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. 2018 Oct 10;9:1412. doi: 10.3389/fphys.2018.01412

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Copyright © 2018 Manonelles, Guiteras, Melilli, Lazzeri, Goma, Crespo, Bestard, Sola, Romagnani and Cruzado.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The presence of uPEC in stable kidney transplant recipients anticipates eGFR decline, albuminuria and glomerulosclerosis. Apart from alloimmune damage and glomerular disease recurrence, pathophysiologic mechanisms of chronic allograft damage occur in certain stable-supposed kidney grafts, progressing along critical steps with (1) podocyte stress and detachment, (2) glomerular rearrangement, (3) PECs proliferation and migration into the glomerular tuft, with uPECs as a novel biomarker of this process, (4) subsequent mesangial expansion and extracellular matrix deposition. This damage-response regenerative process, if sustained in time, might fail in preserve allograft function, and is translated into worse long-term results with eGFR decline, a significant albuminuria appearance, and chronic glomerular histological lesions.