Haemophilus parainfluenzae Antigen and Antibody in Children

With IgA Nephropathy and Henoch-Schönlein Nephritis

Yuko Ogura, BSc, Satoru Suzuki, MD, Taku Shirakawa, PhD, Miwa Masuda, BSc,
Hajime Nakamura, MD, Kazumoto Iijima, MD, and Norishige Yoshikawa, MD

● Although the pathogenesis of immunoglobulin A (IgA) nephropathy and Henoch-Schönlein nephritis (HSN)
remains uncertain, there is substantial evidence that they are immune complex–mediated diseases. Recently,
Haemophilus parainfluenzae antigens were shown in the glomerular mesangium of adult patients with IgA
nephropathy, and greater levels of IgA antibody against H parainfluenzae were also shown in the sera of adult
patients with IgA nephropathy. The present study was performed to detect H parainfluenzae antigens and antibody
against H parainfluenzae in children with IgA nephropathy and HSN. H parainfluenzae antigens in the mesangium
were examined by indirect immunofluorescence, and antibody against H parainfluenzae was examined by enzyme-
linked immunosorbent assay. Diffuse global staining of the mesangium with rabbit antisera against H parainfluen-
zae was shown in 10 of the 32 patients (31%) with IgA nephropathy and 12 of the 34 patients (35%) with HSN.
Conversely, only 2 of the 47 patients (4%) with other renal diseases showed staining of glomeruli with rabbit
antisera against H parainfluenzae (IgA nephropathy versus other renal diseases, P 5 0.003; HSN versus other renal
diseases, P 5 0.0006). Patients with IgA nephropathy and those with HSN showed significantly greater levels of
plasma IgA1 antibody against H parainfluenzae than patients with other renal diseases (IgA nephropathy versus
other renal diseases, P 5 0.008; HSN versus other renal diseases, P 5 0.025). These findings suggest that H
parainfluenzae has a role in the cause of these two conditions in a subset of patients.
r 2000 by the National Kidney Foundation, Inc.
INDEX WORDS: Haemophilus parainfluenzae; immunoglobulin A (IgA) nephropathy; Henoch-Schönlein nephritis
(HSN); children.

I MMUNOGLOBULIN A (IgA) nephropathy

occurs in both children and adults. Children
with IgA nephropathy usually have episodes of
macroscopic or microscopic hematuria with nor-
mal renal function and mild proteinuria. Henoch-
Schönlein nephritis (HSN) occurs predominantly
during childhood and is characterized by a purpu-
ric rash, arthralgia, abdominal pain, and gastroin-
testinal bleeding. Both conditions show the same
glomerular changes, characterized by diffuse
deposition of IgA on immunofluorescence micros-
copy and various degrees of focal or diffuse
mesangial proliferation on light microscopy. On
electron microscopy, numerous electron-dense
deposits in the mesangium are characteristic.1,2
Although the pathogenesis of IgA nephropa-
thy and HSN remains uncertain, there is substan-
tial evidence that they are immune complex–
mediated diseases. Abnormal IgA regulation,
impaired reticuloendothelial cell system phago-
cytic function, and elevated circulating IgA-
containing immune complexes have been
found.3-12 Considerable effort has been directed
toward the search for antigens, but with limited
success. Many antigens, including bacteria, vi-
ruses, and food, have been identified.13,14 How-
ever, no single antigen has yet been positively
identified in a diffuse and global distribution in
the glomeruli. Recently, Suzuki et al15 showed
the presence of Haemophilus parainfluenzae an-
tigens in a diffuse and global distribution in the
glomerular mesangium and the presence of IgA
antibody against H parainfluenzae in the sera of
adult patients with IgA nephropathy.
The present study was performed to detect H
parainfluenzae antigens in the glomerular mesan-
gium and antibody against H parainfluenzae in
the plasma of children with IgA nephropathy,
HSN, and other renal diseases.
PATIENTS AND METHODS
The following methods are in accordance with the ethical
standards for human experimentation stipulated by the Eth-
ics Committee of Kobe University Hospital (Kobe, Japan).
All patients’ parents gave informed consent.
Renal tissues from all children who had undergone renal
From the Faculty of Health Science and Department of
Pediatrics, Kobe University School of Medicine, Kobe; and
the Department of Clinical and Laboratory Medicine, Fukui
Medical University, Fukui, Japan.
Received September 27, 1999; accepted in revised form
February 4, 2000.
Address reprint requests to Norishige Yoshikawa, MD,
Faculty of Health Science, Kobe University School of Medi-
cine, 10-2 Tomogaoka 7 chome, Suma-ku, Kobe 654, Japan.
E-mail: nori@kobe-u.ac.jp
r 2000 by the National Kidney Foundation, Inc.
0272-6386/00/3601-0006$3.00/0
doi:10.1053/ajkd.2000.8264

