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      Is Open Access

      Opioids and the Kidney: A Compendium

      review-article

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          Abstract

          Opioids are a class of medications used in pain management. Unfortunately, long-term use, overprescription, and illicit opioid use have led to one of the greatest threats to mankind: the opioid crisis. Accompanying the classical analgesic properties of opioids, opioids produce a myriad of effects including euphoria, immunosuppression, respiratory depression, and organ damage. It is essential to ascertain the physiological role of the opioid/opioid receptor axis to gain an in-depth understanding of the effects of opioid use. This knowledge will aid in the development of novel therapeutic interventions to combat the increasing mortality rate because of opioid misuse. This review describes the current knowledge of opioids, including the opioid epidemic and opioid/opioid receptor physiology. Furthermore, this review intricately relates opioid use to kidney damage, navigates kidney structure and physiology, and proposes potential ways to prevent opioid-induced kidney damage.

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          Most cited references77

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          CDC Guideline for Prescribing Opioids for Chronic Pain--United States, 2016.

          Primary care clinicians find managing chronic pain challenging. Evidence of long-term efficacy of opioids for chronic pain is limited. Opioid use is associated with serious risks, including opioid use disorder and overdose.
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            Podocyte injury and its consequences.

            Podocytes maintain the glomerular filtration barrier, and the stability of this barrier depends on their highly differentiated postmitotic phenotype, which also defines the particular vulnerability of the glomerulus. Recent podocyte biology and gene disruption studies in vivo indicate a causal relationship between abnormalities of single podocyte molecules and proteinuria and glomerulosclerosis. Podocytes live under various stresses and pathological stimuli. They adapt to maintain homeostasis, but excessive stress leads to maladaptation with complex biological changes including loss of integrity and dysregulation of cellular metabolism. Podocyte injury causes proteinuria and detachment from the glomerular basement membrane. In addition to "sick" podocytes and their detachment, our understanding of glomerular responses following podocyte loss needs to address the pathways from podocyte injury to sclerosis. Studies have found a variety of glomerular responses to podocyte dysfunction in vivo, such as disruption of podocyte-endothelial cross talk and activation of podocyte-parietal cell interactions, all of which help us to understand the complex scenario of podocyte injury and its consequences. This review focuses on the cellular aspects of podocyte dysfunction and the adaptive or maladaptive glomerular responses to podocyte injury that lead to its major consequence, glomerulosclerosis.
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              Podocyte biology and response to injury.

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                Author and article information

                Contributors
                Role: Role: Role:
                Role: Role: Role:
                Role:
                Role: Role: Role:
                Journal
                Kidney360
                Kidney360
                KIDNEY
                Kidney360
                Kidney360
                American Society of Nephrology
                2641-7650
                December 2023
                6 November 2023
                : 4
                : 12
                : 1816-1823
                Affiliations
                [1 ]Department of Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida
                [2 ]James A. Haley Veteran's Hospital, Tampa, Florida
                [3 ]Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin
                [4 ]Hypertension and Kidney Research Center, University of South Florida, Tampa, Florida
                Author notes
                Correspondence: Dr. Alexander Staruschenko, Department of Molecular Pharmacology and Physiology, University of South Florida, 560 Channelside Drive, Tampa, FL 33602. Email: staruschenko@ 123456usf.edu
                Author information
                https://orcid.org/0000-0001-7078-7193
                https://orcid.org/0000-0002-9663-9639
                https://orcid.org/0000-0002-5190-8356
                Article
                K360-2023-000585 00023
                10.34067/KID.0000000000000291
                10758516
                37927032
                0d0e5340-b70d-4cd8-9831-98a2f9a10729
                Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Society of Nephrology

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Page count
                Figures: 3, Tables: 1, References: 77, Pages: 8
                Funding
                Funded by: National Institutes of Health
                Award ID: R35 HL135749
                Award Recipient : Alexander Staruschenko
                Funded by: National Institutes of Health
                Award ID: R21 DK129882
                Award Recipient : Alexander Staruschenko
                Funded by: National Institutes of Health
                Award ID: R01 DK135644
                Award Recipient : Alexander Staruschenko
                Funded by: James A. Haley Veterans' Hospital
                Award ID: I01 BX004024
                Award Recipient : Alexander Staruschenko
                Funded by: American Heart Association
                Award ID: TPA35490039
                Award Recipient : Alexander Staruschenko
                Funded by: American Physiological Society
                Award ID: Postdoctoral Fellowship
                Award Recipient : Biyang Xu
                Funded by: National Institutes of Health
                Award ID: R35 HL135749
                Funded by: National Institutes of Health
                Award ID: R21 DK129882
                Funded by: National Institutes of Health
                Award ID: R01 DK135644
                Funded by: James A. Haley Veterans' Hospital
                Award ID: I01 BX004024
                Funded by: American Heart Association
                Award ID: TPA35490039
                Funded by: American Physiological Society
                Award ID: Postdoctoral Fellowship
                Categories
                Review Article
                Custom metadata
                TRUE
                YES

                opioid physiology,opioid receptors,opioids and kidney damage,podocytopathy

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