential diagnosis. Am J Rentogenol 188:495–501doi:10.2214/AJR.05.1712

9. Wegener M, Börsch G, Schneider J, Wedmann B, Winter R,Zacharias J (1987) Gallbladder wall thickening: a frequent findingin various nonbiliary disorders—a prospective ultrasonographicstudy. J Clin Ultrasound 15:307–312 doi:10.1002/jcu.1870150503

10. Zissin R, Osadchy A, Shapiro-Feinberg M, Gayer G (2003) CT ofa thickened-wall gall bladder. Br J Radiol 76:137–143doi:10.1259/bjr/63382740

Eur J Pediatr (2009) 168:717–719 719