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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 Childrens Hospital, 2School of Population Health, University of Auckland, 3Department of Paediatrics, Kidz First
Hospital Middlemore and 4Childrens Research Unit, Starship Childrens Health, Auckland, New Zealand

Aim: A nationwide 24-month study was conducted (20072009), via the New Zealand Paediatric Surveillance Unit to dene 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 fullling a case denition of denite (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 identied (denite: n = 138, probable: n = 38) with 63% residing in the Auckland metropolitan region.
Sixty-seven percent were in the most deprived quintile. Annual incidence (014 years) was 9.7/100 000 (Pacic 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-specic incidence was highest in age 59
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 signicant disease burden of hospitalised APSGN with socio-economically deprived; Pacic and
Maori children are being over-represented. Signicant 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 preventable 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 (514
years), ethnicity (Pacic 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.15 The disease is preceded by group A
Correspondence: Dr William Wong, Department of Paediatric Nephrology,
Starship Childrens Hospital, Private Bag 92024, Auckland, New Zealand.
Fax: +64 9307 8928; email: wwong@adhb.govt.nz
Conicts of interest: None declared.
Accepted for publication 15 April 2013.

850

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 19941998,8 143 cases
were identified in two childrens 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.911 Yap et al. demonstrated a significant decline in
APSGN in Singaporean children between 1971 and 1985 attributable to improvement in socio-economic status, the healthcare system and urbanisation.12
There is a wide spectrum of clinical presentations, ranging
from subclinical disease to rapidly progressive glomerulonephritis requiring acute dialysis because of severe biochemical
disturbances.1316 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 incidence 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 laboratory 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 paediatrician 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 creatinine, 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

Post-streptococcal glomerulonehritis

Table 1

Case denition 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 signicant 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

JanuaryMarch to enable direct comparison with the Meekin
and Martins dataset.4 Ethnicity was self-defined at hospital
admission and as a population denominator. Age-, ethnicityand geographic-matched population statistics are based upon
the estimated resident population 2006 with prioritised ethnicity (http://www.stats.govt.nz Keming Wang, pers. comm.,
2009). A 2% increase was applied to these data to align them
to 20072009 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 intervals were based on the Poisson distribution. Incidence comparisons 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 nonparametric MannWhitney test. The nominal level of significance 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.

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851

Post-streptococcal glomerulonehritis

W Wong et al.

over 30 years support this association, and it mimics the occurrence of acute rheumatic fever nationally.

Haematuria

Streptococcal titre:
Serum
Complement C3:

high
low
n = 123

normal
n = 12

unknown
n=3

Definite Cases

Fig. 1

normal

unknown

low
n = 37

low
n=1

Probable Cases

Classication of 176 APSGN cases in New Zealand children.

Results
From a total 188 notifications, 12 were excluded as either duplicates or not fitting the case definition (and considered unlikely
to have APSGN). Of the remaining 176 cases, 138 were considered 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 1.414.7 years (mean 7.6 years, standard deviation
3.3 years). The annual incidence for the age groups 04, 59 and
1014 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% confidence interval (CI) = 3.910.0, P < 0.0001); Pacific versus
European/other = 17.8 (95% CI = 11.428.7, P < 0.0001). Similarly to Meekin and Martin,4 APSGN occurred most frequently
in autumn, with a seasonal rate of 3.4 per 100 000 (95% CI
2.64.4), followed by summer 2.6 (95% CI 1.93.4), winter 2.4
(95% CI 1.83.3) and spring 1.3 (95% CI 0.81.9). One
hundred ten cases were reported from the three Auckland metropolitan regions, with the highest incidence in the South Auckland 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 19941998 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 deprivation applies nationally. Clinical observations by the authors
852

Clinical features
Gross haematuria, hypertension, oedema and oliguria were the
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) 143/100180/127). 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 136/97200/130) to be accompanied
with acute encephalopathic symptoms such as headaches, confusion 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 European 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 proliferative glomerulonephritis with 1040% cellular crescents.
Patients were admitted to hospital for monitoring and treatment
for a median of 4 days (95% CI 45). 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 significantly 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

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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.

Table 2

Post-streptococcal glomerulonehritis

Cases and incidence of APSGN in New Zealand children (014 years), September 2007August 2009

Category

Cases (2 years)

Population denominator
(1000s)

Incidence per 100 000 children

(per year)

95% CI

Total
Gender
M
F
Ethnicity
Asian
European/other
Maori
Pacic
Region
Auckland
Rest of NZ
Auckland Region
North/West
Central
South
Auckland Region Deprivation Scale
12
34
56
78
910

176

906

9.7

8.311.3

114
62

464
442

12.3
7.0

10.114.8
5.49.0

0.0004
Ref.

3
27
69
77

73
529
220
85

2.1
2.6
15.7
45.5

0.46.0
1.73.7
12.219.9
35.956.8

0.99
Ref.
<0.0001
<0.0001

110
66

308
598

17.9
5.5

14.721.5
4.37.0

<0.0001
Ref.

13
24
73

110
81
118

5.9
14.9
31.0

3.210.1
9.622.2
24.339.0

0.007
Ref.
0.001

1
3
11
17
78

66
51
52
53
86

0.8
2.9
10.6
16.0
45.3

0.04.2
0.68.6
5.318.9
9.325.7
35.856.6

<0.0001
<0.0001
<0.0001
<0.0001
Ref.

