Henoch–Schönlein purpura nephritis associated with human parvovirus B19 infection
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Human parvovirus B19 (B19) is associated with various diseases, 1 including erythema infectiosum, hydrops fetalis, transient aplastic crisis, neurologic diseases, 2 rheumatologic diseases and vasculitis. In 1985, Lefrère et al. reported the first case of Henoch–Schönlein purpura (HSP) associated with B19 infection. 3 Thereafter several cases of HSP associated with B19 were reported. 4–7 Among these cases, only two patients have had renal involvement. We present in the present paper a patient with clinically and histologically typical Henoch–Schönlein purpura nephritis (HSPN) associated with B19. Patient report A 5-year-old Japanese girl presented in March 1997 with purpura on the bilateral lower extremities, ankle swelling and pain. Two weeks later, urinalysis showed 1+ protein and 3+ blood, with many red blood cells per high-power field. On admission, her weight was 20 kg, blood pressure 98/48 mmHg. Her eyelids were edematous and pretibial pitting edema was present. Laboratory studies revealed hypo- albuminemia (2.45 g/dL), hypercholesterolemia (263 mg/dL) and an increase in erythrocyte sedimentation rate (54 mm/h). Her blood urea nitrogen (BUN) was 18.1 mg/dL, serum creatinine 0.3 mg/dL, hemoglobin 11.6 g/dL, platelet count 319 000 /mm 3 , antistreptolysin O (ASO) 42.91 U/L, serum IgG 899 mg/dL, IgA 188 mg/dL, IgM 89 mg/dL, C3 104 mg/dL, C4 28 mg/dL and creatinine clearance 95.6 mL/min per 1.73 m 2 . Antinuclear antibody (ANA), anti-double stranded DNA antibody and anticardiolipin antibodies were negative. Urinalysis showed 3+ protein, macroscopic hematuria and a few granular and red blood cell casts. Urine protein excretion was 2.2 g/day. Serum electrolyte, liver enzymes and blood coagulation tests were normal. We examined her sera taken on admission (early phase) and 3 months later (late phase) for anti-B19 specific IgG and IgM antibody by enzyme-linked immunosorbent assay and B19 DNA by the polymerase chain reaction (PCR) technique. The early phase serum had anti-B19 IgG antibody (absorbance value was 2.21) and B19 DNA. In the late phase, the titer of anti-B19 IgG antibody was increased (absorbance value was 7.33) and B19 DNA disappeared. These results were compatible with recent B19 infection. The patient was diagnosed as having nephrotic HSPN associated with B19 infection and underwent renal biopsy on the fifth hospital day. A kidney biopsy specimen contained 13 glomeruli. All glomeruli showed moderate mesangial proliferation and segmental neutrophil infiltration into capillary lumens (Fig. 1). No glomeruli had crescents. No interstitial infiltration or fibrosis were present. Immunofluorescence studies showed diffuse granular mesangial staining for IgA and C3 (Fig. 2). These findings represented typical HSPN, International Study of Kidney Diseases in Childhood (ISKDC) grade 2. The patient was treated with oral dypiridamole 6 mg/kg per day, 15 U/kg per h heparin, i.v., and 1 mg/kg per day oral predonisolone for 4 weeks. Thereafter, she was treated 0.1 mg/kg oral warfarin and 1 mg/kg per alternative day oral predonisolone for 6 months. One year later, her proteinuria and hematuria had disappeared and her renal function was normal. Discussion Renal diseases associated with B19 infection have occasionally been reported. Markenson et al. described the nephrotic syndrome and hypoplastic crisis after viral infection in two members of a family with sickle-cell anemia. 8 Although serologic evidence of B19 infection was lacking, concomitant hypoplastic crisis suggested that they suffered from B19 infection. Wierenga et al. have reported seven cases of glomerulonephritis after serologically defined B19 infection in sickle-cell disease. 9 Segmental proliferative glomerulonephritis was found in four patients who Pediatrics International (2000) 42, 94–96 Patient Report Henoch–Schönlein purpura nephritis associated with human parvovirus B19 infection TORU WATANABE AND YOSHIHIKO ODA Department of Pediatrics, Niigata City General Hospital, Niigata, Japan Key words Henoch–Schönlein purpura, Henoch–Schönlein purpura nephritis, human parvovirus B19. Correspondence: Toru Watanabe, Department of Pediatrics, Niigata City General Hospital, 2-6-1 Shichikuyama, Niigata 950-8739, Japan. Email: [email protected] Received 30 October 1998; revised 6 January 1999; accepted 8 January 1999.
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Transcript of Henoch–Schönlein purpura nephritis associated with human parvovirus B19 infection
Human parvovirus B19 (B19) is associated with variousdiseases,1 including erythema infectiosum, hydrops fetalis,transient aplastic crisis, neurologic diseases,2 rheumatologicdiseases and vasculitis. In 1985, Lefrère et al. reported thefirst case of Henoch–Schönlein purpura (HSP) associatedwith B19 infection.3 Thereafter several cases of HSPassociated with B19 were reported.4–7 Among these cases,only two patients have had renal involvement.
We present in the present paper a patient with clinicallyand histologically typical Henoch–Schönlein purpuranephritis (HSPN) associated with B19.
Patient report
A 5-year-old Japanese girl presented in March 1997 withpurpura on the bilateral lower extremities, ankle swelling andpain. Two weeks later, urinalysis showed 1+ protein and3+ blood, with many red blood cells per high-power field.
