304 AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH 2008 vol. 32 no. 4© 2008 The Authors. Journal Compilation © 2008 Public Health Association of Australia

Journal contact detailsMail: Australian and New Zealand Journal of Public Health, PO Box 351, North Melbourne, Victoria 3051.Street deliveries: c/- SUBStitution Pty Ltd, 1st Floor, 484 William Street, Melbourne, Victoria 3003.Phone: (03) 9329 3535 Fax: (03) 9329 3550E-mail: anzjph@substitution.com.au

Editorial

doi: 10.1111/j.1753-6405.2008.00244.x

End-stage kidney failure in Indigenous AustraliansJohn Mathews

Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, The University of Melbourne

As we were reminded recently in these pages, rates of end-stage

kidney failure are 8-10 fold greater for Indigenous people than

for other Australians,1 the differential is 15 fold at age 50 years,2

and even greater for Indigenous Australians living in some remote

communities.1,3

Awareness of this problem was limited until recent decades. Older

readers may remember that Charles Perkins, who first achieved

fame as an Aboriginal leader of the NSW Freedom Ride in 1965,

had received a kidney transplant in 1972. Charlie died at the age

of 64 in 2000, after a lifetime of service to his people; he was the

longest-surviving transplant recipient in Australia.4 Many other

Aboriginal leaders have also died from kidney disease at relatively

young ages. Yet despite such knowledge, and the early work of renal

units at the Queen Elizabeth and other hospitals,5 we can only guess

at the numbers of ordinary Aboriginal people, particularly in remote

communities with limited access to health care, who may have died

in the years before 1990 with their kidney disease undiagnosed.

Over the past 20 years researchers have explored the origins

of kidney disease in Aboriginal communities: albuminuria, a

precursor of renal failure, is frequent, even at younger ages,6-8

associated factors include haematuria,6,8 hypertension, obesity,

type 2 diabetes,7,8 markers of streptococcal infection,6,8,9 and low

birth weight.10 Albuminuria is clearly predictive of renal failure

and all-cause mortality in the Aboriginal population.11

To help understand the Aboriginal epidemic, we can examine

historical trends in kidney failure in the wider community. Before

the advent of dialysis and transplantation, kidney failure was a

death sentence, even in developed countries. Thus, the death rate

from diseases of the genitourinary system12 serves as a proxy for

the incidence of kidney failure until the 1960s. Figure 1 shows

Australian mortality rates from renal failure, which declined

dramatically from the 1930s to the 1980s. The same graph shows

the intake of people onto dialysis and transplantation programs

from 1964-2006; for the age group shown (45-54 years), the

graphs crossed in 1974, when increasing numbers of people with

renal failure went onto renal replacement programs rather than

being allowed to die.

In this issueJohn Mathews gives a sobering account of end-stage kidney

failure among Indigenous Australians, showing an 8 to 10-

fold greater risk, a 15-fold difference by the age of 50, and

even greater risks for Indigenous Australians living in some

remote communities. Yuejen Zhao and colleagues found remote

Aboriginal communities in 2005 had a higher prevalence of various

chronic diseases, with considerable under-diagnosis.

Culture and language are important. Della Maneze and

colleagues surveyed the use of Kava among Tongan men.

Consumption is high and linked to culture. Danielle Esler and

colleagues developed and tested a depression screening tool

modified for use with Indigenous people. Kam Cheong Wong

and Zhiqiang Wang carried out a bilingual health survey in a

Chinese community in Brisbane. Two-thirds of recipients chose to

complete the questionnaire in Chinese and they were significantly

different.

Child abuse and neglect is still with us. Melissa O’Donnell,

Dorothy Scott and Fiona Stanley show high levels of notifications

and argue for a public health approach focused on preventative

services. Marc Tourigny and colleagues in Quebec, in a telephone

survey of more than 1,000 adults, assess the prevalence of sexual,

physical and psychological violence. More than a third had

experienced at least one form of violence. Co-occurring forms

of violence have serious long-term repercussions. Devon Indig

and colleagues used the NSW Minimum Data Set for Alcohol

and other Drug Treatment Service to recommend treatment

better targeted to the needs of young people attending specialist

treatment centres.

