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2007 vol. 31 no. 2 AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH 177© 2007 The Authors. Journal Compilation © 2007 Public Health Association of Australia
Quantifying the excess risk for proteinuria, hypertension
and diabetes in Australian Aborigines: comparison of
profiles in three remote communities in the Northern
Territory with those in the AusDiab study
Wendy E. Hoy, Srinivas Kondalsamy-Chennakesavan, Zhiqiang Wang
Centre for Chronic Disease, Discipline of Medicine, University of Queensland
Esther Briganti Department of Medicine, University of Melbourne, Victoria
Jonathan Shaw International Diabetes Institute, Victoria
Kevan Polkinghorne Monash Medical Centre, Victoria
Steven ChadbanRoyal Prince Alfred Hospital and University of Sydney, New South Wales
The AusDiab Study Group
Abstract
Objective: To estimate the magnitude
of excess risk for proteinuria, high blood
pressure and diabetes in Australian
Aboriginal adults in three remote
communities by comparing them with
nationwide Australian data.
Methods: Adult volunteers from three
remote communities in the Northern
Territory were screened for proteinuria,
high blood pressure, and diabetes between
2000 and mid 2003. Rates for people age
25 to 74 years were compared with those
from the AusDiab study conducted in 1999
and 2000.
Results: Compared with AusDiab, rates
of these conditions were elevated in all
Aboriginal communities, but differed
among them. With adjustment for age and
sex, rates of proteinuria were elevated 2.5-
to 5.3-fold, rates of high blood pressure
were elevated 3.1- to 8.1-fold and rates
of diabetes were elevated 5.4- to 10-fold
(p<0.001 for all). The risk of having any
condition ranged from 3.0- to 8.7-fold and
the risk of having two or more conditions
ranged from 5.8- to 14.2-fold.
Discussion: The data are compatible
with the excess morbidity and mortality
from cardiovascular disease, diabetes and
renal disease in these Aboriginal groups.
They reflect the multitude of risk factors
operating in these environments. They
dictate urgent and systematic intervention
to modify outcomes of established disease
and to prevent their development. However,
the resources required for effective
secondary intervention will differ among
communities according to the disease
burden.
Key words: Australian Aborigine,
proteinuria, hypertension, diabetes,
prevalence, health surveys.
(Aust N Z J Public Health. 2007; 31:177-83)
doi:10.1111/j.1753-6405.2007.00038.x
Non-communicable chronic diseases
(NCDs) represent one of the major
health issues of the 21st century.
Increasing rates of hypertension, type 2
diabetes and chronic kidney disease are
especially prominent in developing countries
and in minority populations undergoing
rapid epidemiologic and lifestyle transition.1
Australian Aborigines are experiencing
an accelerated and often brutal transition
and many are now living in deprived and
marginalised circumstances with poor access
to health services. Prior to the 1980s, almost
no NCDs were recognised, but they are now
rife, with average rates of cardiovascular
death more than three times those of non-
Aboriginal Australians, diabetes deaths
Correspondence to: Professor Wendy Hoy, Clinical Sciences Building, Royal Brisbane Hospital, Herston, Queensland 4029. Fax: (07) 4436 4812; e-mail: [email protected]
Submitted: October 2006 Revision requested: January 2007 Accepted: February 2007
increased eight-fold and renal failure about
10-fold.2,3 Rates are much higher in some
remote areas.4,5
Awareness and management of this
problem have improved in the past 10-
15 years. Screening programs have been
conducted in several regions.6-16 Systematic
management of affected people produces
good results. McDermott et al. showed
that structured diabetes care reduces
hospitalisations,17 and we showed that
systematic treatment for hypertension and
renal disease produces marked reductions in
non-renal and renal deaths,18 with dramatic
cost-savings in dialysis avoided. We also
showed that benefits are quickly lost when
treatment falters.19 Guidelines for chronic
Article Indigenous Health
178 AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH 2007 vol. 31 no. 2© 2007 The Authors. Journal Compilation © 2007 Public Health Association of Australia
disease management have been incorporated into standard care
plans for Aboriginal adults in some regions.20 However, serious
deficiencies persist. The structures for Aboriginal primary health
care, in which chronic disease programs should be nested, are a
chaotic, inscrutable and ever-changing mix. They are inadequately
resourced, have a serious staffing shortage, and average per capita
spending is estimated at less than one-tenth of that for non-
Aboriginal Australians.21 In addition, there is a tacit assumption of
a uniform disease burden across Aboriginal Australia, suggesting
that one resourcing formula will suit all circumstances.