On admission, her weight was 20 kg, blood pressure98/48 mmHg. Her eyelids were edematous and pretibialpitting edema was present. Laboratory studies revealed hypo-albuminemia (2.45 g/dL), hypercholesterolemia (263 mg/dL)and an increase in erythrocyte sedimentation rate (54 mm/h).Her blood urea nitrogen (BUN) was 18.1 mg/dL, serumcreatinine 0.3 mg/dL, hemoglobin 11.6 g/dL, platelet count319 000 /mm3, antistreptolysin O (ASO) 42.91 U/L, serumIgG 899 mg/dL, IgA 188 mg/dL, IgM 89 mg/dL, C3 104mg/dL, C4 28 mg/dL and creatinine clearance 95.6 mL/minper 1.73 m2. Antinuclear antibody (ANA), anti-doublestranded DNA antibody and anticardiolipin antibodies werenegative. Urinalysis showed 3+ protein, macroscopichematuria and a few granular and red blood cell casts. Urineprotein excretion was 2.2 g/day. Serum electrolyte, liverenzymes and blood coagulation tests were normal.
We examined her sera taken on admission (early phase)and 3 months later (late phase) for anti-B19 specific IgG andIgM antibody by enzyme-linked immunosorbent assay andB19 DNA by the polymerase chain reaction (PCR)technique. The early phase serum had anti-B19 IgG antibody(absorbance value was 2.21) and B19 DNA. In the latephase, the titer of anti-B19 IgG antibody was increased(absorbance value was 7.33) and B19 DNA disappeared.These results were compatible with recent B19 infection.
The patient was diagnosed as having nephrotic HSPNassociated with B19 infection and underwent renal biopsyon the fifth hospital day. A kidney biopsy specimencontained 13 glomeruli. All glomeruli showed moderatemesangial proliferation and segmental neutrophil infiltrationinto capillary lumens (Fig. 1).
No glomeruli had crescents. No interstitial infiltration orfibrosis were present. Immunofluorescence studies showeddiffuse granular mesangial staining for IgA and C3 (Fig. 2).These findings represented typical HSPN, InternationalStudy of Kidney Diseases in Childhood (ISKDC) grade 2.
The patient was treated with oral dypiridamole 6 mg/kgper day, 15 U/kg per h heparin, i.v., and 1 mg/kg per dayoral predonisolone for 4 weeks. Thereafter, she was treated0.1 mg/kg oral warfarin and 1 mg/kg per alternative day oralpredonisolone for 6 months. One year later, her proteinuriaand hematuria had disappeared and her renal function wasnormal.
Discussion
Renal diseases associated with B19 infection haveoccasionally been reported. Markenson et al. described thenephrotic syndrome and hypoplastic crisis after viralinfection in two members of a family with sickle-cellanemia.8 Although serologic evidence of B19 infection waslacking, concomitant hypoplastic crisis suggested that theysuffered from B19 infection. Wierenga et al. have reportedseven cases of glomerulonephritis after serologically definedB19 infection in sickle-cell disease.9 Segmental proliferativeglomerulonephritis was found in four patients who
Pediatrics International (2000) 42, 94–96
Patient Report
Henoch–Schönlein purpura nephritis associated with humanparvovirus B19 infection
TORU WATANABE AND YOSHIHIKO ODA
Department of Pediatrics, Niigata City General Hospital, Niigata, Japan
Key words Henoch–Schönlein purpura, Henoch–Schönlein purpura nephritis, human parvovirus B19.
Correspondence: Toru Watanabe, Department of Pediatrics,Niigata City General Hospital, 2-6-1 Shichikuyama, Niigata 950-8739, Japan. Email: [email protected]
Received 30 October 1998; revised 6 January 1999; accepted8 January 1999.
HSPN associated with human parvovirus B19 95
underwent acute renal biopsy. Immunofluorescence for IgGand C1q showed segmental staining, but IgA was negative.9
Since Lefrère reported the first case of HSP associatedwith B19 infection,3 several cases of HSP with B19infection have been described.4–7 Although renal involve-ment in HSP is common complication, it has been reportedin only two cases of HSP with B19 infection. Veraldi andRizzitelli have described an adult case of HSP associatedwith B19 infection who had proteinuria and hematuria.5
Renal biopsy was not performed. Minohara reported a 7-year-old patient with HSP after B19 infection whose renalbiopsy specimen showed diffuse mesangial proliferative
glomerulonephritis, but immunofluorescence findings werenot described.6
The pathogenesis of HSPN is unknown, but themesangial location and the granular IgA and C3 stainingsuggest immune complex disease.10 Our present case washistologically typical of HSPN, including a positiveimmunofluorescence finding. Tanaka et al. have recentlyreported a case of B19 infection resembling systemic lupuserythematosus and suggest that B19 infection could inducean immune complex-mediated phenomenon.11 Infection byB19 could induce direct renal endothelial injury, but inHSPN, at least in our present case, secondary immunologic
Fig. 1 Photograph of a glom-erulus exhibiting mesangialproliferation with neutrophilinfiltration. (periodic acid-Schiffstain).
Fig. 2 Immunofluorescence forIgA and C3 showed granularmesangial staining. (a) Immuno-globulin A, (b) C3.
96 T Watanabe and Y Oda
disturbances caused by B19 may induce immune complex-mediated glomerulonephritis.
References
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