Parents are important too. Belinda Morley and colleagues show

widespread parental concern about food advertising and strong

support for tighter restrictions. Robert Scragg and colleagues

reviewed data from the 2005 New Zealand National Survey finding

that attachment to parents played a major role in low levels of

smoking in adolescence.

Under infectious diseases, Robert Dunstan and colleagues

provide a systematic review of the emerging viral threats to the

Australian blood supply. Kirsty Hope and colleagues show that

emergency department data can lead to early identification of

outbreaks. Clare Heal and Rosanne Muller argue that general

practitioners’ can do better with contact tracing. Sanjyot Vogholkar

and colleagues show that healthcare workers are themselves at risk

of infectious diseases.

Cancer remains an issue of concern. Janet Jopson and Anthony

Reeder support ongoing concerns about indoor tanning services.

Lauren Krnjacki and colleagues demonstrate that pathology

reports are a valid source of information for colorectal cancer.

Colin Luke and colleagues in Adelaide explore the characteristics

of cancers of unknown primary site.

In midlife, in retrospect, many women report having had

unwanted pregnancies according to Edith Weisberg and colleagues.

Steve Riddell show problems with the way in which antenatal

cocaine use has been assessed.

2008 vol. 32 no. 4 AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH 305© 2008 The Authors. Journal Compilation © 2008 Public Health Association of Australia

Editorial

The causes of this historical decline in (non-Indigenous)

mortality from kidney disease in Australia and other developed

countries are poorly understood. However, early in the 20th

century, infections with group A streptococci were still rife,

causing high rates of rheumatic fever and acute nephritis,13 as still

seen in developing countries.14 It was also recognised that an attack

of acute nephritis could sometimes progress to kidney failure over

months or years.13 Thus, the historical decline in kidney failure, and

the parallel decline in rheumatic fever in developed populations,

can be linked to the decline in streptococcal infections,13 driven

by improving social conditions in the first half of the 20th century.

The rapid mortality decline in the late 1940s (Figure 1) was

likely influenced by the more general availability of penicillin,

and possibly by changes in coding practices. It is not suggested

that streptococcal infection caused all kidney disease in past

generations; staphylococcal and other infections can also trigger

kidney damage, particularly in persons with immune deficiency

or diabetes.15 Indeed, as cytokines and other mediators are now

known to have metabolic as well as inflammatory effects,16,17 the

previous distinctions between diabetic and inflammatory pathways

to kidney failure are less clear than previously thought.

In traditional hunter-gatherer times, Aboriginal Australians

were likely protected, by isolation, from many infections. Their

diet was healthy, and with ample exercise, there was an absence

of obesity and diabetes.18 The situation changed dramatically

with the loss of the traditional lifestyle in the 19th century in

the south and east, and later in remote Australia. New infections

were introduced, and people were aggregated in overcrowded

and unhygienic town camps and in new sedentary communities.19

Multiple types of newly introduced bacteria were transmitted,

causing acute illness and death, and becoming established as

causes of endemic infection.6,20 This led to chronic skin-sores and

1920 1930 1940 1950 1960 1970 1980 1990 2000 20100

20

40

60

80

100

120

140

160

180

200

YEAR

INCIDENCEORMORTALITYPER100,000

Australian Incidence of ESKFAustralian Mortality from ESKFAboriginal Incidence of ESKF

Figure 1: Annual rates of mortality (1921-88) from or incidence (1963-2006) of end-stage kidney failure (ESKF) for Australians aged 45-54 years, compared with the incidence (2001-2006) of ESKF for Aboriginal people of the same age.

ear and lung infections, arguably sowing the seeds for the epidemic

of kidney failure that was to follow. Poor diet and lack of exercise

contributed additional risk through obesity, type 2 diabetes and

associated hypertension.11,18 Immune deficiencies3,21,22 or impaired

renal development10,23 arising from poor diet or genetic isolation

may have added to Aboriginal susceptibility. Low birth weight

may affect risk through a reduction in the numbers of functioning

nephrons at birth.2,23 Alcohol abuse may also affect the risk of

kidney disease, although the evidence is inconclusive.24

In effect, the epidemic of kidney disease that afflicted non-

Aboriginal Australians a century ago12 is now attacking Aboriginal

people, driven by the effects of chronic infections and poor diet on

a susceptible population.20 In recent years the incidence of kidney

failure for Australians aged 45-54 has been 10-11 per 100,000;

for Aboriginal people, the corresponding rate was about 160 per

100,000 (Figure 1), although probably two-fold greater in the

Northern Territory.