In this paper we describe the rates of proteinuria, high blood
pressure and diabetes in adults in three remote Aboriginal
communities in one region of Australia, and compare them with a
nationally representative survey of participants from the Australian
Diabetes, Obesity and Lifestyle Study (AusDiab). Our objective is
to define the magnitude of the problem, the degree of homogeneity
or variation, to speculate on causes and associations, and make the
case for systematic, needs-based health services planning.
MethodsThe Aboriginal study communities (named 1 through to 3), were
all situated in the Top End of the Northern Territory, Australia (see
Figure 1). They all represent aggregations of people from several
tribal groups in those regions. These communities have adult (25+
year) Aboriginal populations ranging from 135 to 512.22
Volunteers were tested in the context of programs to improve
the awareness and management of chronic diseases, conducted
between 2000 and 2003. Testing was generally done by Aboriginal
Health Workers who had been trained by nurse co-ordinators.
Results were recorded in hard copy and also entered in an
electronic database. Testing included a brief history, medication
review, anthropomorphic measurements, blood pressure, urine
dipstick for protein and assessment of the presence of diabetes.
The health profiles have been previously described.9,10,23
The AusDiab study was based on a stratified cluster sample of
Figure 1: Study communities in the ‘Top End’ of the Northern Territory, Australia.
11,247 consenting adults aged 25 and above who participated in
a nationwide survey in Australia conducted between 1999 and
2000.24 Only 1% of the study participants in AusDiab were of
Aboriginal or Torres Strait Islander origin.
Data on people age 25 to <75 years of age were used to
compare the Aboriginal and AusDiab findings. This lower limit
was set by the lower age limit in the AusDiab study, and the
upper limit was defined by the paucity of older people in the
Aboriginal group (among screened Aboriginal people age 25+
years, only 2.5% were aged 75+ years, compared with 7.2% for
the AusDiab group). Proteinuria was defined as protein •1+ (30
mg/dl) by urine dipstick. High blood pressure was defined at two
levels: as a blood pressure •140/90 mmHg and as an inclusive
definition of BP•140/90 and/or antihypertensive treatment for a
past diagnosis of hypertension. Diabetes was defined by history,
existing prescription of hypoglycaemic medication and/or by blood
glucose measurement on testing. Aboriginal people not already
known to be diabetic were screened by a fasting or random blood
glucose measurement; those with values of •7.0 mmol/l or •11.1
mmol/l respectively were deemed diabetic. These were confirmed
by repeat screening. AusDiab participants not already known to
be diabetic were screened with an oral glucose tolerance test
and deemed diabetic if the fasting value was •7.0 mmol/l or the
two-hour level •11.1 mmol/l. The prevalence of each of these
conditions was calculated. The prevalences of people with at
least one condition and with more than one condition were also
defined. Unadjusted proportions of people with these conditions
were compared, and the odds ratios (95% confidence intervals)
of the Aboriginal groups relative to the AusDiab population were
estimated using logistic regression, adjusted for age and sex.
Statistical analyses were performed using Stata, version 9.1.25 The Aboriginal data used for analyses in this report were
collected in projects approved by the ethics committees of the
Menzies School of Health Research, the Royal Darwin Hospital,
and the University of Queensland. Comparison with AusDiab data
was approved by the individual communities and by the ethics
committee of the University of Queensland, and publication of
the findings was approved by the individual communities. The
AusDiab study was approved by the ethics committee of the
International Diabetes Institute, and all participants gave written,
informed consent.
ResultsData were compared on 10,434 people in the AusDiab study and
814 Aboriginal people in the specified age range. The Aboriginal
participants represented approximately 71%, •100% and 64% of
the age-eligible populations in communities 1, 2 and 3 respectively.
(Participation in community 2 was greater than the Census
population of age-eligible adults.) Females constituted 55.1% of
the AusDiab group and 53.4% of the Aboriginal group (p=0.36).
Table 1 shows that the mean age of the Aboriginal participants
in each community was younger than the AusDiab population,
which was due to higher proportions of Aboriginal people in
Hoy et al. Article
2007 vol. 31 no. 2 AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH 179© 2007 The Authors. Journal Compilation © 2007 Public Health Association of Australia
the younger age group and lower proportions in the higher age
groups. However, age was well matched within each age stratum
(for age groups 25-<35, 35-<45, 45-<55 and 55-<75 respectively,
AusDiab ages (means) were 29.9, 39.8, 49.5 and 63.6 years, and
for Aboriginal were 29.7, 39.8, 49.0 and 63.0 years). Table 1 also
shows a marked gradation of body mass index (BMI) figures
among the Aboriginal communities, with only those in Community
3 exceeding those of AusDiab.
