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Showing 1–6 of 6 results
Advanced filters: Author: Svjetlana Lovric Clear advanced filters

  • T-cell–mediated rejection (TCMR) remains a major cause of kidney transplant failure with incompletely understood mechanisms. Here the authors use single-nucleus RNA sequencing, spatial transcriptomics and immunofluorescence to show that injured kidney epithelial cell states associate with poor transplant outcomes after T-cell–mediated rejection.

    • Anna Maria Pfefferkorn
    • Lorenz Jahn
    • Christian Hinze
    ResearchOpen Access
    Nature Communications
    Volume: 17, P: 1-19

  • Nephrotic syndrome is the second most common chronic kidney disease but there are no targeted treatment strategies available. Here the authors identify mutations of six genes codifying for proteins involved in cytoskeleton remodelling and modulation of small GTPases in 17 families with nephrotic syndrome.

    • Shazia Ashraf
    • Hiroki Kudo
    • Friedhelm Hildebrandt
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-14

  • Steroid-sensitive nephrotic syndrome (SRNS) can cause CKD and necessitate kidney transplant. Here the authors identify FAT1 mutations by homozygosity mapping and whole-exome sequencing in families with SRNS and provide functional mouse and zebrafish evidence that FAT1 is required for normal glomerular and tubular function and that FAT1 mutations can cause SRNS.

    • Heon Yung Gee
    • Carolin E. Sadowski
    • Friedhelm Hildebrandt
    ResearchOpen Access
    Nature Communications
    Volume: 7, P: 1-11

  • Martin Zenker, Corinne Antignac, Friedhelm Hildebrandt and colleagues report that mutations in OSGEP, TP53RK, TPRKB and LAGE3, genes encoding KEOPS-complex subunits, cause Galloway–Mowat syndrome, a recessive disease characterized by early-onset steroid-resistant nephrotic syndrome and microcephaly. Functional studies suggest that the phenotypes result from impaired protein translation, thus leading to endoplasmic reticulum stress and apoptosis.

    • Daniela A Braun
    • Jia Rao
    • Friedhelm Hildebrandt
    Research
    Nature Genetics
    Volume: 49, P: 1529-1538

  • This Review describes parallels in the injury mechanisms that underlie acute kidney injury, chronic kidney disease and allograft injury, and explains how our understanding of the molecular changes that occur in epithelia in the context of kidney disease may contribute to the therapeutic targeting of specific epithelial cell phenotypes for the treatment of transplantation complications.

    • Christian Hinze
    • Svjetlana Lovric
    • Kai M. Schmidt-Ott
    Reviews
    Nature Reviews Nephrology
    Volume: 20, P: 447-459