Australia now has to deal with the very high rates of kidney

failure in its Indigenous citizens. The burden for Aboriginal people

is even greater because many people with albuminuria will die

from cardiovascular causes before developing kidney failure.1,3,11

In the years 2001 to 2006 respectively, there were 175, 172, 173,

193, 215 and 207 new Indigenous patients presenting for treatment

of kidney failure; if cases are not being missed, the Indigenous

epidemic could now be close to its peak (see also Figure 1). Of

all Indigenous patients on treatment in 2006, 971 were on dialysis

programs, and 147 had previously had a transplant.2 In that year

there were 135 deaths of Indigenous patients on dialysis, and

5 transplant deaths. Because of the difficulties of delivering

effective treatment, particularly for patients from remote Australia,

outcomes have been worse for Indigenous patients. On average the

five0 year survival for Indigenous patients was 60%, compared

with 80% for non-Indigenous patients.2

The Australian Health Ministers’ Conference has endorsed

National Service Guidelines for the management of renal

failure,1 and increased resources for Aboriginal patients have

been made available, both from government and community

sources.1 Nevertheless, most patients in remote locations still

need to relocate to a capital city or regional centre for dialysis; the

logistic and cultural challenges for patients and families led some

patients to withdraw from treatment in the early years.1 However,

earlier reservations about the cultural acceptability of dialysis for

traditional Aboriginal patients are now mostly settled.1

The increased availability of dialysis facilities for Aboriginal

patients, while necessary, has addressed just the tip of the ice-

berg, as little has been done to delay or prevent kidney disease. In

the short-term, treatment of persons with hypertension, diabetes

or albuminuria would be expected to delay the progression of

kidney disease and reduce mortality.11,25 The case is proven for

patients with hypertension. For patients with diabetes but without

hypertension, although treatment with ACE inhibitors will delay

disease progression, the reduction in mortality is not proven in

randomised studies26 Pro-active treatment of 228 persons in an

Aboriginal community, primarily with ACE inhibitors, was said

306 AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH 2008 vol. 32 no. 4© 2008 The Authors. Journal Compilation © 2008 Public Health Association of Australia

to prevent some 27.7 person-years of dialysis over 4.7 years of

follow-up,27 compared with historical controls. The program was

not sustained following changes in management.25,28 Nevertheless,

pro-active treatment of Aboriginal patients seems justified, even if

the likely benefit27 may have been over-estimated, and despite the

difficulties to be solved with service delivery across the cultural

interface.

In the longer-term, much kidney disease can be prevented by

improvements in the social circumstances of Aboriginal people.

Hitherto, their plight has been made worse by the failures of

government, through the education and health care systems, to

solve the problems of cultural transition. We have long known

that the heavy burden of infection and poor nutrition, particularly

in Aboriginal children, was worse than that seen in city slum

populations in generations past.20 Unfortunately, education for

Aboriginal people has not delivered the knowledge and skills29

needed to improve hygiene and diet and to prevent infection,

nor has it explained the rationale for doing so; likewise, the

infrastructure and housing available to Aboriginal people has not

been adequate to support a healthy lifestyle.3,19,30 and the primary

care sector does not yet have sufficient expertise or resources to

diagnose and treat all persons at risk.31 The failures of the education

system have also left many Aboriginal people in the welfare trap,

caught between two cultures and without the resources, knowledge,

language and literacy skills needed to solve their own problems and

to find satisfaction in productive employment; this has fuelled an

existential crisis leading to gambling, alcohol abuse, child abuse

and suicide. The resulting social dysfunction has made it even more

difficult to solve the problems of delivering effective education,

health services and housing for Aboriginal people across a fraught

cultural interface.29,30,31

Australia must act upon the many lessons it is learning from this

epidemic of kidney disease in our Indigenous citizens.

