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doi:10.1111/jpc.12295

ORIGINAL ARTICLE

Prospective population-based study on the burden of disease

from post-streptococcal glomerulonephritis of hospitalised
children in New Zealand: Epidemiology, clinical features
and complications
William Wong,1 Diana R Lennon,2 Sonja Crone,1 Jocelyn M Neutze3 and Peter W Reed4
1
Department of Paediatric Nephrology, Starship Children’s Hospital, 2School of Population Health, University of Auckland, 3Department of Paediatrics, Kidz First
Hospital Middlemore and 4Children’s Research Unit, Starship Children’s Health, Auckland, New Zealand

Aim: A nationwide 24-month study was conducted (2007–2009), via the New Zealand Paediatric Surveillance Unit to define epidemiology and
clinical features of acute poststreptococcal glomerulonephritis (APSGN) in children hospitalised with the illness.
Methods: Paediatricians (n = 215) were requested to report new hospitalised cases fulfilling a case definition of definite (haematuria with low
C3 and high streptococcal titres or biopsy proven APSGN) or probable (haematuria with low C3 or high streptococcal titres).
Results: A total of 176 cases were identified (definite: n = 138, probable: n = 38) with 63% residing in the Auckland metropolitan region.
Sixty-seven percent were in the most deprived quintile. Annual incidence (0–14 years) was 9.7/100 000 (Pacific 45.5, Maori 15.7, European/other
2.6 and Asian 2.1/100 000). Annual incidence was highest in the South Auckland Metropolitan region (31/100 000), Central Auckland 14.9,
West/North Auckland metropolitan region 5.9 and for the remainder of New Zealand 5.5/100 000. Age-specific incidence was highest in age 5–9
years (15.1/100 000). Reduced serum complement C3, gross haematuria, hypertension, impairment of renal function and heavy proteinuria were
present in 93%, 87%, 72%, 67% and 44% of patients, respectively. Severe hypertension was closely associated with either symptoms of an acute
encephalopathy or congestive heart failure.
Conclusions: New Zealand children carry a significant disease burden of hospitalised APSGN with socio-economically deprived; Pacific and
Maori children are being over-represented. Significant short-term complications were observed in hospitalised children with APSGN. Persistently
very low rates in European/other suggest a preventable disease.

Key words: epidemiology; New Zealand; post-streptococcal glomerulonephritis.

What is already known on this topic What this paper adds

1 Acute poststreptococcal glomerulonephritis (APSGN), a pre-
ventable illness, is a common illness affecting New Zealand
children.
2 Hypertension is a frequent complication of APSGN that often
requires appropriate treatment.
3 In New Zealand, APSGN is concentrated by age group (5–14
years), ethnicity (Pacific and Maori children) and geographical
area (The North Island).
1 There is a strong relationship with socio-economic deprivation
with children in the lowest socio-economic quintile accounting
for two-thirds of cases.
2 Some patients present with severe extra-renal complications
such as an acute encephalopathy or congestive heart failure,
which is almost always associated with severe hypertension.
Their atypical presentation occasionally results in a delay
in diagnosis.
3 Acute severe renal failure is uncommon and requires temporary
acute dialysis in a small number of cases.

Acute post-streptococcal glomerulonephritis (APSGN) is one of
the most common causes of acute kidney injury in children of
developing countries.1–5 The disease is preceded by group A
Correspondence: Dr William Wong, Department of Paediatric Nephrology,
Starship Children’s Hospital, Private Bag 92024, Auckland, New Zealand.
Fax: +64 9307 8928; email: wwong@adhb.govt.nz
Conflicts of interest: None declared.
Accepted for publication 15 April 2013.
beta-haemolytic streptococcal infections affecting either the
throat or skin.3,4 APSGN is a common illness affecting New
Zealand children and is the commonest cause of acute severe
glomerulonephritis.1 Small studies undertaken in the 1980s in
localised areas of New Zealand have described clinical features
and short-term outcomes.6,7 There are also pronounced ethnic
differences. In a study undertaken in 1994–1998,8 143 cases
were identified in two children’s inpatient facilities in Auckland,
New Zealand. Annual incidence by ethnicity was 37 for Pacific
children, 17 for Maori and 3 per 100 000 for others.

