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. 2022 Jun 8;8(4):265–274. doi: 10.1159/000524965

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Copyright © 2022 by The Author(s). Published by S. Karger AG, Basel

This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC). Usage and distribution for commercial purposes requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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Fig. 1 — suPAR and the kidney − an evolving story. Membrane-bound uPAR (e.g., podocyte uPAR) could mediate cell signaling in an “autocrine” or “paracrine” manner. uPAR has multiple isoforms due to alternative transcription. Cleavage of the GPI anchor from the cell membrane or direct secretion from cells generates suPAR that circulates in blood. Infection and/or inflammation such as COVID-19 promotes suPAR production from bone marrow myeloid cells. High circulating suPAR levels are associated with both AKI and CKD as a kidney disease factor. In certain circumstance, suPAR alone (i.e., dimerized form) or together with other risk factors (such as CD40 autoantibody, or APOL1 risk variants) causes FSGS-like changes.