Risk of CKD in Australian indigenous and nonindigenous children: a population-based cohort study.

BACKGROUND: Aboriginal Australians have a 9-fold increased risk of end-stage renal disease. There is no information about the natural history and risk of chronic kidney disease (CKD) in Aboriginal and non-Aboriginal children.

STUDY DESIGN: Using a prospective study design, we aimed to determine the prevalence of persistent markers and risk factors for CKD in Australian Aboriginal and non-Aboriginal children and whether Aboriginal children are at increased risk of persistent markers of CKD after accounting for sociodemographic differences.

SETTING & PARTICIPANTS: Children were enrolled from elementary schools throughout New South Wales.

PREDICTOR: Aboriginal (Aboriginal and Torres Strait Islander Australians) versus non-Aboriginal ethnicity.

OUTCOMES & MEASUREMENTS: Urine analysis, height, weight, blood pressure, birth weight, and sociodemographic status were measured at baseline and 2-year follow-up. Albuminuria was defined as albumin-creatinine ratio of 3.4 mg/mmol or greater, hematuria as 25 or greater red blood cells/microL (>or=1+), obesity as body mass index of 2 SDs or greater, and systolic and diastolic hypertension as blood pressure greater than the 90th percentile.

RESULTS: 2,266 children (55.1% Aboriginal; 51.0% boys; mean age, 8.9 +/- 2.0 years [SD] years) were enrolled at baseline. Early markers and predictors of CKD at baseline were frequent: hematuria (5.5%), albuminuria (7.3%), obesity (7.1%), systolic hypertension (7.2%), and diastolic hypertension (5.8%). 1,432 children (63%) were available for retesting at 2-year follow-up (54.0% Aboriginal; 50.5% boys; mean age, 10.5 +/- 2.0 years). Persistent obesity (5.3%) was frequent, but persistent markers of CKD were infrequent (systolic hypertension, 1.1%; diastolic hypertension, 0.2%; hematuria, 1.1%; and albuminuria, 1.5%). Although there were more Aboriginal than non-Aboriginal children with baseline hematuria (7.1% versus 3.6%; P = 0.001), after adjustment for age, sex, birth weight, and sociodemographic status, there was no increased risk of persistent hematuria, albuminuria, obesity, or hypertension in Aboriginal children.

LIMITATIONS: Persistent markers of CKD were much less frequent than anticipated, which may have affected study power. The group lost at follow-up was older children, which may have biased results.

CONCLUSIONS: Overall, only 20% of children found to have markers of early CKD had persistent abnormalities (diastolic and systolic hypertension, albuminuria, and hematuria) 2 years later, equivalent to a population point prevalence of 1% to 2% in children with a mean age of 10 years. Aboriginal children had greater rates of baseline and transient hematuria, but no increased risk of persistent markers of CKD, suggesting that adolescence and young adulthood is a critical time for preventative strategies.