ArticleRenal failure2025
Global research trends in renal anemia: a multidimensional bibliometric study.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Renal anemia, a major complication of chronic kidney disease, contributes to increased cardiovascular risk, mortality, and accelerated progression to kidney failure. However, comprehensive bibliometric analyses evaluating global trends, knowledge gaps, and emerging research hotspots in this field remain lacking. This study retrieved publications related to renal anemia from the Web of Science Core Collection (January 1965-November 2024) and conducted data analysis and visualization using VOSviewer, CiteSpace, Pajek, and Origin. The final dataset included 1,664 publications authored by 7,534 researchers from 2,287 institutions across 72 countries, with Japan, the United States, and China accounting for 45.8% of total publications. Top institutions were Showa University, the University of Tokyo, and King's College Hospital; Iain C. Macdougall was the most prolific author, while Masaomi Nangaku demonstrated the highest citation impact and centrality. Keyword analysis revealed a growing focus on clinical trials and pathophysiology, highlighting three core therapeutic strategies: erythropoiesis-stimulating agents, iron supplementation, and hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs), along with several emerging research topics targeting sodium-glucose cotransporter 2 (SGLT2), hepcidin, fibroblast growth factor 23 (FGF23), gut microbiota, zinc, and stem cells. Our conclusions indicate that the field has evolved from erythropoietin replacement therapy to HIF-PHI-centered physiological modulation. Current hotspots center on HIF-PHI clinical translation, with potential therapeutic avenues including SGLT2 inhibitors, hepcidin antagonists, FGF23 signaling modulation, gut microbiota regulation, zinc supplementation, and stem cell-based therapeutics.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.