Figure 2A shows the aggregate unadjusted rates of proteinuria,
high blood pressure and diabetes. They were excessive in all the
Aboriginal communities relative to AusDiab, but differed among
them. The prevalence of proteinuria varied from 15% to 28%,
of high blood pressure from 34% to 54%, and of diabetes from
17% to 30%. With adjustment for age and sex, as shown in Figure
2B, these corresponded to odds ratios for proteinuria ranging
from 2.5 to 5.3, for high blood pressure from 3.1 to 8.1, and for
diabetes from 5.4 to 10.0. For all conditions the heterogeneity
among Aboriginal communities was significant, with p<0.0001.
As shown in Table 2, the proportions of Aboriginal people with
elevated blood pressure at examination, while still higher than the
AusDiab population, were relatively less elevated than the rates
of hypertension by the expanded definition, probably reflecting
some success in policies to control blood pressure in recent years
in the Aboriginal environments.
Figure 3A shows that between 43% and 68% of people in the
Table 1: Demographics of participants in this study.
Communities n Females % Age in years, mean (SD) BMI, kg/m2 mean (SD) Obese by BMI %AusDiab 10,434 55.1 49.4 (12.6) 27.0 (5.0) 22.9
Community 1 331 47.4 40.6 (12.0) 22.1 (4.7) 6.3
Community 2 157 56.7 41.9 (12.0) 25.7 (5.9) 23.4
Community 3 326 58.0 42.7 (13.2) 28.5 (6.2) 38.6
Figure 2A: Prevalences of proteinuria, hypertension and diabetes, by community.
DefinitionsProteinuria: Urine dipstick •1+.Hypertension: BP•140/90 and/or on antihypertensive medication.Diabetes: Fasting plasma glucose •7.0 or random or two-hour plasma glucose •11.1 mmol/or hypoglycaemic medication.
Figure 2B: Odds ratios for proteinuria, hypertension and diabetes relative to AusDiab, by community (adjusted for age and sex).
DefinitionsProteinuria: Urine dipstick •1+.Hypertension: BP •140/90 and or on antihypertensive medication.Diabetes: Fasting plasma glucose •7.0 or random or two-hour plasma glucose •11.1 mmol/or hypoglycaemic medication.
different Aboriginal communities had at least one of the three
conditions, and 17% to 34% had more than one condition. As
shown in Figure 3B, these correspond to odds ratios, adjusted for
age and sex, varying from 3.0 to 8.7 for any condition and from
5.8 to 14.2 for multiple conditions. In both instances, the apparent
heterogeneity among communities was significant (p<0.0001).
Figure 4A shows that the rates of these conditions were strongly
correlated with age in the Aboriginal communities. In the AusDiab
population, high blood pressure and diabetes also correlated
strongly with age, but proteinuria did not. Rates in Aboriginal
people were higher than those in the AusDiab population in every
age group. Figure 4B shows an elevated risk for proteinuria in all
age groups, but the risk accentuation was higher after age 35 years.
The figure shows that the risk accentuation for hypertension was
highest in younger Aboriginal adults. Finally, it shows a 19.5-fold
exacerbation of risk for diabetes among the youngest Aboriginal
adults and although the relative risk fell somewhat with age, it
remained very high throughout life.
Figure 5A shows that the probability of having at least one
condition rose with age in both populations, but was always greater
in the Aboriginal group. By age 35-44 years, 59% of Aboriginal
people had at least one condition and by age 55+ years, 79%
were affected. The probability of having multiple conditions was
strikingly higher at all ages among the Aboriginal people, and
reached 35% by middle age. Figure 5B shows that the adjusted
Indigenous Health Quantifying the excess risk for proteinuria
180 AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH 2007 vol. 31 no. 2© 2007 The Authors. Journal Compilation © 2007 Public Health Association of Australia
Figure 3A: Prevalences of any and of multiple conditions, by community.
Figure 4A: Prevalences of proteinuria, hypertension and diabetes, by age group and Aboriginal status.
DefinitionsProteinuria: Urine dipstick •1+.Hypertension: BP•140/90 and/or on antihypertensive medication.Diabetes: Fasting plasma glucose •7.0 or random or two-hour plasma glucose •11.1 mmol/or hypoglycaemic medication.