American Journal of Kidney Diseases, Vol 36, No 1 (July), 2000: pp 47-52 47

48
biopsy at Kobe University Hospital from December 1997 to
November 1998 were examined. Renal tissue from all chil-
dren with IgA nephropathy who underwent biopsy from
January 1997 to November 1997 and renal tissue from all
children with HSN who underwent biopsy from July 1993 to
November 1997 were also examined.
The diagnosis of IgA nephropathy was based on the
presence of IgA as the sole or predominant immunoglobulin
in the glomerular mesangium, with no evidence of such
systemic diseases as Henoch-Schönlein purpura or systemic
lupus nephritis.1 HSN was diagnosed when hematuria and
proteinuria were associated with a characteristic purpuric
rash and either abdominal or joint pain or both.2
The biopsies were performed by the percutaneous tech-
nique using a Tru-Cut needle (Baxter Healthcare Co) under
radiograph or ultrasound control. Renal biopsy specimens
were examined by light microscopy, immunofluorescence,
and electron microscopy. Biopsy tissue for immunofluores-
cence was snap frozen in acetone-dry ice, cut at 4 µm, and
stained with fluorescein-tagged commercial antisera to hu-
man IgG, IgA, IgM, C1q, C4, C3, and fibrinogen (Cappel,
Ohio, PA). Cryostat sections were incubated with antiserum
against H parainfluenzae in moist chambers at 4°C over-
night, washed three times with phosphate-buffered saline
(PBS), and incubated with fluorescein isothiocyanate–
labeled swine antibody against rabbit immunoglobulin (Dako,
Glostrup, Denmark) for 30 minutes. Antiserum against H
parainfluenzae was produced as previously described.15 H
parainfluenzae antigen was prepared from a strain isolated
from the pharynx of a healthy individual. Sonicate of H
parainfluenzae was prepared by high-power ultrasound
pulses. Sonicate of H parainfluenzae was injected with
complete Freund’s adjuvant into white rabbits. The IgG
fraction isolated from rabbit serum was shown to have
specificity for sonicate of H parainfluenzae. Sections were
viewed with an Olympus BH2-RFCA reflecting microscope
(Olympus, Tokyo, Japan).
Enzyme-linked immunosorbent assay was performed ac-
cording to the modified method of Borradori et al.16 Briefly,
each well of a 96-well polystyrene microtiter plate was
coated with 100 µL of sonicate of H parainfluenzae at a final
protein concentration of 1.07 µg/mL in 0.05 mol/L of carbon-
ate buffer (pH 9.5). After incubation overnight at 4°C, wells
were washed three times with PBS-Tween (Yatoron, Tokyo,
Japan) and shaken dry. Unoccupied absorption sites in the
wells were blocked by overnight incubation at 4°C with
PBS-Tween containing 0.5% (w/v) bovine serum albumin.
One hundred microliters of patient plasma diluted 1 in 100
with PBS-Tween was added to the wells of the microtiter
plates and incubated for 60 minutes at 37°C. Plates were
then washed three times with PBS-Tween; 100 µL of peroxi-
dase-conjugated monoclonal antibody against human IgA1
and IgA2 (Nordic Laboratories, Tilburg, The Netherlands)
diluted 1 in 10 with PBS-Tween was added to each well; and
after incubation for 60 minutes at 37°C, the wells were
washed three times. One hundred microliters of 0.1 mol/L of
phosphate-citrate buffer (pH 4.9) containing o-phenylenedi-
amine (33 mg/mL) and hydrogen peroxide (0.018% w/v) in
0.1 mol/L of phosphate-citrate buffer (pH 4.9) was added to
each well. After incubation at room temperature for 30
minutes in the dark, the reaction was stopped by the addition
OGURA ET AL
of 100 µL of 0.75 mol/L of H2SO4. Absorbance was then
read at 492 nm.
The results were analyzed with StatView J-4.02 software
(SAS Institute, Cary, NC).17 The associations of categorical
variables were examined by Fisher’s exact test. Continuous
characteristics of the groups were compared using the Mann-
Whitney U test or analysis of variance. Two-tailed P less
than 0.05 is considered significant.
RESULTS
Biopsy specimens from 32 patients with IgA
nephropathy (19 boys, 13 girls; age range, 8 to
19 years; mean age, 12.7 years), 34 patients with
HSN (16 boys, 18 girls; age range, 3 to 19 years;
mean age, 9.1 years), and 47 patients with other
renal diseases (34 boys, 13 girls; age range, 1 to
19 years; mean age, 10.4 years) were examined.
Diffuse global deposits of IgA in the mesangial
area, often expanding into the adjacent capillary
walls, were observed in all patients with IgA
nephropathy and HSN. IgA deposits were associ-
ated with IgG in 28 patients with IgA nephropa-
thy and 31 patients with HSN, with IgM in 18
patients with IgA nephropathy and 11 patients
with HSN, with C1q in 2 patients with HSN,
with C4 in 1 patient with HSN, and with C3 in 17
patients with IgA nephropathy and 23 patients
with HSN. Glomerular deposition of IgA was
observed in 8 of 47 patients with renal diseases
other than IgA nephropathy or HSN (diffuse
global mesangial deposition, 2 patients; focal
segmental deposition, 6 patients); IgG was pres-
ent in 17 patients, IgM in 16 patients, C1q in 9
patients, C4 in 6 patients, and C3 in 9 patients.
Diffuse global staining of the mesangium with
rabbit antisera against H parainfluenzae was
shown in 10 of the 32 patients (31%) with IgA
nephropathy and 12 of the 34 patients (35%)
with HSN (Table 1; Fig 1). In contrast, only 2 of
the 47 patients (4%) with other renal diseases
showed staining of glomeruli with rabbit antisera
against H parainfluenzae (IgA nephropathy ver-
sus other renal diseases, P 5 0.003; HSN versus
other renal diseases, P 5 0.0006). Diffuse global
staining of the mesangium with rabbit antisera
against H parainfluenzae often expanded into the
adjacent capillary walls, and the distribution of H
parainfluenzae antigen was similar to the distri-
bution of IgA. Extraglomerular staining for H
parainfluenzae antigen was not observed.
Plasma levels of IgA1 and IgA2 antibodies
against H parainfluenzae are listed in Table 2.
H PARAINFLUENZAE IN IgA-ASSOCIATED DISEASES 49