References1. Preston-Thomas A, Cass A, O’Rourke P. Trends in the incidence of treated end-

stage kidney disease among Indigenous Australians and access to treatment. Aust N Z J Public Health. 2007;31(5):419-21.

2. McDonald S, Chang S, Excell L, editors. ANZDATA Registry Report 2007. Adelaide (AUST): Australia and New Zealand Dialysis and Transplant Registry; 2007.

3. Cass A, Cunningham J, Snelling P, Wang Z, Hoy W. Exploring the pathways leading from disadvantage to end-stage renal disease for Indigenous Australians (review). Soc Sci Med. 2004;58(4):767-85.

4. Read P. Charles Perkins: A Biography. Revised ed. Melbourne (AUST): Penguin; 2001.

5. Kirubakaran MG, Pugsley DJ. Morbidity and mortality among Australian aboriginal renal transplant recipients. Transplant Proc. 1992;24(5):1808.

6. Van Buynder PG, Gaggin JA, Martin D, Pugsley D, Mathews JD. Streptococcal infection and renal disease markers in Australian aboriginal children. Med J Aust. 1992;156(8):537-40.

7. Van Buynder PG, Gaggin JA, Mathews JD. Renal disease patterns in aboriginal Australians. A family-based study in a high incidence community. Med J Aust. 1993;159(2):82-7. Erratum in: Med J Aust. 1993;159(6):432.

8. 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.

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10. 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.

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15. Nasr SH, Markowitz GS, Stokes MB, Said SM, Valeri AM, D’Agati VD. Acute postinfectious glomerulonephritis in the modern era: experience with 86 adults and review of the literature. Medicine (Baltimore). 2008;87(1):21-32.

16. O’Connor JC, McCusker RH, Strle K, Johnson RW, Dantzer R, Kelley KW. Regulation of IGF-I function by proinflammatory cytokines: At the interface of immunology and endocrinology. Cell Immunol. Epub 2008 Mar 4.

17. Cameron NE, Cotter MA. Pro-inflammatory mechanisms in diabetic neuropathy: focus on the nuclear factor kappa B pathway (review). Curr Drug Targets. 2008;9(1):60-7.

18. O’Dea K. Westernisation, insulin resistance and diabetes in Australian aborigines (review). Med J Aust. 1991;155(4):258-64.

19. Munoz E, Powers JR, Nienhuys TG, Mathews JD. Social and environmental factors in 10 aboriginal communities in the Northern Territory: relationship to hospital admissions of children. Med J Aust. 1992;156(8):529-33.

20. Mathews JD. The Menzies School of Health Research offers a new paradigm of cooperative research. Med J Aust. 1998;169(11-12):625-9.

21. Jose DG, Shelton M, Tauro GP, Belbin R, Hosking CS. Deficiency of immunological and phagocytic function in aboriginal children with protein-calorie malnutrition. Med J Aust. 1975;2(18):699-705.

22. Turner MW, Dinan L, Heatley S, Jack DL, Boettcher B, Lester S, et al. Restricted polymorphism of the mannose-binding lectin gene of Indigenous Australians. Hum Mol Genet. 2000;9(10):1481-6.

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24. Reynolds K, Gu D, Chen J, Tang X, Yau CL, Yu L, et al. Alcohol consumption and the risk of end-stage renal disease among Chinese men. Kidney Int. 2008;73(7):870-6.

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26. Strippoli GF, Craig M, Craig JC. Antihypertensive agents for preventing diabetic kidney disease (Cochrane Review). In: The Cochrane Database of Systematic Reviews, Issue 4, 2005. Oxford (UK): Update Software; 2005.

27. 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.

28. 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):66-73.

29. Hughes H. Indigenous Education in the Northern Territory. Sydney (AUST): Centre for Independent Studies; 2008. CIS Policy Monographs No.: 83.

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Correspondance to:John Mathews, Centre for Molecular, Environmental, Genetic and Analytical Epidemiology, University of Melbourne, Level 2, 723 Swanston St, Melbourne, Victoria 3010. E-mail: mathews@unimelb.edu.au