Figure 4B: Odds ratios for proteinuria, hypertension and diabetes among Aborigines relative to AusDiab, by age group (adjusted for age and sex).
DefinitionsProteinuria: Urine dipstick •1+.Hypertension: BP•140/90 and/or on antihypertensive medication.Diabetes: Fasting plasma glucose •7.0 or random or two-hour plasma glucose •11.1 mmol/or hypoglycaemic medication.
Figure 5A: Prevalences of any and of multiple conditions by age group and Aboriginal status.
Figure 5B: Odds ratios for any and for multiple conditions relative to AusDiab, by age group (adjusted for age and sex).
Figure 3B: Odds ratios for any and for multiple conditions relative to AusDiab, by community (adjusted for age and sex).
Hoy et al. Article
2007 vol. 31 no. 2 AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH 181© 2007 The Authors. Journal Compilation © 2007 Public Health Association of Australia
risk of having any condition was more than four times that of
AusDiab among the youngest adults, and peaked at 7.1-fold
increase among those age 35-44 years. The adjusted relative risk
for multiple conditions was greatest among the younger adults,
with an 18-fold increase.
DiscussionRates of proteinuria, high blood pressure and diabetes were
excessive in each of these Aboriginal communities relative to those
in the AusDiab study. The accentuations of risk in Community
1, with a 2.5-fold increase in proteinuria, a 3.1-fold increase
in hypertension and a 5.3-fold increase in diabetes, are serious
indeed; the 5.3-fold increase in proteinuria, 8.1-fold increase in
hypertension and a 10-fold increase in diabetes in Community 3
are truly striking. The risk of having any condition was increased
as much as nine-fold and the risk of having multiple conditions
was increased 14-fold and more.
Several factors limit the precision of our findings, although they
could not have caused a major distortion of the true relationships.
The groups were tested by different teams, measurements of blood
pressures might have varied with observers and, while reported
blood pressures were averaged from two or three readings in
AusDiab participants, they represent a single reading in the
Aboriginal people. The dipsticks for measuring proteinuria were
not necessarily the same brand, and urine protein concentration
could have been accentuated by the generally hot ambient
temperature in the Aboriginal settings. The accentuation of risk
for diabetes in Aboriginal people is probably understated, because
a glucose tolerance test was not routinely performed on those
without a known diagnosis of diabetes. Also, glucose screening
might have missed some people with unsuspected IGT/IFG/
diabetes by accepting ‘normal range’ fasting or random glucose
screening. This will result in understatement by estimates of the
risk exacerbation of the Aboriginal group compared with the
AusDiab data. The possible effect of differential participation by
age and gender among the communities is discussed below.
Striking as the risk accentuations are, the figures nonetheless
markedly understate the real burden of these conditions in the
Aboriginal communities. Participants in cross-sectional studies
are, by definition, survivors to that point: in the Aboriginal
context this means they have so far escaped the greatly excessive
risk for premature death carried by proteinuria, hypertension and
diabetes.26,27 According to nationwide estimates, about half the
males and only a marginally lower proportion of females have
already died before the age of 55 years, with the deaths heavily
segregated among those with the morbidities under study. This
must be contributing, at least in part, to the lower risk ratios in
older Aboriginal participants.
The data are compatible with the >20-fold increase in renal
failure and the three- to six-fold increase in premature deaths
in general, and cardiovascular deaths in particular, in these
regions, and with the nine-fold increase in deaths from ischaemic
heart disease and 28-fold increase in diabetes deaths in remote
Aboriginal Australia more generally.3,4,5,32 These are crisis-level
statistics.
It is challenging to consider the mix and balance of risks factors
that allows expression of disease at such levels. It is also important
to consider the implications for health services policy and needs-
based planning.
The very substantial overlap of conditions, described in more
detail elsewhere and demonstrated in the high rates of people
with more than one condition, suggests that they are, in part,
elements of a single vascular/renal/metabolic syndrome.9,10,14,28-30
Such integration suggests a shared base of risk factors. It also
supports integrated rather than disease-specific programs for
surveillance and containment and the need for multiple arms of
management. With almost 60% of Aboriginal people having at
least one morbidity by age 35-44 years, most people will need
medical treatment by middle age and many will need treatment
with multiple drugs. Treatment will need to be sustained for many
years if they are to aspire to a life span that approximates that of
non-Aboriginal Australians.
