All renal failure develops out of a background of persistent albuminuria in this population. More important, albuminuria and, inversely, GFR are powerful markers of risk for nonrenal natural death, including, but not restricted to, cardiovascular deaths. Most of the risk for premature death can be assessed by a simple urine test, and interventions that prevent development and progression of albuminuria and loss of GFR should not only prevent renal insufficiency, but powerfully reduce mortality from natural causes as well.

Albuminuria progresses and GFR is lost over time in individuals in this community, at rates that are strongly dependent on levels of pre-existing albuminuria. Much loss of GFR and all renal failure should be avoided by preventing the development of albuminuria and minimizing its progression. This depends on improving the weight, blood pressure, and metabolic profile of the entire community and reducing infections. Modification of the course in people with established disease depends on vigorous control of blood pressure and the metabolic profile and the specific use of angiotensin-converting enzyme inhibitors.

SUMMARY: Aborigines in remote Australia are living in profound socio‐economic disadvantage and epidemiological transition. They are also experiencing an epidemic of cardiovascular disease, with deaths increased > threefold and renal failure increased > 20‐fold. Dialysis costs pose a crisis, but premature death is the greater human catastrophe. In one high‐risk group, we identified renal disease through the urinary albumin/creatinine ratio and assessed it distribution, its correlations, its associations with other morbidities and overall mortality and its natural history. We later introduced systematic antihypertensive and renal‐protective treatment for afflicted persons. Albuminuria was detected in 55% of adults. It was inversely correlated with glomerular filtration rate (GFR) and generally progressed over time. It was strongly correlated with cardiovascular risk, and its intensity predicted not only renal failure but also all‐cause natural death. Factors correlated with renal disease included increasing age, low birthweight and infant malnutrition, adult weight gain and its syndrome X metabolic accompaniments, skin infections, post‐streptococcal glomerulonephritis, heavy drinking, multiparity and a family history of renal disease. Nephron endowment probably also influences risk, with birthweight being one important driving force. Ironically, improved health services have probably contributed to the epidemic of renal failure in at least two ways: increased survival of low‐birthweight infants and increased longevity in adults, allowing the full progression or renal disease to its terminal state. The treatment programme was associated with swift and massive reductions in end‐stage renal failure, overall mortality and costs. Renal disease is multideterminant, with the simultaneous operation of several risk factors amplifying the increase in albuminuria and decrease in GFR that accompany increasing age. While many risk factors and mechanisms remain to be identified, our findings provide ample grounds for immediate intervention in similarly afflicted communities, with expectation of excellent outcome. Improved services will probably result in additional ascertainment of disease and more opportunity for its expression, so that disease prevention and modification become even more pressing obligations. Major shifts in our political, social, academic and clinical priorities are needed to effectively address these issues for all Aboriginal communities.