Post-infectious glomerulonephritis in a patient with vesicorenal malacoplakiacoincidence or causal relationship?
An Hang Yang1,4,,
Der Cherng Tarng2,
Jinn Yang Chen2 and
Shing Hwa Lu3
1 Department of Pathology,
2 Division of Nephrology, Department of Medicine and
3 Division of Urology, Department of Surgery, Veterans General Hospital, Taipei, and
4 Department of Pathology, School of Medicine, National Yang-Ming University, Taipei, Taiwan
Keywords: Escherichia coli; glomerulonephritis; malacoplakia
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Introduction
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Malacoplakia is an inflammatory disease involving mainly the urinary tract. Many studies indicate that it is an unusual host response to various micro-organisms, of which Escherichia coli is the most common [1]. Persistent infection associated with malacoplakia is considered to be non-nephritogenic. It has never been reported in association with post-infectious glomerulonephritis.
We report a patient with post-infectious type proliferative glomerulonephritis who suffered from malacoplakia of kidney and urinary bladder. A causal relationship between urinary E. coli and glomerulonephritis is discussed.
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Case
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A 62-year-old woman was admitted for evaluation of renal function impairment. She had a previous history of chronic headache, gouty arthritis, and gastric ulcer. Prominent urinary symptoms including pain and frequency presented at the time of admission. Urinary culture yielded E. coli. Upper abdominal MRI revealed bilateral enlargement of the kidneys and multiple low-density areas in both cortex and medulla. MR examination of urinary bladder showed thickening of the posterior wall. Physical examination revealed neither hypertension (blood pressure 110/70 mmHg) nor oedema. Laboratory data included blood urea nitrogen 59 mg/dl, serum creatinine 5.4 mg/dl, creatinine clearance 3.1 ml/min, serum total protein 8.0 g/dl, serum albumin 3.1 g/dl, serum C-reactive protein 4.1 mg/dl, erythrocyte sedimentation rate 129 mm/h, and serum antistreptolysin-O titre, <80 IU. Search for anti-neutrophil cytoplasmic antibody was negative. Urinalysis revealed proteinuria (24-h urinary protein up to 1 g), microscopic haematuria, pyuria, and bacteriuria. Peripheral blood WBC count was 14 200. Immunological studies showed serum IgG 765 mg/dl, IgM 127 mg/dl, IgA, 765 mg/dl, C3 99 mg/dl, and C4 23 mg/dl.
Cystoscopic biopsy and renal needle biopsy were performed. Light microscopic examination of both biopsy specimens revealed characteristic features of malacoplakia, as described previously (Figure 1A
) [1,2]. The pathognomonic spherical or targetoid bodies (MichaelisGutmann bodies, Figure 1A
) were mainly located in the large histiocytes (von Hansemann cells). In addition to the typical interstitial changes, the glomeruli in renal biopsy showed diffuse intracapillary proliferative glomerulonephritis (Figure 1A
). The ultrastructural features of glomerular disease were compatible with the description in acute post-infectious glomerulonephritis (Figure 1B
and C
). Immunofluorescence microscopy revealed diffuse granular pattern of IgG and C3 deposition along the glomerular capillary walls (not shown). The patient received antibiotic treatment (ciprofloxacin, 500 mg every 12 h) for 8 weeks. Pyuria disappeared and urinary culture became negative after treatment. However, renal function remained severely impaired 12 months later (blood urea nitrogen 85 mg/dl, serum creatinine 7.3 mg/dl, and creatinine clearance 7.2 ml/min).

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Fig. 1. (A) Light microscopy finding of a glomerulus showing an increase in size and cellularity with broadening of lobules and segmental reduction of capillary lumina. Typical MichaelisGutmann bodies (arrows) are easily identified in large histiocytes (von Hansemann cells) in renal interstitium; 1-µm plastic section. Toluidine blue and basic fuchsine, x207. (B) Polymorphonuclear leukocytes are present in glomerular capillary lumina and in Bowman's space. Uranyl acetate and lead citrate, x3680. (C) Large, discrete, hump-like electron-dense deposits are frequently located in the subepithelial region (arrow). There is prominent effacement of the foot processes of glomerular visceral epithelial cells. Uranyl acetate and lead citrate, x4780.
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Discussion
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Arguments may arise as to whether the glomerulonephritis in our case was an independent disease, brought to attention by superimposed malacoplakia, or whether it was causally related to the E. coli infection. Since the glomerulonephritis occurred in a clearly related time course with malacoplakia, without evidence of prior streptococcal or other infection, it could conceivably be associated with E. coli infection.
Post-infectious glomerulonephritis of non-streptococcal origin is not uncommon. A variety of bacterial, viral, protozoan, and fungal infections have been reported to give rise to acute glomerulonephritis [3]. Escherichia coli-associated acute glomerulonephritis in humans has been documented although it is very rare [4]. One animal study demonstrated that infection of mice with living E. coli led to anti-E. coli DNA antibodies with subsequent development of immune complex glomerulonephritis [5]. Direct immunization of normal mice with E. coli DNA has also been reported to induce glomerular deposition of anti-DNA antibodies and acute proliferative glomerulonephritis [6]. Thus E. coli infection may be an alternative nephritogenic mechanism in addition to the classic concept of immunogenic reactions to bacterial protein fraction.
The major cause of persistent renal function impairment in our case may be attributed to the bilateral renal involvement of malacoplakia with extensive, irreversible destruction of renal parenchyma. The lack of a prominent acute nephritic syndrome with hypertension, oedema, and oliguria in the present case suggests that the glomerular disease was a form of subclinical or mild post-infectious glomerulonephritis. However, we are unable to provide definitive proof for our hypothesis of a possible implication of glomerulonephritis in the severity of renal failure. The potential risk of progressive damage of glomeruli leading to progressive nephron loss is, however, possible. Its contribution to the course of renal failure could only be ascertained by repeated renal biopsy.
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Acknowledgments
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The present study was supported by Veterans-General HospitalTaipei, under research grant No. VGH-360 (C-project, 1998).
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Notes
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Correspondence and offprint requests to: Dr An Hang Yang, Department of Pathology, Veterans General Hospital-Taipei, Taipei, Taiwan 112. 
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References
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Received for publication: 11. 8.99
Revision received 21. 2.00.