Some of the factors associated with these morbidities are
being defined.9-16,28,29,32-35 In addition to increasing age, they
include higher levels of body fat, which is particularly flagged
by higher waist measurements. A role for body fat is suggested
here by the fact that the differential rates of morbidities in the
Aboriginal groups follow the same pattern as their weights and
their BMIs.9 Alone, however, they do not account for most of the
excessive rates, for only in Community 3 are the BMIs greater
than in the AusDiab population. We have previously described
the body habitus profiles of these Aboriginal communities.9,10 The
associations of Aboriginal body size measurements with chronic
conditions and their comparisons with the AusDiab population
are subjects of proposed reports (Dr Kondalsamy-Chennakesavan,
University of Queensland). Other demonstrated risk factors
include birthweight (inversely), skin infections, noncutaneous
infections, inflammation, excessive alcohol use (for renal disease
at least), and grand multiparity, while high rates of smoking (up
to 80% in men and up to 50% of women) and psychosocial stress
are also probably instrumental.9-12,14,36-40 All the conditions are
Table 2: Proportion of participants with high blood pressure using two definitions, and odds ratios relative to AusDiab, adjusted for age and sex.
BP•140/90 OR (95% CI) BP•140/90 and/or on medication OR (95% CI)AusDiab 23.0% Referent 29.0% Referent
Community 1 24.6% 2.3 (1.7-3.1) 33.7% 3.1 (2.4-4.1)
Community 2 32.7% 3.6 (2.5-5.2) 47.1% 6.0 (4.2-8.5)
Community 3 35.4% 3.7 (2.8-4.8) 54.4% 8.1 (6.2-10.6)
Indigenous Health Quantifying the excess risk for proteinuria
182 AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH 2007 vol. 31 no. 2© 2007 The Authors. Journal Compilation © 2007 Public Health Association of Australia
probably multi-determinant, with the simultaneous or sequential
operation of more than one risk factor amplifying effects of the
others.11,41 We have already defined this in relationship to renal
disease in an Aboriginal setting,10,33 and an important precedent
exists internationally in the polyfactorial model for ischaemic
heart disease.42 Such models help explain the massively higher
rates of disease in environments with a high density of risk factors.
We have also emphasised that the emergence of this epidemic is
a consequence, in part, of prior health triumphs. The recent vast
reduction in infant mortality since the 1950s, as a result of better
hospital management of sick babies, has allowed cohorts of low
birthweight babies to survive to adult life where, as proposed by
Barker and becoming manifest in the Aboriginal setting, they are
at increased risk for chronic disease.33-35 In addition, reduction in
competing mortality, particularly due to fewer infectious deaths,
has increased adult longevity and thus the opportunity for chronic
disease expression.
The uniformly excessive rates support clinical impressions that
all remote communities are afflicted by this epidemic of chronic
disease. The variation in rates, however, shows that the magnitude
of the situation cannot be generalised at any one particular time.
Plausible reasons for the differences include obvious variations
in body habitus, differences in diet, alcohol use and rates of
smoking, differences in timing of the improved infant survival
phenomenon, in the duration and intensity of lifestyle changes,
in palpably different degrees of disadvantage at this point in
time and, potentially, differences in genetic predisposition. Men
constituted a somewhat larger proportion of the total screened
population in Community 1 than in the other sites (see Table 1),
and they tended to be somewhat younger. These phenomena were
driven by an all-male screening team and a paucity of males aged
45+ years in this community due to premature deaths, in large
part associated with substance abuse and violence. However, the
differences in rates of morbidities by community, and particularly
the lowest rates in Community 1, are very real. They applied for
all the three conditions, except arguably for proteinuria, for any
morbidity and for multiple morbidities in both sexes, and for all
age groups below 55 years, after which small numbers sometimes
became limiting.
The situation constitutes an emergency by any standards.
With the clinical benefits and cost savings of effective treatment
demonstrated, there can be no rational argument against early
screening and intervention programs.18,44-46 There are also
plenty of avenues for primary prevention, targeting exercise,
nutrition, hygiene, smoking and infections, which can be
implemented or strengthened even while working to understand
the pathophysiology more precisely. A problem of equal magnitude
among non-Indigenous Australians, adequately exposed, would
excite a vigorous and systematic response.
