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C3-glomerulonephritis in New Zealand - a case series
Luke J Sutherland1, Hari Talreja2
1Auckland City Hospital, Auckland, New Zealand.
Insights
C3-glomerulonephritis incidence in New Zealand is 1.3 per million, with higher rates in Pacific Islanders. Immunosuppression may improve outcomes for this complement-mediated kidney disease.
Area of Science:
- Nephrology
- Immunology
- Complement System
Background:
- C3-glomerulonephritis (C3-GN) is a rare kidney disease characterized by complement-mediated glomerular injury.
- It can lead to progressive renal impairment, but its incidence and outcomes in New Zealand are unknown.
Purpose of the Study:
- To determine the incidence and clinical outcomes of C3-glomerulonephritis in New Zealand.
- To investigate potential ethnic disparities in disease incidence and outcomes.
Main Methods:
- A retrospective review of all C3-GN cases over 10 years at a New Zealand tertiary referral center.
- Collection of descriptive data on patient characteristics and clinical outcomes.
Main Results:
- The incidence of C3-GN was 1.3 cases per million individuals.
- Pacific Islanders represented 42% of cases, suggesting a higher susceptibility.
- 27% of patients progressed to end-stage renal disease (ESRD), and 8% died; outcomes appeared better with immunosuppression.
Conclusions:
- Findings align with global C3-GN descriptions, highlighting complement dysfunction in Pacific Islanders.
- A potential benefit of immunosuppression for C3-GN patients warrants further investigation.
Background:
C3-glomerulonephritis can lead to progressive renal impairment from complement-mediated glomerular injury. Incidence and outcomes of C3-glomerulonephritis are not known in the New Zealand population.
Methods:
We reviewed all cases of C3-glomerulonephritis from the past 10 years at a tertiary referral centre in New Zealand. Descriptive information on baseline characteristics and clinical outcomes was collected.
Results:
Twenty-six patients were included (16 men; mean ± SD age 44 ± 25 years) with a median follow-up of 30 months. Disease incidence was 1.3 cases per million individuals, of which 42% were Pacific Islanders. Most patients presented with renal impairment, with a median (IQR) creatinine at diagnosis of 210 (146-300) μmol/L, and 11 (42%) patients presented with nephrotic syndrome. Seven (27%) patients progressed to end stage renal disease and 2 (8%) had died. End stage renal disease occurred in 20% of patients treated with immunosuppression and in 50% of those not treated. Complete remission was seen in 25% of patients treated with some form of immunosuppression and in 17% of those not treated.
Conclusions:
Our results are consistent with previous descriptions of C3-glomerulonephritis. There was a suggestion of better clinical outcomes in patients treated with immunosuppression. There was a higher disease incidence in Pacific Islanders, which may indicate an underlying susceptibility to complement dysfunction in this population.
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