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Moresco RN, Speeckaert MM, Zmonarski SC, et al. Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis. BBA Clin. 2016;5:79-84doi: 10.1016/j.bbacli.2016.02.002.
Moresco, R. N., Speeckaert, M. M., Zmonarski, S. C., Krajewska, M., Komuda-Leszek, E., Perkowska-Ptasinska, A., Gesualdo, L., Rocchetti, M. T., Delanghe, S. E., Vanholder, R., Van Biesen, W., & Delanghe, J. R. (2016). Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis. BBA clinical, 579-84. https://doi.org/10.1016/j.bbacli.2016.02.002
Moresco, Rafael N, et al. "Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis." BBA clinical vol. 5 (2016): 79-84. doi: https://doi.org/10.1016/j.bbacli.2016.02.002
Moresco RN, Speeckaert MM, Zmonarski SC, Krajewska M, Komuda-Leszek E, Perkowska-Ptasinska A, Gesualdo L, Rocchetti MT, Delanghe SE, Vanholder R, Van Biesen W, Delanghe JR. Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis. BBA Clin. 2016 Feb 17;5:79-84. doi: 10.1016/j.bbacli.2016.02.002. eCollection 2016 Jun. PMID: 27051593; PMCID: PMC4802400.
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BBA Clin. 2016 Feb 17;5:79-84. doi: 10.1016/j.bbacli.2016.02.002. eCollection 2016 Jun.

Urinary myeloid IgA Fc alpha receptor (CD89) and transglutaminase-2 as new biomarkers for active IgA nephropathy and henoch-Schönlein purpura nephritis.

BBA clinical

Rafael N Moresco, Marijn M Speeckaert, Slawomir C Zmonarski, Magdalena Krajewska, Ewa Komuda-Leszek, Agnieszka Perkowska-Ptasinska, Loreto Gesualdo, Maria T Rocchetti, Sigurd E Delanghe, Raymond Vanholder, Wim Van Biesen, Joris R Delanghe

Affiliations

  1. Department of Clinical and Toxicological Analysis, Federal University of Santa Maria, Santa Maria, Brazil; Department of Clinical Chemistry, Ghent University Hospital, Gent, Belgium.
  2. Department of Nephrology, Ghent University Hospital, Gent, Belgium.
  3. Department of Nephrology and Transplantation Medicine, Wroclaw Medical University, Wroclaw, Poland.
  4. Department of Transplantation Medicine and Nephrology, Medical University of Warsaw, Warsaw, Poland.
  5. Department of Emergency and Organ Transplantation, Section of Nephrology, University of Bari "Aldo Moro", Bari, Italy.
  6. Department of Clinical Chemistry, Ghent University Hospital, Gent, Belgium.

PMID: 27051593 PMCID: PMC4802400 DOI: 10.1016/j.bbacli.2016.02.002

Abstract

BACKGROUND: IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) are glomerular diseases that share a common and central pathogenic mechanism. The formation of immune complexes containing IgA1, myeloid IgA Fc alpha receptor (FcαRI/CD89) and transglutaminase-2 (TG2) is observed in both conditions. Therefore, urinary CD89 and TG2 could be potential biomarkers to identify active IgAN/HSPN.

METHODS: In this multicenter study, 160 patients with IgAN or HSPN were enrolled. Urinary concentrations of CD89 and TG2, as well as some other biochemical parameters, were measured.

RESULTS: Urinary CD89 and TG2 were lower in patients with active IgAN/HSPN compared to IgAN/HSPN patients in complete remission (P < 0.001). The CD89xTG2 formula had a high ability to discriminate active from inactive IgAN/HSPN in both situations: CD89xTG2/proteinuria ratio (AUC: 0.84, P < 0.001, sensitivity: 76%, specificity: 74%) and CD89xTG2/urinary creatinine ratio (AUC: 0.82, P < 0.001, sensitivity: 75%, specificity: 74%). Significant correlations between urinary CD89 and TG2 (r = 0.711, P < 0.001), proteinuria and urinary CD89 (r = - 0.585, P < 0.001), and proteinuria and urinary TG2 (r = - 0.620, P < 0.001) were observed.

CONCLUSIONS: Determination of CD89 and TG2 in urine samples can be useful to identify patients with active IgAN/HSPN.

Keywords: Henoch-Schönlein purpura nephritis; IgA nephropathy; Myeloid IgA Fc alpha receptor; Transglutaminase-2

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