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Journal of Paediatrics and Child Health © 2013 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
W Wong et al.
In 2005, childhood incidence in the developing world was
reported to be two cases per 100 000 person-years and 0.3 in
developed regions.5 Over the past 30 years, the disease has
declined throughout the world, especially in developed
countries.9–11 Yap et al. demonstrated a significant decline in
APSGN in Singaporean children between 1971 and 1985 attrib-
utable to improvement in socio-economic status, the health-
care system and urbanisation.12
There is a wide spectrum of clinical presentations, ranging
from subclinical disease to rapidly progressive glomerulonephri-
tis requiring acute dialysis because of severe biochemical
disturbances.13–16 In a recent retrospective study of our own
experience, the outcome of children with severe APSGN showed
that most recovered in the short to medium term, albeit with
continuing proteinuria.1 Other studies have shown similar
degrees of recovery from severe disease.17,18 APSGN is considered
to be a preventable illness with chronic disease implications.
The New Zealand Paediatric Surveillance Unit (NZPSU) was
established in 1997 to enable paediatricians to study the inci-
dence of rare diseases in New Zealand children. Although
APSGN is not a rare disease, the NZPSU is an excellent vehicle
to study the disease burden, clinical characteristics and labora-
tory features of this illness because of the consistently high
surveillance card return rates observed over the past decade or
more.19 There is limited current data on the epidemiology of
APSGN in New Zealand. The aims of this study were to define
the epidemiological features and clinical characteristics of
APSGN in New Zealand, compare some of the epidemiological
aspects with previous data, identify trends or patterns, and to
guide future prevention strategies.
Materials and Methods
A prospective nationwide study was conducted via the NZPSU
between 1 September 2007 and 31 August 2009. This involved
voluntary reporting by paediatricians of APSGN cases admitted
to hospital aged less than 15 years. The mean response rate of
clinicians replying to the monthly APSGN surveillance card was
95% for 2008 and 93% for 2009 (http://www.otago.ac.nz/
nzpsu).
Following identification of a possible case by the principal
investigator, a questionnaire was sent to the reporting paedia-
trician requesting patient demographics including health district
residence at time of diagnosis and clinical and management
details of the children including patient historical data, clinical
characteristics, laboratory investigations including serum creati-
nine, urea, albumin, streptococcal serology, serum complement
C3, C4 levels, treatment and course of illness with follow-up
care details. The case definition of APSGN used for this study is
given in Table 1.
Also requested was the New Zealand Health Domicile Code
for the patient, which can be matched to New Zealand Census
Area Units. Socio-economic status (SES) was determined using
the census-based New Zealand Deprivation Index of 2006
(NZDep2006). The NZDep2006 scores localities on an ordinal
scale of deciles, where 1 represents areas with highest SES and
10 represents areas with lowest SES, and the average score
nationwide is 5.5.22
Journal of Paediatrics and Child Health 49 (2013) 850–855
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Journal of Paediatrics and Child Health © 2013 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
Post-streptococcal glomerulonehritis
Table 1 Case definition of APSGN2
Haematuria and or heavy proteinuria† associated with recent evidence
of streptococcal infection‡ in absence of clinical or histological
evidence of previous renal disease in the presence of transient C3
hypocomplementaemia (normalising within 8 weeks). Oedema and
or azotemia with or without hypertension§ may be present. For this
study, we included cases where C3 was normal or unknown, where
other diagnostic features were present or the case was biopsy
proven.
Probable cases
For this study we also included cases where the streptococcal titre/s
were normal or unknown, but the patient otherwise had all the
clinical hallmarks of APSGN and evidence of alternate complement
pathway activation indicating reaction to a bacterial antigen. The
