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      Vadadustat for anemia in chronic kidney disease patients on peritoneal dialysis: A phase 3 open‐label study in Japan

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          Abstract

          Vadadustat is an oral hypoxia‐inducible factor prolyl hydroxylase inhibitor for the treatment of anemia in patients with chronic kidney disease (CKD). This phase 3, open‐label, 24‐week single‐arm study evaluated the efficacy and safety of vadadustat in 42 Japanese CKD patients with anemia undergoing peritoneal dialysis. Patients received oral vadadustat for 24 weeks, initiated at 300 mg/day and doses were adjusted to achieve the target hemoglobin (Hb) range of 11.0‐13.0 g/dL. Least squares mean of average Hb at weeks 20 and 24 was 11.35 g/dL, which was within the target range. The most frequent adverse events were catheter site infections (23.8%), which were not related to vadadustat treatment. Vadadustat was generally well tolerated and effective in controlling Hb levels within the target range, indicating the usefulness of vadadustat for treating anemia in Japanese CKD patients undergoing peritoneal dialysis.

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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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            Hypoxia-Inducible Factors: Master Regulators of Cancer Progression

            Luana Schito, Gregg L. Semenza (2016)
            Intratumoral hypoxia (reduced O2 availability) is a common finding in human cancer and leads to increased activity of hypoxia-inducible factors (HIFs), which regulate the expression of genes that contribute to angiogenesis, metabolic reprogramming, extracellular matrix remodeling, epithelial-mesenchymal transition, motility, invasion, metastasis, cancer stem cell maintenance, immune evasion, and resistance to chemotherapy and radiation therapy. Conventional anticancer therapies target well-oxygenated and proliferating cancer cells, whereas there are no approved therapies that target hypoxic cancer cells, despite growing clinical and experimental evidence indicating that intratumoral hypoxia is a critical microenvironmental factor driving cancer progression. In this review, our current understanding of the consequences of HIF activity and the translational potential of targeting HIFs for cancer therapy are discussed.
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              HIF1α and HIF2α: sibling rivalry in hypoxic tumour growth and progression.

              Brian Keith, Randall Johnson, M. Celeste Simon (2011)
              Hypoxia-inducible factors (HIFs) are broadly expressed in human cancers, and HIF1α and HIF2α were previously suspected to promote tumour progression through largely overlapping functions. However, this relatively simple model has now been challenged in light of recent data from various approaches that reveal unique and sometimes opposing activities of these HIFα isoforms in both normal physiology and disease. These effects are mediated in part through the regulation of unique target genes, as well as through direct and indirect interactions with important oncoproteins and tumour suppressors, including MYC and p53. As HIF inhibitors are currently undergoing clinical evaluation as cancer therapeutics, a more thorough understanding of the unique roles performed by HIF1α and HIF2α in human neoplasia is warranted.
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                Author and article information

                Contributors
                Souichirou Takabe:
                ORCID: https://orcid.org/0000-0001-9132-2109
                takabe.souichirou@ma.mt-pharma.co.jp
                Journal
                Journal ID (nlm-ta): Ther Apher Dial
                Journal ID (iso-abbrev): Ther Apher Dial
                Journal ID (doi): 10.1111/(ISSN)1744-9987
                Journal ID (publisher-id): TAP
                Title: Therapeutic Apheresis and Dialysis
                Publisher: John Wiley & Sons Australia, Ltd (Kyoto, Japan )
                ISSN (Print): 1744-9979
                ISSN (Electronic): 1744-9987
                Publication date (Electronic): 29 December 2020
                Publication date (Print): October 2021
                Volume: 25
                Issue: 5 ( doiID: 10.1111/tap.v25.5 )
                Pages: 642-653
                Affiliations
                [ 1 ] Graduate School of Medicine, The University of Tokyo Tokyo Japan
                [ 2 ] Integrated Value Development Division, Medical Intelligence Department Mitsubishi Tanabe Pharma Corporation Tokyo Japan
                [ 3 ] Graduate School of Medicine, Gunma University Maebashi Gunma Japan
                Author notes
                [*] [* ] Correspondence

                Dr Souichirou Takabe, Mitsubishi Tanabe Pharma Corporation, 17‐10, Nihonbashi‐Koamicho Chuo‐Ku, Tokyo 103‐8405, Japan.

                Email: takabe.souichirou@ 123456ma.mt-pharma.co.jp

                Author information
                https://orcid.org/0000-0001-9132-2109
                Article
                Publisher ID: TAP13611
                DOI: 10.1111/1744-9987.13611
                PMC ID: 8451920
                PubMed ID: 33283981
                SO-VID: b6a6772c-1081-4721-8c18-8428a6aaa4ac
                Copyright © © 2020 The Authors. Therapeutic Apheresis and Dialysis published by John Wiley & Sons Australia, Ltd on behalf of International Society for Apheresis, Japanese Society for Apheresis, and Japanese Society for Dialysis Therapy.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                Date revision received : 27 November 2020
                Date received : 02 September 2020
                Date accepted : 01 December 2020
                Page count
                Figures: 6, Tables: 3, Pages: 12, Words: 6409
                Funding
                Funded by: Mitsubishi Tanabe Pharma Corporation , doi 10.13039/501100012351;
                Award ID: Not applicable
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date October 2021
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.0.7 mode:remove_FC converted:20.09.2021

                Keywords: anemia,chronic kidney disease,hypoxia‐inducible factor prolyl hydroxylase inhibitor,peritoneal dialysis,vadadustat
                Data availability:
                Keywords: anemia, chronic kidney disease, hypoxia‐inducible factor prolyl hydroxylase inhibitor, peritoneal dialysis, vadadustat

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