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

Fig. 2 APSGN in Auckland children (014 years) ethnic incidence. ,

Pacic; , Maori; , NZ Euro; , Total. *Lennon et al.2 Bhatia et al.8
Current study.

deprivation, crowded housing increasing transmission of infection and poor access and utilisation of health services.23 Children of Maori descent showed a significant reduction in
admission numbers in Auckland between 1988 and the mid1990s; however, rates in Auckland have risen again, and nationally 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 59 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.15,2729 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 presentations, 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 severity 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 undifferentiated 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)

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Table 3 Clinical and laboratory features of children with APSGN

(n = 176) in New Zealand, September 2007August 2009
Clinical feature

n (%)

Gross haematuria
Microscopic haematuria only
Hypertension
Oedema
Oliguria
12 days
34 days
>5 days
Anuria
Encephalopathy (seizures incl.)
Dyspnoea
Congestive heart failure
Laboratory feature
Streptococcus pyogenes from pharynx
S. pyogenes from skin
Elevated ASOT/AntiDNase B
Low C3 complement
Mean time to APSGN in pharyngeal infections
Mean time to APSGN with skin infection
Heavy proteinuria (U/Pc > 250/4+ dipstix)
Nephrotic syndrome
Serum creatinine 2 standard deviations
>250 mmol/L

153 (87)
23 (13)
126 (72)
109 (62)
86/167 (51)
56 (65)
18 (21)
12 (14)
3 (2)
16 (9)
12 (7)
8 (5)
24/75 (32)
8/20 (40)
138/175 (79)
161/173 (93)
9.1 days
10.9 days
58/133 (44)
4/58 (7)
120 (68)
6 (3)

Mean time to APSGN was derived from the time of onset of infection
(skin or pharyngeal) to onset of acute glomerulonephritis (usually gross
haematuria or oedema). APSGN, acute post-streptococcal glomerulonephritis; ASOT, antistreptolysin O titre; CI, condence interval.

found to have severe crescentic glomerulonephritis. This confirms the findings of a recent retrospective study, the rarity of
rapidly progressive or crescentic glomerulonephritis due to
APSGN.1
There have been few population-based national studies of
APSGN in the past 20 years. A recent study from French Polynesia27 showed cardiac failure as a presentation occurred in 14%
of their study group but only 5% in our cohort. Overall severe
presentations (cardiac failure, severe hypertension and with or
without encephalopathy) occurred in 22% of their group,
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 presenting a representative picture of hospitalised APSGN in New
Zealand. With the development of group A streptococcal vaccines, the present study provides an important estimate of the
associated disease burden and its sequelae.
Severe hypertension was also closely associated with abnormal neurological symptoms in a small group of patients who
presented with a generalised seizure as the first manifestations
of APSGN. In a child presenting with a first generalised seizure
and examination shows severe hypertension, a urinalysis for
blood and protein should be obtained at the bedside as this will
quickly establish the diagnosis of acute glomerulonephritis,
which can be later confirmed with streptococcal serology and
854

serum complement levels. Delays in the diagnosis of APSGN

have been reported by other authors.9
There are limitations to this study, common to observational
studies. The large number of different clinical observers may
introduce inconsistencies in clinical observations. Although the
presence of clinical signs such as gross haematuria, hypertension
and congestive heart failure are less open to differing interpretations, other clinical signs and symptoms like oliguria or oedema
are more subjective. There was a lack of complete follow-up
clinical and laboratory data on some patients that may indicate
that some of them may not have APSGN but possibly a chronic
glomerulonephritis. Many of the children diagnosed with
APSGN were discharged to primary or secondary health-care
providers for follow-up but failed to attend. The estimates of
prevalence are likely to be an underestimate as children with
milder disease, such as those with microscopic haematuria only,
may escape attention by care givers or health workers.
Our results have implications for the prevention and management of APSGN in New Zealand. The continuing high rates
demonstrate that sequelae of group A streptococcal disease continues to present a large disease burden to New Zealand children, in particular the 33% who are of Pacific and Maori descent
and those in low socio-economically areas. A primary prevention programme improving access to health care in those highrisk populations may provide a feasible and efficient means to
approaching these health inequities. Aggressive treatment of
sore throats and impetigo in these populations is warranted.
Targeted interventions like these have the potential to reduce
rates of acute rheumatic fever in New Zealand.23,30
The prevalence of long-term complications of APSGN in this
cohort is unknown. Those with persistent proteinuria have been
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
children and found higher levels of albuminuria and frequency
of chronic renal insufficiency compared with controls.32 They
concluded that APSGN contributes to the very serious burden of
chronic kidney disease in that community. We are currently
setting up a long-term follow-up study to evaluate this issue in
a cohort of children diagnosed to have APSGN more than 10
years ago. This may assist us in developing more evidence-based
guidelines on long-term surveillance and may demonstrate that
APSGN has long-term kidney health implications in susceptible
populations.

Acknowledgement
The authors gratefully thank the paediatricians who contributed
data of patients from around New Zealand.

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Journal of Paediatrics and Child Health 49 (2013) 850855

2013 The Authors
Journal of Paediatrics and Child Health 2013 Paediatrics and Child Health Division (Royal Australasian College of Physicians)

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