absence of a high streptococcal titre could be due to a delay in, or
lack of, testing so we considered those cases ‘probable’.
†A urine protein to creatinine ratio >250 mg/mmol, or 4+ on urine
dipstix. ‡A positive throat culture or skin swab or both for group A
beta-haemolytic streptococcus or a significant elevation in at least one of
the streptococcal titres (ASOT, anti-DNAse B20). §Systolic blood pressure
> 95th percentile for age and sex.21 APSGN, acute post-streptococcal
glomerulonephritis; ASOT, antistreptolysin O titre.
Seasons were three monthly, with summer defined as
January–March to enable direct comparison with the Meekin
and Martins dataset.4 Ethnicity was self-defined at hospital
admission and as a population denominator. Age-, ethnicity-
and geographic-matched population statistics are based upon
the ‘estimated resident population’ 2006 with prioritised eth-
nicity (http://www.stats.govt.nz – Keming Wang, pers. comm.,
2009). A 2% increase was applied to these data to align them
to 2007–2009 estimates. In 2006, the total population of New
Zealand was just over 4 million, with children aged <15 years
comprising 21%, divided into ethnic groups of European/other
(58%), Maori (24%), Pacific (9%) and Asian (8%). Auckland
is the largest urban area in New Zealand with a population of
1.4 million serviced by three of the 20 District Health Boards
(DHBs) nationwide. DHBs are organisations responsible for
ensuring the provision of health and disability services to
populations within a defined geographical area. The three
Auckland DHBs service similarly sized populations, broadly
geographically defined as North/West Auckland (‘Waitemata’),
Central Auckland (‘Auckland’) and South Auckland (‘Counties
Manukau’). The South Auckland region is characterised by a
higher proportion of Maori and Pacific peoples (33%) and
lower SES (average NZDep2006 score = 6.2).
Data were analysed using StatsDirect V2.7.8 (StatsDirect Ltd,
Cheshire, UK). Incidence and incidence rate confidence inter-
vals were based on the Poisson distribution. Incidence compari-
sons were undertaken by c2 test. Comparisons of categorical
clinical or demographic parameters were undertaken by c2
test. Time to APSGN was compared using the t-test/analysis of
variance. Creatinine levels were compared using the non-
parametric Mann–Whitney test. The nominal level of signifi-
cance P < 0.05 was used for all tests.
Ethical approval was obtained from the Multi Region Ethics
Committee of the Ministry of Health, New Zealand.
851
Post-streptococcal glomerulonehritis
Haematuria
Streptococcal titre: high normal
Serum low normal unknown low
Complement C3: n = 123 n = 12 n=3 n = 37
Definite Cases Probable Cases
Fig. 1 Classification of 176 APSGN cases in New Zealand children.
Results
From a total 188 notifications, 12 were excluded as either dupli-
cates or not fitting the case definition (and considered unlikely
to have APSGN). Of the remaining 176 cases, 138 were consid-
ered definite and 38 probable as per the case definitions (Fig. 1).
There was no difference between the definite and probable cases
(comparing, age, frequency with gross haematuria, ethnicity,
time to APSGN, initial or peak plasma, time to peak plasma
creatinine, C3 complement levels, frequency or severity of
hypertension, oedema, oliguria and duration of hospitalisation.
Data not shown), so they were combined for analysis.
Case distribution and incidence
Sixty-five percent of APSGN cases were male (Table 2), and age
range was 1.4–14.7 years (mean 7.6 years, standard deviation
3.3 years). The annual incidence for the age groups 0–4, 5–9 and
10–14 was 7.0, 15.1 and 7.1 per 100 000, respectively. Maori
and Pacific children account for the majority of cases, 39% and
44%, respectively. Of those identified as Pacific, 58% were
Samoan, 19% were Tongan, 13% were Cook Island and 9%
other Pacific. Incidence by ethnicity was highest in Pacific (45.5
per 100 000) and Maori (15.7 per 100 000) (Table 2). Incidence
rate ratios were: Maori versus European/other = 6.2 (95% con-
fidence interval (CI) = 3.9–10.0, P < 0.0001); Pacific versus
European/other = 17.8 (95% CI = 11.4–28.7, P < 0.0001). Simi-
larly to Meekin and Martin,4 APSGN occurred most frequently
in autumn, with a seasonal rate of 3.4 per 100 000 (95% CI
2.6–4.4), followed by summer 2.6 (95% CI 1.9–3.4), winter 2.4
(95% CI 1.8–3.3) and spring 1.3 (95% CI 0.8–1.9). One
