ArticleFrontiers in pharmacology2023
Quantitative systems pharmacology model of erythropoiesis to simulate therapies targeting anemia due to chronic kidney disease.
Article in Frontiers in pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it, 1 citations in OpenAlex.
- Roxadustat for CKD-related anemia in patients undergoing peritoneal dialysis: a systematic review and meta-analysis.BMC nephrology · 2026Pooled it
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anemia induced by chronic kidney disease (CKD) has multiple underlying mechanistic causes and generally worsens as CKD progresses. Erythropoietin (EPO) is a key endogenous protein which increases the number of erythrocyte progenitors that mature into red blood cells that carry hemoglobin (Hb). Recombinant human erythropoietin (rHuEPO) in its native and re-engineered forms is used as a therapeutic to alleviate CKD-induced anemia by stimulating erythropoiesis. However, due to safety risks associated with erythropoiesis-stimulating agents (ESAs), a new class of drugs, prolyl hydroxylase inhibitors (PHIs), has been developed. Instead of administering exogenous EPO, PHIs facilitate the accumulation of HIF-α, which results in the increased production of endogenous EPO. Clinical trials for ESAs and PHIs generally involve balancing decisions related to safety and efficacy by carefully evaluating the criteria for patient selection and adaptive trial design. To enable such decisions, we developed a quantitative systems pharmacology (QSP) model of erythropoiesis which captures key aspects of physiology and its disruption in CKD. Furthermore, CKD virtual populations of varying severities were developed, calibrated, and validated against public data. Such a model can be used to simulate alternative trial protocols while designing phase 3 clinical trials, as well as an asset for reverse translation in understanding emerging clinical data.
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