Prediction of corticosteroid responsiveness based on fibroblast-specific protein 1 (FSP1) in patients with IgA nephropathy

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Abstract

Background. Corticosteroids are frequently used to treat patients with active IgA nephropathy (IgAN); however, there have been few reports describing factors that are predictive of the response to corticosteroid treatment. The purpose of this study is to determine the extent to which fibroblast-specific protein 1-positive (FSP1+) cells are predictive of corticosteroid responsiveness in patients with IgAN. Methods. Fifty biopsy-proven IgAN patients who received corticosteroid therapy were enrolled and followed for 7.1 ± 3.0 years. FSP1+ cells were identified using an anti-FSP1 antibody. Results. Twelve patients showed progression of renal impairment or no reduction of urinary protein (non-responders) after steroid therapy. In the remaining 38 patients, renal function was stable during follow-up, and their urinary protein declined to <1.0 g/day (responders). Serum creatinine, estimated GFR, severity of mesangial proliferation, percent glomerulosclerosis/total glomeruli, extent of interstitial damage and FSP1+ cell number were all significantly higher in non-responders than in responders. Cox regression analysis using two covariates with every possible combination of factors indicated that FSP1+ cell number was the strongest and most significant predictor of corticosteroid responsiveness. When IgAN patients had >32.6 FSP1+ cells/HPF at diagnosis, they were the more likely to show steroid resistance. Conclusion. FSP1+ cell number can serve as an excellent predictor of corticosteroid responsiveness in patients with IgAN. © The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

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Harada, K., Akai, Y., Yamaguchi, Y., Kimura, K., Nishitani, Y., Nakatani, K., … Saito, Y. (2008). Prediction of corticosteroid responsiveness based on fibroblast-specific protein 1 (FSP1) in patients with IgA nephropathy. Nephrology Dialysis Transplantation, 23(10), 3152–3159. https://doi.org/10.1093/ndt/gfn240

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