hundred ten cases were reported from the three Auckland met-
ropolitan regions, with the highest incidence in the South Auck-
land region (Table 2). The ethnic-specific incidences for the
Auckland metropolitan region for Maori and Pacific children
(29.5 and 55.5 per 100 000, respectively) were higher than
those reported for 1994–1998 and represent no improvement
for Pacific children since 1988, although the incidence in Maori
remains lower than 1988 (Fig. 2). Patient Domicile codes, which
were only fully reported for cases in the Auckland region (63%
of all cases), showed the incidence was highest in children of
lowest SES (highest deprivation scale) (Table 1). Of all patients
where SES was known (n = 140), 67% were in the lowest SES
quintile, and of those patients outside Auckland, 53% were in
the lowest SES quintile, suggesting the correlation with depri-
vation applies nationally. Clinical observations by the authors
852
Journal of Paediatrics and Child Health © 2013 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
W Wong et al.
over 30 years support this association, and it mimics the occur-
rence of acute rheumatic fever nationally.
unknown Clinical features
low Gross haematuria, hypertension, oedema and oliguria were the
n=1 most common signs and symptoms (Table 3).
Ten of 176 (6%) had pulmonary symptoms of fluid overload
with eight patients showing overt congestive cardiac failure.
All 10 children had acute severe hypertension (blood pressure
(BP) 143/100–180/127). There was no significant relationship
between the presence of cardiac failure and the severity of
hypoalbuminaemia, proteinuria or degree of impairment of
renal function. Hypertension occurred more frequently in
Maori children than other ethnic groups (85% vs. 62%, P =
0.002), but the severity of hypertension was not significantly
different. There was no effect of age or time to presentation on
the severity or frequency of hypertension. There was a trend for
severe hypertension (BP 136/97–200/130) to be accompanied
with acute encephalopathic symptoms such as headaches, con-
fusion and seizures.
There was no significant difference in the mean time to
APSGN in patients who had pharyngeal infections compared
with those with skin sepsis (P = 0.06) and ethnicity did not
influence time to APSGN (P = 0.11). The proportion of Euro-
pean and Maori children with a history of sore throat or skin
sepsis was similar; however, in Pacific children, sore throats
occurred 1.7 times as frequently as skin sepsis (P = 0.01).
There were no significant differences in the maximum serum
creatinine between Maori and Pacific and non-Maori children
either at presentation or during the course of the illness. The
severity of renal dysfunction was not related to geographical
location of the patient. Nine children (5%) had renal biopsies
for the following indications: acute severe glomerulonephritis
(n = 4), recurrent haematuria (n = 3), persistent proteinuria (n
= 1) and persistent hypertension (n = 1). In the four patients
biopsied for acute severe nephritis, all showed diffuse prolifera-
tive glomerulonephritis with 10–40% cellular crescents.
Patients were admitted to hospital for monitoring and treatment
for a median of 4 days (95% CI 4–5). Treatment of hypertension
and/or oedema was recorded in 71 patients of whom 68 (96%)
were given frusemide, including 48 patients (68%) also treated
with a calcium channel blocking medication. Three children
required temporary dialysis for anuric renal failure ranging from
4 to 11 days.
Discussion
This prospective, hospitalised, population-based study describes
the disease burden of APSGN over a 2-year period in New
Zealand children, where the disease is a significant cause of
acute presentation to hospital. Sixty-seven percent of cases in
this study were from the lowest socio-economic quintile.
Clear ethnic disparities exist, with Pacific children signifi-
cantly over-represented with an annual incidence of 45.5 per
10 000. The incidence in Pacific children in the Auckland region
is higher than nationally and is essentially unchanged from
1988.2,8 Pacific children are most likely over-represented due
to multiple factors including higher rates of socio-economic
Journal of Paediatrics and Child Health 49 (2013) 850–855
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W Wong et al. Post-streptococcal glomerulonehritis

