Abstract

THE CLINICAL SIGNIFICANCE OF ANTI -C1Q ANTIBODIES IN IGA NEPHROPATHY Hemender Vats, Masoud Haghi, Alexander Yevzlin, Henry Young, Weixiong Zhong, Micah Chan. University of Wisconsin, Madison. Immunoglobulin A Nephropathy (IgAN) is the most common form of glomerulonephritis worldwide and is defined by deposition of IgA in glomerular mesangium. Exact pathogenesis of the loss of renal function is not clear; however activation of the complement via classical, alternative and lectin pathways is implicated. C1q antibodies are associated with worse outcomes in SLE patients; however their role in IgAN is not clear despite reported elevated levels of anti C1q IgA antibodies. We studied the outcomes of patients with C1q deposits in biopsy proven IgAN in respect to rate of decline of glomerular filtration rate (GFR) and progression on to ESRD. This retrospective study included all patients with biopsy proven IgAN from February 2002 to October 2009. Data for age, sex, diabetes, hypertension, yearly creatinine (and GFR), urine protein/ creatinine ratio and biopsy findings including glomerular sclerosis, fibrosis, C1q, IgG and IgM deposits was abstracted. Multivariate regression analyses were conducted to examine the relationships between the presence of C1q deposits and the decline of GFR and progression on to ESRD. 220 cases of biopsy proven IgAN were reviewed. Eighty patients had sufficient data for analysis (32 female, 48 male). Twenty-two patients were C1q positive and 58 negative. Analysis did not reveal any significant association between C1q deposits and risk of progression to ESRD [OR 1.79, p=0.57, C.I. 0.23-13.44]. There was slightly higher risk with higher age at diagnosis [OR 1.06, p=0.022]. Other variables did not have significant bearing on progression to ESRD. Analyses also did not reveal any significant association between C1q deposits and the change in gfr at one year from date of biopsy. [β= 12.24, p= 0.11, C.I. 2.92, 27.4] Conclusion: The presence of C1q deposits does not confer a higher risk of development of ESRD in IgAN, nor does it affect the rate of progression of disease as measured by decline in eGFR at one year after diagnosis.

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