ABSTRACT
Objective: This cross-sectional study investigated the relationship between individual-level markers of disadvantage, renal function and cardio-metabolic risk within an Indigenous population characterised by a heavy burden of chronic kidney disease and disadvantage.
Design: Using data from 20 Indigenous communities across Australia, an aggregate socio-economic status (SES) score was created from individual-level socio-economic variables reported by participants. Logistic regression was used to assess the association of individual-level socio-economic variables and the SES score with kidney function (an estimated glomerular function rate (eGFR) cut-point of <60 ml/min/1.73 m2) as well as clinical indicators of cardio-metabolic risk.
Results: The combination of lower education and unemployment was associated with poorer kidney function and higher cardio-metabolic risk factors. Regression models adjusted for age and gender showed that an eGFR < 60 ml/min/1.73 m2 was associated with a low socio-economic score (lowest vs. highest 3.24 [95% CI 1.43–6.97]), remote living (remote vs. highly to moderately accessible 3.24 [95% CI 1.28–8.23]), renting (renting vs. owning/being purchased 5.76[95% CI 1.91–17.33]), unemployment (unemployed vs employed 2.85 [95% CI 1.31–6.19]) and receiving welfare (welfare vs. salary 2.49 [95% CI 1.42–4.37]). A higher aggregate socio-economic score was inversely associated with an eGFR < 60 ml/min/1.73 m2 (0.75 [95% CI 063–0.89]).
Conclusion: This study extends upon our understanding of associations between area-level markers of disadvantage and burden of end stage kidney disease amongst Indigenous populations to a detailed analysis of a range of well-characterised individual-level factors such as overall low socio-economic status, remote living, renting, unemployment and welfare. With the increasing burden of end-stage kidney disease amongst Indigenous people, the underlying socio-economic conditions and social and cultural determinants of health need to be understood at an individual as well as community-level, to develop, implement, target and sustain interventions.
Acknowledgements
The authors gratefully acknowledge the support of eGFR study participants, study staff, and partner organisations and the eGFR Study Investigators not included as co-authors on this manuscript: G Jerums, R MacIsaac, L Ward, M Thomas, A Sinha, R McDermott, G Jones, A Ellis, LS Piers, K Warr, S Cherian, W Majoni. We thank Dr. Kevin Warr and Dr. William Majoni for facilitating participant recruitment at the sites of their employing organisation and Loyla Leysley, Sian Graham, Mary Ward, and Joseph Fitz for assistance with follow-up in their communities. The authors also acknowledges the support and mentorship of Kevin Rowley for RR. Thank you to Melbourne Pathology for providing the technical support in the enzymatic creatinine analysis and Roche Diagnostics for supplying the enzymatic creatinine reagent kit for this study.
Disclosure statement
No potential conflict of interest was reported by the authors.
ORCID
Wendy Hoy http://orcid.org/0000-0002-8405-1539