Table 2 Cases and incidence of APSGN in New Zealand children (0–14 years), September 2007–August 2009

Category Cases (2 years) Population denominator Incidence per 100 000 children 95% CI P
(1000s) (per year)

Total 176 906 9.7 8.3–11.3

Gender
M 114 464 12.3 10.1–14.8 0.0004
F 62 442 7.0 5.4–9.0 Ref.
Ethnicity
Asian 3 73 2.1 0.4–6.0 0.99
European/other 27 529 2.6 1.7–3.7 Ref.
Maori 69 220 15.7 12.2–19.9 <0.0001
Pacific 77 85 45.5 35.9–56.8 <0.0001
Region
Auckland 110 308 17.9 14.7–21.5 <0.0001
Rest of NZ 66 598 5.5 4.3–7.0 Ref.
Auckland Region
North/West 13 110 5.9 3.2–10.1 0.007
Central 24 81 14.9 9.6–22.2 Ref.
South 73 118 31.0 24.3–39.0 0.001
Auckland Region Deprivation Scale
1–2 1 66 0.8 0.0–4.2 <0.0001
3–4 3 51 2.9 0.6–8.6 <0.0001
5–6 11 52 10.6 5.3–18.9 <0.0001
7–8 17 53 16.0 9.3–25.7 <0.0001
9–10 78 86 45.3 35.8–56.6 Ref.

APSGN, acute post-streptococcal glomerulonephritis; CI, confidence interval.

Fig. 2 APSGN in Auckland children (0–14 years) ethnic incidence. ,
Pacific; , Maori; , NZ Euro; , Total. *Lennon et al.2 †Bhatia et al.8
‡Current study.
deprivation, crowded housing increasing transmission of infec-
tion and poor access and utilisation of health services.23 Chil-
dren of Maori descent showed a significant reduction in
admission numbers in Auckland between 1988 and the mid-
1990s; however, rates in Auckland have risen again, and nation-
ally the rate in Maori is six times higher than European/other
children. Although children of European/other ethnicity have
the lowest rates of APSGN in New Zealand, these remain almost
10-fold higher than other developed countries where the inci-
dence has been calculated at 0.3 per 100 000 childhood years.5,24
Other potentially avoidable infectious diseases such as cellulitis,
rheumatic fever and respiratory illness are also more frequent
among Maori and Pacific Island children. This is due to multiple
factors but includes poverty, poor education, crowded housing
and access to health care.25,26 By age, incidence of infection is
highest in the 5–9 year age group (P < 0.0001).
The spectrum of clinical signs, symptoms and complications
associated with APSGN is well described in many large studies of
children.1–5,27–29 Whereas most of those studies have been single
centres based on referrals to tertiary paediatric facilities and
therefore more likely to be skewed to more severe presenta-
tions, a strength of the present study is it was a countrywide
population-based study of consecutive children with APSGN
referred to secondary and tertiary health-care facilities. The
scope of this study informs local paediatricians and parents of
children affected with the condition of the frequency and sever-
ity of some of the complications of APSGN that they are likely
to encounter. For example, severe acute renal failure is very
uncommon; however, more than 60% of the study group had
significantly elevated serum creatinine values at presentation.
These children require careful monitoring to ensure that their
renal function normalise after the acute phase of the illness.
Occasionally, children with APSGN present with undifferenti-
ated and rapidly progressive severe acute renal failure where a
renal biopsy is needed to exclude other causes of this syndrome,
which may have more specific treatments. In this present study,
only four patients needed urgent renal biopsies, and none were

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Journal of Paediatrics and Child Health © 2013 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
Post-streptococcal glomerulonehritis W Wong et al.

