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Ethnic, clinical and immunological factors in systemic lupus erythematosus and the development of lupus nephritis: results from a multi-ethnic New Zealand cohort

Department of Medicine, Middlemore Hospital, Private Bag 93311, Auckland, New Zealand, socrates{at}internet.co.nz, Rheumatology and Musculo-Skeletal Clinic, 5/110 Remuera Road, Remuera, Auckland, New Zealand

J. Ng

Department of Medicine, Middlemore Hospital, Private Bag 93311, Auckland, New Zealand

H. Thein

Department of Medicine, Middlemore Hospital, Private Bag 93311, Auckland, New Zealand

J. Ly

Rheumatology Registrar, Auckland City Hospital, New Zealand

M.R. Marshall

Department of Medicine, Middlemore Hospital, Private Bag 93311, Auckland, New Zealand

P. Gow

Department of Medicine, Middlemore Hospital, Private Bag 93311, Auckland, New Zealand

The aim of this study was to identify risk factors for lupus nephritis including clinical, laboratory, and ethnic factors in a cohort of lupus patients in New Zealand. A retrospective study of patients from two teaching hospitals in Auckland, New Zealand. Patients were selected if they had attended as either an inpatient, or a rheumatology outpatient between 2000 and 2005. 170 patients had SLE according to ACR classification. Lupus nephritis (LN) was diagnosed according to ACR criteria. Clinical, laboratory, and ethnic data were gathered from the patient notes. Twenty-four patients had LN at diagnosis and 32 patients developed LN after diagnosis. LN was associated with serositis (P = 0.008), cutaneous vasculitis (P = 0.026), anaemia (P = 0.005), CRP elevation >6 months (P < 0.001), hypocomplementaemia >6 months (P < 0.0001). Patients with elevated doublestranded DNA (dsDNA) (>5 x normal) were more likely to develop type IV LN (P = 0.0096). Forty-one percent of patients were Caucasian, 12% Maori, 23% Pacific People, 16% Asian, 6% Indian. Maori patients with SLE (odds ratio (OR) = 8.47, 95% confidence interval (CI) = 2.11—33.96, P = 0.002), and Pacific People (OR = 3.11, 95% CI = 1.29—11.48, P = 0.014) had increased risk for developing LN. Anaemia at presentation (hazard ratio (HR) 3.2, 95% CI = 1.4—7.1, P = 0.004), and low complement >6 months (HR = 3.4, 95% CI = 1.4—8.7, P = 0.008) were independent risk factors for developing LN after SLE diagnosis. In New Zealand, Pacific People and Maori patients with SLE have a higher incidence of LN, and patients with anaemia and hypocomplementaemia are more likely to develop LN after diagnosis. Patients with high dsDNA levels are more likely to develop Type IV lupus nephritis. Lupus (2007) 16, 830—837.

Key Words: anaemia • dsDNA • lupus nephritis • Maori • systemic lupus erythematosis

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