TY - DATA T1 - Supplementary Material for: Uromodulin and α1-Antitrypsin Urinary Peptide Analysis to Differentiate Glomerular Kidney Diseases PY - 2017/03/23 AU - Navarro-Muñoz M. AU - Ibernon M. AU - Bonet J. AU - Pérez V. AU - Pastor M.C. AU - Bayés B. AU - Casado-Vela J. AU - Navarro M. AU - Ara J. AU - Espinal A. AU - Fluvià L. AU - Serra A. AU - López D. AU - Romero R. UR - https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Uromodulin_and_1-Antitrypsin_Urinary_Peptide_Analysis_to_Differentiate_Glomerular_Kidney_Diseases/4780939 DO - 10.6084/m9.figshare.4780939.v1 L4 - https://ndownloader.figshare.com/files/7852279 L4 - https://ndownloader.figshare.com/files/7852282 L4 - https://ndownloader.figshare.com/files/7852285 L4 - https://ndownloader.figshare.com/files/7852288 L4 - https://ndownloader.figshare.com/files/7852291 L4 - https://ndownloader.figshare.com/files/7852294 L4 - https://ndownloader.figshare.com/files/7852300 L4 - https://ndownloader.figshare.com/files/7852303 L4 - https://ndownloader.figshare.com/files/7852306 KW - α1-Antitrypsin KW - Glomerular kidney disease KW - MALDI-TOF MS analysis KW - Peptide profiling KW - Proteinuria KW - Urine proteomics KW - Uromodulin N2 - Background/Aims: Glomerular kidney disease (GKD) is suspected in patients based on proteinuria, but its diagnosis relies primarily on renal biopsy. We used urine peptide profiling as a noninvasive means to link GKD-associated changes to each glomerular entity. Methods: Urinary peptide profiles of 60 biopsy-proven glomerular patients and 14 controls were analyzed by combining magnetic bead peptide enrichment, MALDI-TOF MS analysis, and ClinProTools v2.0 to select differential peptides. Tentative identification of the differential peptides was carried out by HPLC-MS/MS. Results: The HPLC-MS/MS results suggest that uromodulin (UMOD; m/z: 1682, 1898 and 1913) and α1-antitrypsin (A1AT; m/z: 1945, 2392 and 2505) are differentially expressed urinary peptides that distinguish between GKD patients and healthy subjects. Low UMOD and high A1AT peptide abundance was observed in 80–92% of patients with GKD. Proliferative forms of GKD were distinguished from nonproliferative forms, based on a combination of UMOD and A1AT peptides. Nonproliferative forms correlated with higher A1AT peptide levels – focal segmental glomerulosclerosis was linked more closely to high levels of the m/z 1945 peptide than minimal change disease. Conclusion: We describe a workflow – urinary peptide profiling coupled with histological findings – that can be used to distinguish GKD accurately and noninvasively, particularly its nonproliferative forms. ER -