The variation in rates by community, however, dictates needs-
based health services planning.9 Primary prevention strategies
might vary little across communities, but the level of resourcing
for programs of screening and treatment will depend on the disease
burden. Disease burden might influence the optimal frequency
of regular testing throughout life, but will certainly influence the
requirements of personnel, reagents, facilities, medicines, tests
and documentation needed for proper treatment and intensified
surveillance of people with morbidities. The capacity for a high
treatment burden to overwhelm poorly resourced chronic disease
intervention programs has already been demonstrated in such
settings.19,23
The governments of the Northern Territory and most other States
have endorsed the need for good chronic disease surveillance and
management, and protocols have been incorporated into standard
care guidelines for Aboriginal people.20 Our observations in these
outreach communities, in an ongoing relationship with the Tiwi
community, and in the radically different environments of two
large and empowered Aboriginal Medical Services in Western
Australia, combined with much anecdotal information more
broadly, indicate that systematic application of these principles is
constrained by limited resources.19,47 Ironically, hospital services
and renal replacement therapy offered to Aboriginal people are of
good quality and essentially uncapped, with the latter now posing
a fiscal crisis for health care budgets.44 The problem requires a
rethinking of Aboriginal health services, adequate resourcing,
strategies to combat the obstacles and hardships associated with
remote locations and placements, and accountability at every
level of the system.
AcknowledgementsWe thank all the remote Aboriginal communities and their
councils who participated in this study, and all the community
liaison people, health workers, nurses and doctors working in
these communities. We also thank the project teams working
with the Menzies School of Health Research in the 1990s,
and more recently with the Chronic Disease Outreach Team,
including Rebecca Davey, Gaye Gokel, Kiernan McKendry,
Suresh Sharma, Joanne Smith and Phillip Hoy. The data on
which the analyses in Aboriginal communities were done were
derived from studies supported by Kidney Health Australia (then
the Australian Kidney Foundation), the Office of Aboriginal and
Torres Strait Islander Health, Rio Tinto, Janssen-Cilag, Helen
Hayes, the Colonial Foundation and the National Health and
Medical Research Council of Australia. The AusDiab study was
supported by the Commonwealth Department of Health and
Aged Care, Abbott Australasia Pty Ltd, Alphapharm Pty Ltd,
Aventis Pharmaceutical, AstraZeneca, Bristol-Myers Squibb
Pharmaceuticals, Eli Lilly (Aust) Pty Ltd, GlaxoSmithKline,
Janssen-Cilag (Aust) Pty Ltd, Merck Lipha s.a., Merck Sharp &
Dohme (Aust), Novartis Pharmaceutical (Aust) Pty Ltd, Novo
Nordisk Pharmaceutical Pty Ltd, Pharmacia and Upjohn Pty Ltd,
Pfizer Pty Ltd, Roche Diagnostics, Sanofi Synthelabo (Aust) Pty
Ltd, Servier Laboratories (Aust) Pty Ltd, BioRad Laboratories
Pty Ltd, HITECH Pathology Pty Ltd, the Australian Kidney
Foundation, Diabetes Australia, Diabetes Australia (Northern
Territory), Queensland Health, South Australian Department of
Human Services, Tasmanian Department of Health and Human
Hoy et al. Article
2007 vol. 31 no. 2 AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH 183© 2007 The Authors. Journal Compilation © 2007 Public Health Association of Australia
Services, Territory Health Services, Victorian Department of
Human Services, and Health Department of Western Australia.
Also, for their invaluable contribution to the set-up and field
activities of AusDiab, we are enormously grateful to A. Allman,
B. Atkins, S. Bennett, S. Colagiuri, M. de Courten, M. Dalton, M.
D’Embden, D. Dunstan, T. Dwyer, D. Jolley, I. Kemp, P. Magnus,
J. Mathews, D. McCarty, A. Meehan, K. O’Dea, P. Phillips, P.
Popplewell, C. Reid, A. Stewart, R. Tapp, H. Taylor, T. Welborn,
F. Wilson and P Zimmet.
References1. Boutayeb A, Boutayeb S. The burden of non communicable diseases
in developing countries. International Journal for Equity in Health. 2005;4(1):2.
2. McDonald SP, Russ GR. Burden of end-stage renal disease among indigenous peoples in Australia and New Zealand. Kidney Int Suppl. 2003(83):S123-7.
3. Australian Bureau of Statistics. The Health and Welfare of Austrtalia’s Aboriginal & Torres Strait Islander Peoples. Canberra (AUST): ABS; 2001. Report No.: 4704.0.
4. Australian Institute of Health and Welfare. Rural, Regional and Remote Health – Mortality Trends 1992–2003. Canberra (AUST): AIHW; 2006. AIHW Catalogue No.: PHE 71.
