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.
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 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 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.