ArticleAmerican journal of physiology. Renal physiology2016
Lack of hepcidin ameliorates anemia and improves growth in an adenine-induced mouse model of chronic kidney disease.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Transgenic augmentation of erythroferrone in mice ameliorates anemia in adenine-induced chronic kidney disease.JCI insight · 2025Article
- Hypoferremic Response to Chronic Inflammation Is Controlled via the Hemojuvelin/Hepcidin/Ferroportin Axis and Does Not Involve Hepcidin-Independent Regulation of Fpn mRNA.American journal of hematology · 2025Article
- Renal damage-induced hepcidin accumulation contributes to anemia in angiotensinogen-deficient mice.Clinical science (London, England : 1979) · 2025Article
- Predictive Value of Serum Hepcidin Levels for the Risk of Incident End-Stage Kidney Disease in Patients with Chronic Kidney Disease: The KNOW-CKD.Kidney diseases (Basel, Switzerland) · 2024Article
- Adiposity and Mineral Balance in Chronic Kidney Disease.Current osteoporosis reports · 2024Review
- Response to oral iron therapy in children with anemia of chronic kidney disease.Pediatric nephrology (Berlin, Germany) · 2024Review
- Conventional and complementary alternative medicine therapies for renal anemia: a literature review.Frontiers in endocrinology · 2024Review
- Iron therapy mitigates chronic kidney disease progression by regulating intracellular iron status of kidney macrophages.JCI insight · 2023Article
- Iron Supplementation Improves Skeletal Muscle Contractile Properties in Mice with CKD.Kidney360 · 2022Article
- Erythropoiesis-independent effects of iron in chronic kidney disease.Pediatric nephrology (Berlin, Germany) · 2022Article
- The HIF-PHI BAY 85-3934 (Molidustat) Improves Anemia and Is Associated With Reduced Levels of Circulating FGF23 in a CKD Mouse Model.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Saccharated ferric oxide attenuates haematopoietic response induced by epoetin beta pegol in patients undergoing haemodialysis.BMC nephrology · 2021Article
- Nomogram prediction model for renal anaemia in IgA nephropathy patients.Open medicine (Warsaw, Poland) · 2021Article
- Potential hazards of recent trends in liberal iron use for renal anemia.Clinical kidney journal · 2021Review
- Carbonyl iron and iron dextran therapies cause adverse effects on bone health in juveniles with chronic kidney disease.Kidney international · 2020Article
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- Assessment of Thrombotic and Bleeding Tendency in Two Mouse Models of Chronic Kidney Disease: Adenine-Diet and 5/6th Nephrectomy.TH open : companion journal to thrombosis and haemostasis · 2020Article
- Polysaccharide from Angelica Sinensis Suppresses Inflammation and Reverses Anemia in Complete Freund's Adjuvant-induced Rats.Current medical science · 2020Article
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Authors and funding
9 authors at 4 institutions in 1 country.
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Abstract
Growth delay is common in children with chronic kidney disease (CKD), often associated with poor quality of life. The role of anemia in uremic growth delay is poorly understood. Here we describe an induction of uremic growth retardation by a 0.2% adenine diet in wild-type (WT) and hepcidin gene (Hamp) knockout (KO) mice, compared with their respective littermates fed a regular diet. Experiments were started at weaning (3 wk). After 8 wk, blood was collected and mice were euthanized. Adenine-fed WT mice developed CKD (blood urea nitrogen 82.8 ± 11.6 mg/dl and creatinine 0.57 ± 0.07 mg/dl) and were 2.1 cm shorter compared with WT controls. WT adenine-fed mice were anemic and had low serum iron, elevated Hamp, and elevated IL6 and TNF-α. WT adenine-fed mice had advanced mineral bone disease (serum phosphorus 16.9 ± 3.1 mg/dl and FGF23 204.0 ± 115.0 ng/ml) with loss of cortical and trabecular bone volume seen on microcomputed tomography. Hamp disruption rescued the anemia phenotype resulting in improved growth rate in mice with CKD, thus providing direct experimental evidence of the relationship between Hamp pathway and growth impairment in CKD. Hamp disruption ameliorated CKD-induced growth hormone-insulin-like growth factor 1 axis derangements and growth plate alterations. Disruption of Hamp did not mitigate the development of uremia, inflammation, and mineral and bone disease in this model. Taken together, these results indicate that an adenine diet can be successfully used to study growth in mice with CKD. Hepcidin appears to be related to pathways of growth retardation in CKD suggesting that investigation of hepcidin-lowering therapies in juvenile CKD is warranted.
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