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serpin family A member 1 (\n                            <jats:italic toggle=\"yes\">SERPINA1<\/jats:italic>\n                            ) in primary FSGS, distinguishing it from other proteinuric kidney diseases.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            <jats:italic toggle=\"yes\">Serpina1<\/jats:italic>\n                            knockdown in zebrafish causes proteinuria and edema, supporting its functional relevance in glomerular disease.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            <jats:italic toggle=\"yes\">SERPINA1<\/jats:italic>\n                            may exert compartment-specific functions, and its decrease may permit protease activity to contribute to podocyte injury in primary FSGS.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Primary FSGS (pFSGS) is caused by circulating permeability factors. Despite extensive efforts, no single causative factor or biomarker signature has been identified that reliably predicts disease or therapeutic outcomes across all patients. By using liquid chromatography-mass spectrometry\u2013based proteomics on serum samples from patients with pFSGS, compared with controls, we aimed to identify disease-specific protein signatures.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Liquid chromatography-mass spectrometry\u2013based proteomics analysis was performed on 103 serum samples from 36 patients with pFSGS, 33 patients with other proteinuric diseases, and 34 healthy controls. Selected proteins found to be dysregulated in pFSGS were tested in cell culture experiments in immortalized human podocytes. Knockdown experiments were performed in zebrafish larvae, which were screened for proteinuria, edema, and podocyte marker expression. Immunofluorescent staining on zebrafish sections and patients' kidney biopsies was used to confirm findings.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Mass spectrometry of sera from patients revealed a set of 27 proteins specifically affected in pFSGS, including a dysbalance of proteases and protease inhibitors. A subset of younger pFSGS patients with frequent relapses showed a distinct serum protein profile based on 23 dysregulated proteins. From proteomics results, serpin family A member 1 (\n                      <jats:italic toggle=\"yes\">SERPINA1<\/jats:italic>\n                      ;\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      -1-antitrypsin) was selected for further investigations. Urinary\n                      <jats:italic toggle=\"yes\">SERPINA1<\/jats:italic>\n                      increased across nephrotic syndromes, whereas serum\n                      <jats:italic toggle=\"yes\">SERPINA1<\/jats:italic>\n                      reduction was specific to pFSGS, suggesting a distinct underlying pathophysiology involving immune modulation, increased protease activity, or systemic depletion. Glomerular\n                      <jats:italic toggle=\"yes\">SERPINA1<\/jats:italic>\n                      expression was selectively increased in sclerotic lesions, likely reflecting a local compensatory response to protease stress. Podocytes constitutively secreted\n                      <jats:italic toggle=\"yes\">SERPINA1<\/jats:italic>\n                      , with limited adaptive response under protease stress. Finally, systemic\n                      <jats:italic toggle=\"yes\">Serpina1<\/jats:italic>\n                      knockdown in zebrafish induced edema, proteinuria, and loss of slit diaphragm markers.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our findings support a causal and compartment-specific role of\n                      <jats:italic toggle=\"yes\">SERPINA1<\/jats:italic>\n                      and suggest that reduced circulating protease inhibitors may shift the local protease-antiprotease balance, potentially facilitating podocyte injury in pFSGS.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.34067\/kid.0000001021","type":"journal-article","created":{"date-parts":[[2025,11,10]],"date-time":"2025-11-10T17:00:40Z","timestamp":1762794040000},"page":"487-500","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Dysregulated Protease Homeostasis Defines Primary FSGS"],"prefix":"10.34067","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2026-9715","authenticated-orcid":false,"given":"Johannes","family":"Schmidt","sequence":"first","affiliation":[{"name":"Department of Preclinical Development and Validation, Fraunhofer Institute for Cell Therapy and Immunology IZI, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nina","family":"Sopel","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Uniklinikum Erlangen, Friedrich-Alexander-Universit\u00e4t (FAU) Erlangen-N\u00fcrnberg, Erlangen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-4906-0123","authenticated-orcid":false,"given":"Carmen","family":"Rist","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Uniklinikum Erlangen, Friedrich-Alexander-Universit\u00e4t (FAU) Erlangen-N\u00fcrnberg, Erlangen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9409-9619","authenticated-orcid":false,"given":"Alexandra","family":"Ohs","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Uniklinikum Erlangen, Friedrich-Alexander-Universit\u00e4t (FAU) Erlangen-N\u00fcrnberg, Erlangen, Germany"},{"name":"Research Center on Rare Kidney Diseases (RECORD), Uniklinikum Erlangen, Erlangen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Dawid","sequence":"additional","affiliation":[{"name":"Department of Preclinical Development and Validation, Fraunhofer Institute for Cell Therapy and Immunology IZI, Leipzig, Germany"},{"name":"Institute for Bioanalysis, University of Applied Sciences Coburg, Coburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9371-2709","authenticated-orcid":false,"given":"Stefan","family":"Simm","sequence":"additional","affiliation":[{"name":"Institute for Bioanalysis, University of Applied Sciences Coburg, Coburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9933-8364","authenticated-orcid":false,"given":"Lorenzo","family":"Catanese","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Angiology and Rheumatology, Klinikum Bayreuth GmbH, Bayreuth, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harald","family":"Rupprecht","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Angiology 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