Table 1. Prevalence of H parainfluenzae Antigen Table 2. Plasma IgA1 and IgA2 Antibodies Against
in Glomeruli of Children With Various H parainfluenzae
Glomerular Diseases
IgA1 IgA2
Glomerular No. of Antibody Antibody
Deposition Patients Level Level
of IgA Diagnosis Examined (ELISA OD) (ELISA OD)
(diffuse
Glomerular global IgA nephropathy 24 0.37 6 0.11* 0.094 6 0.006
No. of Deposition mesangial Henoch-Schön-
Diagnosis Patients of Antigen deposition) lein nephritis 20 0.35 6 0.16† 0.095 6 0.006
Other glomerular
IgA nephropathy 32 10 (31%)* 32 (32) diseases 37 0.27 6 0.10 0.098 6 0.008
Henoch-Schönlein
nephritis 34 12 (35%)† 34 (34) NOTE. Values expressed as mean 6 SD of the mean.
Other glomerular diseases 47 2 (4%) 8 (2) Abbreviations: ELISA, enzyme-linked immunosorbent
Minimal change assay; OD, optical density.
nephrotic syndrome 22 0 0 *IgA nephropathy versus other renal diseases; P 5
Focal segmental glo- 0.008.
merulosclerosis 5 0 2 (0) †Henoch-Schönlein nephritis versus other renal dis-
Membranous glomerulo- ease; P 5 0.03.
nephritis 3 0 0
Membranoproliferative
glomerulonephritis 4 0 0 Patients with IgA nephropathy and those with
Hereditary nephritis 2 0 0 HSN showed significantly greater levels of
Lupus nephritis 3 1 3 (2) plasma IgA1 antibody against H parainfluenzae
Allograft kidney 6 1 1 (0)
Hemolytic uremic syn-
than patients with other renal diseases (IgA ne-
drome 1 0 1 (0) phropathy versus other renal disease, P 5 0.008;
Mesangial proliferative HSN versus other renal diseases, P 5 0.025)
glomerulonephritis 1 0 1 (0) The incidence of episodes of upper respiratory
infection within the 3 months before biopsy,
*IgA nephropathy versus other renal diseases; P 5
0.003.
gross hematuria before biopsy, decreased renal
†Henoch-Schönlein nephritis versus other renal dis- function, heavy proteinuria, mesangial IgA depos-
eases; P 5 0.0006. its, and mesangial C3 deposits; mean age at
biopsy; and mean time of biopsy from onset of
disease were similar in patients with and without
glomerular H parainfluenzae antigen (Table 3).
The mean level of plasma IgA1 antibody
against H parainfluenzae was greater in patients
with than without glomerular H parainfluenzae
antigen, but the difference was not statistically
significant. There was no correlation between
level of plasma IgA1 antibody against H parain-
fluenzae and age (Fig 2). The incidence of epi-
sodes of upper respiratory infection within the 3
months before biopsy, mesangial IgA deposits,
mesangial C3 deposits, and mean age at biopsy
were similar in patients with greater levels of
plasma IgA1 antibody against H parainfluenzae
and those with lower levels of plasma IgA1
antibody against H parainfluenzae (Table 4). The
incidence of glomerular H parainfluenzae anti-
gen was greater in patients with greater levels of
Fig 1. Immunofluorescence micrograph of a glo- plasma IgA1 antibody against H parainfluenzae
merulus from a patient with IgA nephropathy. H parain-
fluenzae antigen is mainly in mesangial areas (original than in those with lower levels, but the difference
magnification 3520). was not statistically significant.
50 OGURA ET AL