5. Cass A, Cunningham J, Wang Z, Hoy W. Regional variation in the incidence of end-stage renal disease in Indigenous Australians. Med J Aust. 2001;175(1):24-7.
6. Guest CS, O’Dea K, Hopper JL, Larkins RG. Hyperinsulinaemia and obesity in aborigines of south-eastern Australia, with comparisons from rural and urban Europid populations. Diabetes Res Clin Pract. 1993;20(2):155-64.
7. Guest CS, O’Dea K, Hopper JL, Nankervis AJ, Larkins RG. The prevalence of glucose intolerance in aborigines and Europids of south-eastern Australia. Diabetes Res Clin Pract. 1992;15(3):227-35.
8. Guest CS, Ratnaike S, Larkins RG. Albuminuria in aborigines and Europids of south-eastern Australia. Med J Aust. 1993;159(5):335-8.
9. Hoy WE, Kondalsamy-Chennakesavan S, Scheppingen J, Sharma S, Katz I. A chronic disease outreach program for Aboriginal communities. Kidney Int Suppl. 2005;Sep(98):S76-82.
10. Hoy W, Kondalsamy-Chennakesavan S, Scheppingen J, Sharma S. Kidney and related chronic disease profiles and risk factors in three remote Australian Aboriginal communities. Adv Chronic Kidney Dis. 2005;12(1):64-70.
11. Hoy WE, Mathews JD, McCredie DA, Pugsley DJ, Hayhurst BG, Rees M, et al. The multidimensional nature of renal disease: rates and associations of albuminuria in an Australian Aboriginal community. Kidney Int. 1998;54(4):1296-304.
12. Hoy WE, Norman RJ, Hayhurst BG, Pugsley DJ. A health profile of adults in a Northern Territory aboriginal community, with an emphasis on preventable morbidities. Aust N Z J Public Health. 1997;21(2):121-6.
13. Leonard D, McDermott R, Odea K, Rowley KG, Pensio P, Sambo E, et al. Obesity, diabetes and associated cardiovascular risk factors among Torres Strait Islander people. Aust N Z J Public Health. 2002;26(2):144-9.
14. McDonald SP, Maguire GP, Hoy WE. Renal function and cardiovascular risk markers in a remote Australian Aboriginal community. Nephrol Dial Transplant. 2003;18(8):1555-61.
15. Rowley KG, Iser DM, Best JD, O’Dea K, Leonard D, McDermott R. Albuminuria in Australian Aboriginal people: prevalence and associations with components of the metabolic syndrome. Diabetologia. 2000;43(11):1397-403.
16. Shephard MD, Allen GG, Barratt LJ, Barbara JA, Paizis K, McLeod G, et al. Albuminuria in a remote South Australian Aboriginal community: results of a community-based screening program for renal disease. Rural Remote Health. 2003;3(1):156.
17. McDermott R, Tulip F, Schmidt B, Sinha A. Sustaining better diabetes care in remote indigenous Australian communities. Br Med J. 2003;327(7412):428-30.
18. Hoy WE, Wang Z, Baker PR, Kelly AM. Reduction in natural death and renal failure from a systematic screening and treatment program in an Australian Aboriginal community. Kidney Int Suppl. 2003(83):S66-73.
19. Hoy WE, Kondalsamy-Chennakesavan SN, Nicol JL. Clinical outcomes associated with changes in a chronic disease treatment program in an Australian Aboriginal community. Med J Aust. 2005;183(6):305-9.
20. Weeramanthri T, Hendy S, Connors C, Ashbridge D, Rae C, Dunn M, et al. The Northern Territory preventable chronic disease strategy – promoting an integrated and life course approach to chronic disease in Australia. Aust Health Rev. 2003;26(3):31-42.
21. Deeble J. Expenditures on Aboriginal and Torres Strait Islander Health. Public Report Card. Canberra (AUST): Australian Medical Association; 2003.
22. Australian Bureau of Statistics. Census of Population and Housing. Selected Characteristics by Indigenous Status by Sex. Indigenous Remote Areas, Communities 1-3. Canberra (AUST): ABS; 2001.
23. Katz IJ, Hoy WE, Kondalsamy-Chennakesavan S, Gerntholtz T, Scheppingen J, Sharma S, et al. Chronic kidney disease management – what can we learn from South African and Australian efforts? Blood Purif. 2006;24(1):115-22.
