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      Call for Papers: Digital Platforms and Artificial Intelligence in Dementia

      Submit here by August 31, 2025

      About Dementia and Geriatric Cognitive Disorders: 2.2 Impact Factor I 4.7 CiteScore I 0.809 Scimago Journal & Country Rank (SJR)

      Call for Papers: Epidemiology of CKD and its Complications

      Submit here by August 31, 2024

      About Kidney and Blood Pressure Research: 2.3 Impact Factor I 4.8 CiteScore I 0.674 Scimago Journal & Country Rank (SJR)

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      Updates on Hypoxia-Inducible Factor Prolyl Hydroxylase Inhibitors in the Treatment of Renal Anemia

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          Abstract

          Background

          Anemia is a common complication of chronic kidney disease. The hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI) is a new class of oral drugs for the treatment of renal anemia.

          Summary

          Clinical trials have consistently shown that HIF-PHIs can effectively increase hemoglobin in both the dialysis population and the nondialysis population. The effects of HIF-PHIs in treating renal anemia include promoting endogenous erythropoietin production and facilitating iron mobilization. Several studies suggest that the erythropoiesis effect of roxadustat is less affected by inflammation. Careful monitoring of thromboembolic events and tumor before and during HIF-PHI treatment is necessary.

          Key Messages

          HIF-PHIs are effective in correcting renal anemia. The long-term safety of HIF-PHIs needs to be further studied.

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          Most cited references100

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          Correction of anemia with epoetin alfa in chronic kidney disease.

          Ajay K. Singh, Lynda Szczech, Kezhen L. Tang … (2006)
          Anemia, a common complication of chronic kidney disease, usually develops as a consequence of erythropoietin deficiency. Recombinant human erythropoietin (epoetin alfa) is indicated for the correction of anemia associated with this condition. However, the optimal level of hemoglobin correction is not defined. In this open-label trial, we studied 1432 patients with chronic kidney disease, 715 of whom were randomly assigned to receive a dose of epoetin alfa targeted to achieve a hemoglobin level of 13.5 g per deciliter and 717 of whom were assigned to receive a dose targeted to achieve a level of 11.3 g per deciliter. The median study duration was 16 months. The primary end point was a composite of death, myocardial infarction, hospitalization for congestive heart failure (without renal replacement therapy), and stroke. A total of 222 composite events occurred: 125 events in the high-hemoglobin group, as compared with 97 events in the low-hemoglobin group (hazard ratio, 1.34; 95% confidence interval, 1.03 to 1.74; P=0.03). There were 65 deaths (29.3%), 101 hospitalizations for congestive heart failure (45.5%), 25 myocardial infarctions (11.3%), and 23 strokes (10.4%). Seven patients (3.2%) were hospitalized for congestive heart failure and myocardial infarction combined, and one patient (0.5%) died after having a stroke. Improvements in the quality of life were similar in the two groups. More patients in the high-hemoglobin group had at least one serious adverse event. The use of a target hemoglobin level of 13.5 g per deciliter (as compared with 11.3 g per deciliter) was associated with increased risk and no incremental improvement in the quality of life. (ClinicalTrials.gov number, NCT00211120 [ClinicalTrials.gov].). Copyright 2006 Massachusetts Medical Society.
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            A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease.

            Marc Pfeffer, Emmanuel A. Burdmann, Chao-Yin Chen … (2009)
            Anemia is associated with an increased risk of cardiovascular and renal events among patients with type 2 diabetes and chronic kidney disease. Although darbepoetin alfa can effectively increase hemoglobin levels, its effect on clinical outcomes in these patients has not been adequately tested. In this study involving 4038 patients with diabetes, chronic kidney disease, and anemia, we randomly assigned 2012 patients to darbepoetin alfa to achieve a hemoglobin level of approximately 13 g per deciliter and 2026 patients to placebo, with rescue darbepoetin alfa when the hemoglobin level was less than 9.0 g per deciliter. The primary end points were the composite outcomes of death or a cardiovascular event (nonfatal myocardial infarction, congestive heart failure, stroke, or hospitalization for myocardial ischemia) and of death or end-stage renal disease. Death or a cardiovascular event occurred in 632 patients assigned to darbepoetin alfa and 602 patients assigned to placebo (hazard ratio for darbepoetin alfa vs. placebo, 1.05; 95% confidence interval [CI], 0.94 to 1.17; P=0.41). Death or end-stage renal disease occurred in 652 patients assigned to darbepoetin alfa and 618 patients assigned to placebo (hazard ratio, 1.06; 95% CI, 0.95 to 1.19; P=0.29). Fatal or nonfatal stroke occurred in 101 patients assigned to darbepoetin alfa and 53 patients assigned to placebo (hazard ratio, 1.92; 95% CI, 1.38 to 2.68; P<0.001). Red-cell transfusions were administered to 297 patients assigned to darbepoetin alfa and 496 patients assigned to placebo (P<0.001). There was only a modest improvement in patient-reported fatigue in the darbepoetin alfa group as compared with the placebo group. The use of darbepoetin alfa in patients with diabetes, chronic kidney disease, and moderate anemia who were not undergoing dialysis did not reduce the risk of either of the two primary composite outcomes (either death or a cardiovascular event or death or a renal event) and was associated with an increased risk of stroke. For many persons involved in clinical decision making, this risk will outweigh the potential benefits. (ClinicalTrials.gov number, NCT00093015.) 2009 Massachusetts Medical Society
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              Mechanisms of anemia in CKD.

              Jodie L. Babitt, Herbert Y. Lin (2012)
              Anemia is a common feature of CKD associated with poor outcomes. The current management of patients with anemia in CKD is controversial, with recent clinical trials demonstrating increased morbidity and mortality related to erythropoiesis stimulating agents. Here, we examine recent insights into the molecular mechanisms underlying anemia of CKD. These insights hold promise for the development of new diagnostic tests and therapies that directly target the pathophysiologic processes underlying this form of anemia.
              Article 0 comments Cited 383 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Kidney Dis (Basel)
                Journal ID (iso-abbrev): Kidney Dis (Basel)
                Journal ID (publisher-id): KDD
                Title: Kidney Diseases
                Publisher: S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.com )
                ISSN (Print): 2296-9381
                ISSN (Electronic): 2296-9357
                Publication date Collection: January 2023
                Publication date (Electronic): 31 October 2022
                Publication date PMC-release: 31 October 2022
                Volume: 9
                Issue: 1
                Pages: 1-11
                Affiliations
                [1] aDivision of Nephrology, Huashan Hospital, Fudan University, Shanghai, China
                [2] bDepartment of Medicine, Vanderbilt University Medical Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA
                [3] cDepartment of Molecular Physiology & Biophysics and Program in Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
                [4] dSection of Integrative Physiology, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
                Author notes
                Article
                Publisher ID: kdd-0009-0001
                DOI: 10.1159/000527835
                PMC ID: 9900466
                PubMed ID: 36756084
                SO-VID: 75210f0e-156b-4f6b-9320-fdef2be2bacc
                Copyright © Copyright © 2022 by The Author(s). Published by S. Karger AG, Basel
                License:

                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.

                History
                Date received : 1 July 2022
                Date accepted : 24 October 2022
                Date: 2023
                Page count
                Figures: 2, Tables: 2, References: 93, Pages: 11
                Funding
                This research received no particular grant from any funding agency in the public, private, or not-for-profit sectors.
                Categories
                Subject: Review Article

                Keywords: hypoxia-inducible factor,chronic kidney disease,anemia,iron
                Data availability:
                Keywords: hypoxia-inducible factor, chronic kidney disease, anemia, iron

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