serum complement levels. Delays in the diagnosis of APSGN

Table 3 Clinical and laboratory features of children with APSGN have been reported by other authors.9
(n = 176) in New Zealand, September 2007–August 2009 There are limitations to this study, common to observational
Clinical feature n (%) studies. The large number of different clinical observers may
introduce inconsistencies in clinical observations. Although the
Gross haematuria 153 (87) presence of clinical signs such as gross haematuria, hypertension
Microscopic haematuria only 23 (13) and congestive heart failure are less open to differing interpreta-
Hypertension 126 (72) tions, other clinical signs and symptoms like oliguria or oedema
Oedema 109 (62)
are more subjective. There was a lack of complete follow-up
Oliguria 86/167 (51)
clinical and laboratory data on some patients that may indicate
1–2 days 56 (65)
that some of them may not have APSGN but possibly a chronic
3–4 days 18 (21)
glomerulonephritis. Many of the children diagnosed with
>5 days 12 (14)
APSGN were discharged to primary or secondary health-care
Anuria 3 (2)
Encephalopathy (seizures incl.) 16 (9)
providers for follow-up but failed to attend. The estimates of
Dyspnoea 12 (7) prevalence are likely to be an underestimate as children with
Congestive heart failure 8 (5) milder disease, such as those with microscopic haematuria only,
Laboratory feature may escape attention by care givers or health workers.
Streptococcus pyogenes from pharynx 24/75 (32) Our results have implications for the prevention and manage-
S. pyogenes from skin 8/20 (40) ment of APSGN in New Zealand. The continuing high rates
Elevated ASOT/AntiDNase B 138/175 (79) demonstrate that sequelae of group A streptococcal disease con-
Low C3 complement 161/173 (93) tinues to present a large disease burden to New Zealand chil-
Mean time to APSGN in pharyngeal infections† 9.1 days dren, in particular the 33% who are of Pacific and Maori descent
Mean time to APSGN with skin infection 10.9 days and those in low socio-economically areas. A primary preven-
Heavy proteinuria (U/Pc > 250/4+ dipstix) 58/133 (44) tion programme improving access to health care in those high-
Nephrotic syndrome 4/58 (7) risk populations may provide a feasible and efficient means to
Serum creatinine ⱖ2 standard deviations 120 (68) approaching these health inequities. Aggressive treatment of
>250 mmol/L 6 (3) sore throats and impetigo in these populations is warranted.
Targeted interventions like these have the potential to reduce
†Mean time to APSGN was derived from the time of onset of infection
rates of acute rheumatic fever in New Zealand.23,30
(skin or pharyngeal) to onset of acute glomerulonephritis (usually gross
The prevalence of long-term complications of APSGN in this
haematuria or oedema). APSGN, acute post-streptococcal glomerulone-
cohort is unknown. Those with persistent proteinuria have been
phritis; ASOT, antistreptolysin O titre; CI, confidence interval.
shown to be at increased risk of chronic kidney disease.31
Hoy and White recently provided information on extended
follow-up of a cohort of Aboriginal adults who had APSGN as
found to have severe crescentic glomerulonephritis. This con- children and found higher levels of albuminuria and frequency
firms the findings of a recent retrospective study, the rarity of of chronic renal insufficiency compared with controls.32 They
rapidly progressive or crescentic glomerulonephritis due to concluded that APSGN contributes to the very serious burden of
APSGN.1 chronic kidney disease in that community. We are currently
There have been few population-based national studies of setting up a long-term follow-up study to evaluate this issue in
APSGN in the past 20 years. A recent study from French Poly- a cohort of children diagnosed to have APSGN more than 10
nesia27 showed cardiac failure as a presentation occurred in 14% years ago. This may assist us in developing more evidence-based
of their study group but only 5% in our cohort. Overall severe guidelines on long-term surveillance and may demonstrate that
presentations (cardiac failure, severe hypertension and with or APSGN has long-term kidney health implications in susceptible
without encephalopathy) occurred in 22% of their group, populations.
which may be related to late presentation in their group.27
Eighty percent of the patients in our study were managed in
secondary care hospitals around the country, therefore present- Acknowledgement
ing a representative picture of hospitalised APSGN in New The authors gratefully thank the paediatricians who contributed
Zealand. With the development of group A streptococcal vac- data of patients from around New Zealand.
cines, the present study provides an important estimate of the
associated disease burden and its sequelae.
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