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Comparative Study
Journal Article
Renal histology in Indigenous Australians with lupus nephritis.
International Journal of Rheumatic Diseases 2018 January
BACKGROUND: Lupus nephritis (LN) is a feared complication of systemic lupus erythematosus (SLE). Renal biopsy is valuable to assess disease severity and prognosis, but no histological data are available for Indigenous Australians (IA). We compared histopathology between IA and non-IA patients (NI) with LN in northern Australia and describe main outcomes.
METHODS: Retrospective cohort study of all patients with biopsy evidence of LN at Royal Darwin Hospital over a 10-year period. Biopsies were classified by International Society of Nephrology criteria with clinical finding and vital status obtained from electronic health records. Data analyses used Australian Bureau of Statistics 2011 census population, nonparametric testing and lifetable estimates.
RESULTS: The study cohort contained 42 patients (mean age 30 years,86% female and 74% IA). The estimated annual incidence of biopsy-proven LN was 7/100 000 for IA versus 0.7/100 000 for NI (P < 0.01). More IA patients had full-house immune complex deposition (79% vs. 21%, P < 0.05), but fewer IA patients had proliferative LN (classes III + IV) (42% vs. 72%) (P < 0.01). Five and 10-year patient (69% and 50%) and renal survival (87% and 53%) in IA were much worse than for NI patients. The reported causes of death were infections (38.6%), end-stage renal disease (23%), cardiovascular events (15.4%).
CONCLUSION: Indigenous Australians more frequently have histological evidence of LN with a broader spectrum of immune complex deposition but less severe renal inflammation compared to non-Indigenous patients. The relative contribution of LN to reduced patient and renal survival for Indigenous Australians thus requires further study.
METHODS: Retrospective cohort study of all patients with biopsy evidence of LN at Royal Darwin Hospital over a 10-year period. Biopsies were classified by International Society of Nephrology criteria with clinical finding and vital status obtained from electronic health records. Data analyses used Australian Bureau of Statistics 2011 census population, nonparametric testing and lifetable estimates.
RESULTS: The study cohort contained 42 patients (mean age 30 years,86% female and 74% IA). The estimated annual incidence of biopsy-proven LN was 7/100 000 for IA versus 0.7/100 000 for NI (P < 0.01). More IA patients had full-house immune complex deposition (79% vs. 21%, P < 0.05), but fewer IA patients had proliferative LN (classes III + IV) (42% vs. 72%) (P < 0.01). Five and 10-year patient (69% and 50%) and renal survival (87% and 53%) in IA were much worse than for NI patients. The reported causes of death were infections (38.6%), end-stage renal disease (23%), cardiovascular events (15.4%).
CONCLUSION: Indigenous Australians more frequently have histological evidence of LN with a broader spectrum of immune complex deposition but less severe renal inflammation compared to non-Indigenous patients. The relative contribution of LN to reduced patient and renal survival for Indigenous Australians thus requires further study.
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