Connect
MJA
MJA

Kidney disease in Australian Aboriginals: time for decisive action

Med J Aust 1998; 168 (11): 532-533.
Published online: 1 June 1998

Kidney disease in Australian Aboriginals: time for decisive action

Can governments and healthcare services in northern and central Australia afford not to get organised?

MJA 1998; 168: 532-533  

            

 

The continued alarming rise in incidence of renal failure in Australian Aboriginals living in the Top End of the Northern Territory (NT) is documented in this issue of the Journal by Spencer and coworkers1 from the Royal Darwin Hospital and the Menzies Institute of Health Research.

Are their findings an isolated observation, why is it happening, and what should be done to address the problem?

The numbers are real. The Darwin incidence and prevalence figures for endstage renal disease (ESRD) in Aboriginals are entirely consistent with figures from other Aboriginal community surveys of the Kimberley, Pilbara and Goldfields regions of Western Australia (WA). The WA Health Services Research Linked Database shows that in the past 8 years there has been a yearly rise in (age-standardised) incidence of dialysis from 67 to 819 per million in Aboriginal men, and from 130 to 758 per million in Aboriginal women. The current rates are, respectively, 12-fold and 20-fold more than the non-Aboriginal rates (Ms K Brameld, Research Officer, Department of Public Health, University of Western Australia, personal communication).

Whole-of-Australia incidence data recorded by the Australian and New Zealand Dialysis and Transplant Registry (ANZDATA Registry) also support these findings (Box), with a marked disparity increasing over time between rates for Aboriginals and non-Aboriginals, particularly in the north of Australia.


The difference in ESRD rates between Aboriginal and non-Aboriginal populations, described by Spencer et al, increases after age-standardisation and is further accentuated by the non-Aboriginal population in Darwin having a lower ESRD rate (37-47 per million) than the non-Aboriginal population of the rest of Australia (62 per million in the same time period). This lower rate probably reflects the "healthy migrant worker" phenomenon, seen in other isolated cities such as Perth, with relatively low rates of chronic diseases.

The increasing number of new cases over time represents a combination of better ascertainment, with the development of the Aboriginal Medical Services, greater acceptance of ESRD therapy by the Aboriginal community, as well as a probable true increase in incidence of renal disease. The trends predate the appointment of a full-time nephrologist in Darwin in 1996.

Why is it happening?

The problem has multiple causes. An unfortunate mix of racial predisposition is aggravated by multiple adverse environmental and metabolic factors.3 Aboriginal kidney biopsy and autopsy data from the University of Melbourne have shown a range of pathological states (diabetic, hypertensive, and proliferative), underpinned by a remarkable increase in glomerular size of up to threefold normal.4 Whether this unusual glomerular change is entirely genetic or is exacerbated by intrauterine malnutrition followed by subsequent dietary excess has yet to be resolved.

The infective insults present in Aboriginal communities have been amply documented,5 with repeated bacterial infections of ears, nose, chest, skin, gut and genitourinary systems, as well as endemic intestinal parasites. Even in the absence of recognised nephritogenic organisms, systemic infection will activate glomerular proliferation, affecting mesangial cells in particular.6

It is probably the development of widespread obesity and "Syndrome X" (raised body mass index, blood pressure, blood glucose, and triglyceride levels; and insulin resistance, and disordered uric acid metabolism) that most closely parallels the renal disease epidemic.7 The background social and legal factors involved are well described:8 loss of employment after voting rights and equal-pay legislation were enacted, access to alcohol, increased welfare benefits, and availability of a high-fat, high-carbohydrate diet. It is ironic that the outstanding success in correcting malnutrition and infective disease in Aboriginal children over the past 30 years should have contributed to creating a cohort of obese adults with hypertension and diabetes.9

Alcohol has several indirect but definite adverse renal effects. Each 10 g of alcohol consumed causes a rise in blood pressure in both white10 and Aboriginal11 populations. The carbohydrate load causes obesity, increasing the risk of diabetes and subsequent diabetic nephropathy. Alcohol both stimulates intestinal production and reduces hepatic clearance of IgA, increasing the risk of IgA nephropathy. (Although this is the commonest form of chronic glomerulonephritis in the non-Aboriginal population, it accounts for only a minority of cases of renal disease in Aboriginals.) Smoking is also recognised in epidemiological surveys as an independent risk factor for renal disease.12 Both these behaviours are very common in Aboriginal communities.13

What can be done about this renal disease epidemic?

