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

• IgAN and HSPN are glomerular diseases with a common central pathogenic mechanism.
• Anatomopathological analysis of renal biopsies is required for diagnosis.
• Urinary CD89 and urinary TG2 are decreased in patients with active IgAN/HSPN.
• The CD89xTG2 product has a high ability to discriminate active IgAN/HSPN.

BackgroundIgA 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.MethodsIn 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.ResultsUrinary 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.ConclusionsDetermination of CD89 and TG2 in urine samples can be useful to identify patients with active IgAN/HSPN.