Table 3. Relationship Between Clinical and Pathological Features, Level of Plasma IgA1 Antibody Against
H parainfluenzae, and Presence or Absence of Glomerular H parainfluenzae Antigen in Children With IgA
Nephropathy and Henoch-Schönlein Nephritis

Glomerular
H parainfluenzae Antigen

Present (n 5 22) Absent (n 5 44)

No. of patients with upper respiratory infection within 3 months before biopsy 4 (18) 7 (16)
No. of patients with gross hematuria before biopsy 7 (32) 16 (36)
Age at biopsy (y) 11.1 6 4.2 10.7 6 3.8
Time of biopsy from onset of disease (mo) 35 6 46 25 6 35
No. of patients with creatinine clearance ,80 mL/min/1.73 m2 of body surface area at biopsy 1 (5) 5 (11)
No. of patients with proteinuria .1 g/d of protein at biopsy 11 (50) 22 (50)
Level of plasma IgA1 antibody against H parainfluenzae (ELISA OD) 0.39 6 0.17 0.34 6 0.11
No. of patients with mesangial IgA deposits 22 (100) 44 (100)
No. of patients with mesangial C3 deposits 15 (68) 25 (57)

NOTE. Values expressed as mean 6 SD or number (percent).

Abbreviations: ELISA, enzyme-linked immunosorbent assay; OD, optical density.

DISCUSSION immune complex have been reported in patients

There is substantial evidence to suggest that
IgA nephropathy and HSN are immune complex–
mediated diseases. Granular electron-dense de-
posits are observed in the glomerular mesangial
areas by electron microscopy and can be con-
firmed as containing IgA and C3 by immunoflu-
orescence microscopy. Circulating IgA immune
complexes, often associated with IgG immune
complex, have been detected by several different
specific assays.3,4,18,19 Many immunologic abnor-
malities that may lead to the formation of IgA
with IgA nephropathy and HSN. Recurrences of
mesangial IgA deposits are frequent in allo-
grafted kidneys in patients with IgA nephropathy
and HSN,20-23 and this evidence indicates that the
mesangial IgA must be of host origin. Moreover,
glomerular IgA deposits associated with histologi-
cal lesions similar to those of human IgA ne-
phropathy and HSN can be induced in laboratory
Table 4. Relationship Between Clinical and
Pathological Features and Level of Plasma IgA1
Antibody Against H parainfluenzae in Children With
IgA Nephropathy and Henoch-Schönlein Nephritis