24. Dunstan DW, Zimmet PZ, Welborn TA, Cameron AJ, Shaw J, de Courten M, et al. The Australian Diabetes, Obesity and Lifestyle Study (AusDiab) –methods and response rates. Diabetes Res Clin Pract. 2002;57(2):119-29.
25. STATA: statistical software [computer program]. Version 9.2. College Station (TX): Stata Corporation; 2005.
26. Spencer JL, Silva DT, Snelling P, Hoy WE. An epidemic of renal failure among Australian Aboriginals. Med J Aust. 1998;168(11):537-41.
27. Phillips CB, Patel MS, Weeramanthri TS. High mortality from renal disease and infection in Aboriginal central Australians with diabetes. Aust J Public Health. 1995;19(5):482-6.
28. O’Dea K. Preventable chronic diseases among indigenous Australians: the need for a comprehensive national approach. Heart Lung Circ. 2005;14(3):167-71.
29. McDonald S, Maguire G, Duarte N, Wang XL, Hoy W. C-reactive protein, cardiovascular risk, and renal disease in a remote Australian Aboriginal community. Clin Sci (Lond). 2004;106(2):121-8.
30. Hoy W, McDonald SP. Albuminuria: marker or target in indigenous populations. Kidney Int Suppl. 2004;(92):S25-31.
31. Dunstan DW, Zimmet PZ, Welborn TA, De Courten MP, Cameron AJ, Sicree RA, et al. The rising prevalence of diabetes and impaired glucose tolerance: the Australian Diabetes, Obesity and Lifestyle Study. Diabetes Care. 2002;25(5):829-34.
32. McDonald S. Indigenous transplant outcomes in Australia: what the ANZDATA Registry tells us. Nephrology (Carlton). 2004;9 Suppl 4:138-43.
33. Singh GR, Hoy WE. The association between birthweight and current blood pressure: a cross-sectional study in an Australian Aboriginal community. Med J Aust. 2003;179(10):532-5.
34. Hoy WE, Rees M, Kile E, Mathews JD, Wang Z. A new dimension to the Barker hypothesis: low birthweight and susceptibility to renal disease. Kidney Int. 1999;56(3):1072-7.
35. Hoy WE, Rees M, Kile E, Mathews JD, McCredie DA, Pugsley DJ, et al. Low birthweight and renal disease in Australian aborigines. Lancet. 1998;352(9143):1826-7.
36. Paradies Y. A systematic review of empirical research on self-reported racism and health. Int J Epidemiol. 2006;35(4):888-901.
37. Paradies Y. A review of psychosocial stress and chronic disease for 4th world indigenous peoples and African Americans. Ethn Dis. 2006;16(1):295-308.
38. O’Dea K, Rowley KG. Macrovascular disease risk factors and insulin resistance in Aboriginal and Torres Strait Islander people. J Diabetes Complications. 2002;16(1):9-16.
39. Strogatz DS, Croft JB, James SA, Keenan NL, Browning SR, Garrett JM, et al. Social support, stress, and blood pressure in black adults. Epidemiology. 1997;8(5):482-7.
40. Bjorntorp P, Holm G, Rosmond R, Folkow B. Hypertension and the Metabolic Syndrome: Closely Related Central Origin? Blood Press. 2000;9(2):71-82.
41. Barker DJ. The developmental origins of adult disease. Eur J Epidemiol. 2003;18(8):733-6.
42. Nenov VD, Taal MW, Sakharova OV, Brenner BM. Multi-hit nature of chronic renal disease. Curr Opin Nephrol Hypertens. 2000;9(2):85-97.
43. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004;364(9438):937-52.
44. You J, Hoy W, Zhao Y, Beaver C, Eagar K. End-stage renal disease in the Northern Territory: current and future treatment costs. Med J Aust. 2002;176(10):461-5.
45. McDermott RA, Schmidt BA, Sinha A, Mills P. Improving diabetes care in the primary healthcare setting: a randomised cluster trial in remote Indigenous communities. Med J Aust. 2001;174(10):497-502.
46. Baker PR, Hoy WE, Thomas RE. Cost-effectiveness analysis of a kidney and cardiovascular disease treatment program in an Australian Aboriginal population. Adv Chronic Kidney Dis. 2005;12(1):22-31.
47. Simmons D. Impact of an integrated approach to diabetes care at the Rumbalara Aboriginal Health Service. Intern Med J. 2003;33(12):581-5.
Indigenous Health Quantifying the excess risk for proteinuria