New studies in autoimmune kidney disease demonstrate the complex interplay between immune and non-immune cells that underlies kidney inflammation and fibrosis. Differences between these autoimmune responses and those observed in kidney allograft rejection, as well as insights from clinical responses to immunotherapy, provide further clues on key pathways driving kidney inflammation.
Key advances
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Platelet-derived growth factor signalling is associated with proliferation of parietal epithelial cells (PECs) in multiple autoimmune diseases; transforming growth factor-β (TGFβ) signalling correlates with glomerulosclerosis in those diseases.
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An expanded population of myeloid cells in the tubulointerstitial space characterizes lupus nephritis; by contrast, kidney allograft rejection is characterized by expanded myeloid and T cell populations.
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Kidney transplant rejection risk is elevated when donor and recipient are not matched at the SIRPA locus.
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Chimaeric antigen receptor (CAR)-T cell-mediated B cell depletion improves frequency and accelerates complete clinic response compared with approved therapies in lupus nephritis, suggesting a need to reconsider how inflammation is sustained in the kidney.
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Arazi, A., Diamond, B. The continued odyssey to unravel the secrets of kidney inflammation. Nat Rev Nephrol 22, 93–94 (2026). https://doi.org/10.1038/s41581-025-01041-1
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DOI: https://doi.org/10.1038/s41581-025-01041-1
