{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T05:05:57Z","timestamp":1784264757914,"version":"3.55.0"},"reference-count":65,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T00:00:00Z","timestamp":1784246400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Nephrol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Staphylococcus<\/jats:italic>\n                      infection-associated glomerulonephritis (SAGN) has emerged as the leading cause of infection-related glomerulonephritis (IRGN) in the Western subcontinents, but pathogenesis remains poorly understood in the absence of animal models and detailed molecular mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>To dissect the complex underlying immunopathology, we analyzed formalin-fixed paraffin-embedded kidney biopsy tissues from three patients with SAGN and one normal control kidney (NCK) using single-cell spatial transcriptomics (analyzing a total of 3,993 cell-specific transcriptomes). The SAGN biopsies showed diffuse endocapillary hypercellularity with focal crescents. Following annotation of various cell types, we constructed cell communication networks using CellChat to identify ligand\u2013receptor interactions in normal and SAGN kidneys.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Secreted phosphoprotein 1 (SPP1\/osteopontin) emerged as the most enriched signaling network in SAGN with markedly increased autocrine and paracrine SPP1\u2013CD44 activity among tubular segments and parietal epithelial cells (PECs). In contrast, SPP1-integrin signaling was mainly observed in healthy control kidneys. Consistent with previous reports, complement pathway activation was detected exclusively in diseased kidneys, with PECs as principal signal receivers, suggesting the potential role in crescent formation. Transcripts for C2, C3, CD55, Factor B, and Factor D showed significant upregulation in SAGN. In contrast, vascular endothelial growth factor (VEGF), angiopoietin-like proteins (ANG PTL), and progranulin\/granulin networks exhibited decreased communication probabilities in SAGN versus NCK, suggesting the suppression of protective angiogenic and anti-inflammatory signaling. Immunofluorescence staining for SPP1 showed increased staining in renal tubular segments in SAGN biopsies, supporting our transcriptomic data.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>SPP1 and complement pathways appear to drive pro-inflammatory responses, while protective VEGF signaling is compromised, providing potential therapeutic targets for this disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fneph.2026.1863912","type":"journal-article","created":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T04:23:55Z","timestamp":1784262235000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Spatial transcriptomic analysis of kidney biopsies identifies activation of complement and SPP1 networks in Staphylococcus infection-associated 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V.","family":"Parikh","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Nephrology Division, The Ohio State University","place":["Columbus, OH, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brad H.","family":"Rovin","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Nephrology Division, The Ohio State University","place":["Columbus, OH, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tibor","family":"Nadasdy","sequence":"additional","affiliation":[{"name":"Department of Pathology, Renal and Transplant Pathology Division, The Ohio State University","place":["Columbus, OH, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hira L.","family":"Nakhasi","sequence":"additional","affiliation":[{"name":"Division of Emerging and Transfusion Transmitted Diseases, Office of Blood Research and Review Center for Biologics Evaluation and 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