Remote-area dialysis works. Although renal transplantation usually gives the best rehabilitation at the lowest cost, its application is limited by scarcity of donors (cadaveric or fit live-related), disparate tissue typing between Aboriginal and white populations, and unsuitability of some recipients because of infections or poor medication compliance. The next-best option is self-care dialysis.

There is a natural and understandable cultural imperative for patients in kidney failure to wish to return to their families and homes. How to deliver dialysis in remote areas is a challenge that has been successfully met by a number of nephrology units around Australia. In Townsville, Queensland, with a semi-urbanised and relatively sophisticated Aboriginal population, a chronic ambulatory peritoneal dialysis program has been in place for over a decade (Dr P de Jersey, Nephrologist, Townsville Base Hospital, personal communication).

In Western Australia, since 1989, both CAPD and self-care haemodialysis have been delivered in areas up to 3500 km away from the parent nephrology unit. This has required some innovative technical approaches (such as inline water coolers, and repressurisation pumps) and training of staff to ensure cultural sensitivity (eg, using photographic rather than written instructions, and showing respect for name avoidance after family deaths).14

These nephrology units have shown that the challenge can be met with complication rates and dialysis survival that approach and occasionally better those observed in metropolitan dialysis units treating white populations.15 While about 25% more expensive than metropolitan self-care dialysis, remote-area dialysis is still half the cost of maintaining dependent, depressed and non-compliant patients against their will in the city.

However, there remain patients and areas where self-care dialysis is not practicable. Hospital dialysis units can benefit from the use of Aboriginal liaison officers to improve cultural awareness, and to limit the sense of alienation for patients. Reorganisation of renal referral patterns around geographical proximity rather than along State borders (eg, referring patients from East Kimberley to Darwin, rather than to Perth) would also reduce the extent of dislocation.

Screening and intervention programs are a priority. Most of the necessary components of such programs are in place and merely require coordination for maximum efficiency and effectiveness. Chronic disease screening (diabetes, hypertension, obesity) easily lends itself to the incorporation of urinalysis for protein, which, if positive, can be followed by serum creatinine estimation. Given the high rate of medical clinic attendance in Aboriginal communities, such screening can be opportunistic, reserving targeted case finding for a select identified few.16

The prime target remains improved environmental conditions.17 Availability of healthier food choices can reduce renal injury.18 Improvements in lifestyle and medication compliance have been achieved in a sizeable proportion of communities with active programs, particularly where there is Aboriginal "ownership" of the service. Reducing the blood pressure level below 140/90 mmHg (with a target of 125/85 mmHg) can slow the rate of progression of renal disease by up to 50%.19 Further, there is a particular role for angiotensin-converting enzyme inhibitors in proteinuric renal diseases, with or without diabetes.20

The cost-benefit equation is obvious. Every year of dialysis deferred for a single patient could pay the salary of another Aboriginal health worker. Can northern and central Australia healthcare services and governments afford not to get organised?

Mark A B Thomas
Head, Department of Nephrology
Royal Perth Hospital, WA

Acknowledgements: The data reported here were supplied by the Australia and New Zealand Dialysis and Transplant Registry. The interpretation and reporting of these data are the responsibility of the author and in no way should be seen as an official policy or interpretation of the Australia and New Zealand Dialysis and Transplant Registry.