Level of Plasma IgA1

Antibody Against
H parainfluenzae
(ELISA OD)

.0.4 ,0.4
(n 5 12) (n 5 32)

No. of patients with upper respira-

tory infection within 3 months
before biopsy 1 (8) 6 (19)
Age at biopsy (y) 11.8 6 4.4 9.8 6 4.1
No. of patients with glomerular
H parainfluenzae antigen 6 (50) 9 (28)
No. of patients with mesangial IgA
deposits 12 (100) 32 (100)
No. of patients with mesangial C3
deposits 7 (58) 20 (63)
Fig 2. Relationship between level of plasma IgA1
antibody against H parainfluenzae and age in children NOTE. Values expressed as number (percent) or
with IgA nephropathy and Henoch-Schönlein nephri- mean 6 SD.
tis. Abbreviations: ELISA, enzyme-linked immunosor- Abbreviations: ELISA, enzyme-linked immunosorbent
bent assay; OD, optical density. assay; OD, optical density.
H PARAINFLUENZAE IN IgA-ASSOCIATED DISEASES
animals by the passive administration of pre-
formed polymeric IgA–concanavalin A com-
plex.24
The predominance of IgA in the mesangium in
IgA nephropathy and HSN strongly suggests that
these deposits are the consequence of an immune
response initiated at mucosal surfaces. The asso-
ciation of recurrent macroscopic hematuria with
infections of the upper respiratory tract further
suggests that the IgA immune response is in-
duced by microbial antigens.25 Suzuki et al15
showed the presence of H parainfluenzae anti-
gens in the glomerular mesangium in all adult
patients with IgA nephropathy and a greater level
of serum IgA antibody against H parainfluenzae
in these patients. In the present study, H parain-
fluenzae antigens in the mesangium were shown
in 31% of the children with IgA nephropathy,
35% of the children with HSN, and only 4% of
the children with other renal diseases (IgA ne-
phropathy versus other renal diseases, P 5 0.003;
HSN versus other renal diseases, P 5 0.0006).
Patients with IgA nephropathy and patients with
HSN showed significantly greater levels of
plasma IgA1 antibody against H parainfluenzae
than patients with other renal diseases (IgA ne-
phropathy versus other renal diseases, P 5 0.008;
HSN versus other renal diseases, P 5 0.025).
The majority of investigators have indicated that
IgA1 is the predominant subclass present in the
glomeruli of patients with IgA nephropathy and
HSN.26,27 These findings suggest that H parain-
fluenzae antigens and antibody against H parain-
fluenzae may be involved in the pathogenesis of
glomerulonephritis in approximately one third of
the children with IgA nephropathy and HSN. The
difference in frequency of mesangial H parainflu-
enzae antigen deposition in IgA nephropathy
between the present study and the previous
study15 may be caused by the difference between
children and adults. There may be antigenic
heterogeneity in childhood IgA nephropathy.
The relationship between IgA nephropathy
and HSN is complex. The morphological and
immunopathological features are similar in the
two conditions.28 The two disorders have been
reported to coexist in different members of the
same family,29,30 including a pair of monozygotic
twins who developed them simultaneously after
a well-documented adenovirus infection,31 and
to affect the same patient at different times.32 It
51
has been suggested that the two conditions are
variants of the same process, and that IgA ne-
phropathy is HSN without the rash.31 This study
shows that H parainfluenzae antigens were de-
tected nearly exclusively in the mesangium of
children with IgA nephropathy and HSN. Their
detection in both diseases suggests a common
pathogenesis of glomerular injury in at least a
subset of patients.
In conclusion, H parainfluenzae antigens were
detected nearly exclusively in the mesangium of
approximately one third of the children with IgA
nephropathy and HSN, and patients with IgA
nephropathy and HSN showed significantly
greater levels of plasma IgA1 antibody against H
parainfluenzae than patients with other renal
diseases. These findings suggest that H parainflu-
enzae has a role in the cause of these two
conditions in a subset of patients.
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