  1. Spencer J, Silva D, Snelling P, Hoy WE. An epidemic of renal failure among Australian Aboriginals. Med J Aust 1998; 168: 537-541.
  2. Disney APS, Russ GR, Walker R, Sheil AGR, editors. Twentieth report of the Australian and New Zealand Dialysis and Transplant Registry 1997. Adelaide: Queen Elizabeth Hospital, 1997.
  3. Hoy WE, Mathews JD, McCredie DA, et al. The multidimensional nature of renal disease: findings in a high risk Australian Aboriginal community. Kidney Int 1998. In press.
  4. Bertram JF, Young RJ, Seymour AE, et al. Glomerulomegaly in Australian Aborigines. Nephrology 1998. In press.
  5. Gracey M, Spargo RM, Smith P, et al. Risk factors for ill-health in a remote desert-dwelling Aboriginal community in Western Australia. Aust N Z J Med 1996; 26: 171-179.
  6. Lovett DH, Bursten SL, Gemsa D, et al. Activation of glomerular mesangial cells by gram-negative bacterial cell wall components. Am J Pathol 1988; 133: 472-484.
  7. Hoy WE. Markers for cardiovascular and renal morbidity: expectations for an intervention program in an Australian Aboriginal community. Clin Exp Pharmacol Physiol 1996; 23(Suppl 1): S33-S37.
  8. Reid J, Trompf P, editors. The health of Aboriginal Australia. Sydney: Harcourt Brace Jovanovich, 1991.
  9. O'Dea K, Trainedes K, Hopper JL, Larkins RG. Impaired glucose tolerance, hyperinsulinaemia, and hypertriglyceridaemia in Australian Aborigines from the desert. Diabetes Care 1988; 11: 23-29.
  10. Puddey IB, Beilin LJ, Vandongen R, et al. Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men. A randomised controlled trial. Hypertension 1985; 7: 707-713.
  11. Smith RM, Spargo RM, King RA, et al. Risk factors for hypertension in Kimberley Aborigines. Med J Aust 1992; 156: 562-566.
  12. Orth SR, Ritz E, Schrier RW. The renal risks of smoking. Kidney Int 1997; 51: 1669-1677.
  13. 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: 121-126.
  14. Lim C, Matthews M, Whishaw J. Self-care dialysis training for Aboriginal patients. Dial Transplantation 1994; 23: 137-139.
  15. Feutrill J, Thomas L, Lazberger J, et al. Determinants of CAPD peritonitis rates in Aboriginal and non-Aboriginal patients. Kidney Int 1996; 50: 1411.
  16. Couzos S, Murray RB. Chronic renal failure. In: Aboriginal primary health care -- an evidence-based approach. Melbourne: Oxford University Press, 1999. In press.
  17. Gracey M, Williams P, Houston S. Environmental health conditions in remote and rural Aboriginal communities in Western Australia. Aust N Z J Public Health 1997; 21: 511-518.
  18. Nath KA, Grande J, Croatt A, et al. Redox regulation of renal DNA synthesis, transforming growth factor-b1 and collagen expression. Kidney Int 1998; 53: 367-381.
  19. Zucchelli P, Zuccala A, Borghi M, et al. Long-term comparison between captopril and nifedipine in the progression of renal insufficiency. Kidney Int 1992; 42: 452-458.
  20. Ruggenenti P, Remuzzi G. Angiotensin-converting enzyme inhibitor therapy for non-diabetic progressive renal disease. Curr Opin Nephrol Hypertens 1997; 6: 489-495.

-



Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company
Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>".

<URL: http://www.mja.com.au/>



Correspondence: 

Author

remove_circle_outline Delete Author
add_circle_outline Add Author

Comment
Do you have any competing interests to declare? *

I/we agree to assign copyright to the Medical Journal of Australia and agree to the Conditions of publication *
I/we agree to the Terms of use of the Medical Journal of Australia *
Email me when people comment on this article

Online responses are no longer available. Please refer to our instructions for authors page for more information.