The iron cycle in chronic kidney disease (CKD): from genetics and experimental models to CKD patients.
Iron is essential for most living organisms but iron excess can be toxic. Cellular and systemic iron balance is therefore tightly controlled. Iron homeostasis is dysregulated in chronic kidney disease (CKD) and contributes to the anemia that is prevalent in this patient population. Iron supplementation is one cornerstone of anemia management in CKD patients, but has not been rigorously studied in large prospective randomized controlled trials. This review highlights important advances from genetic studies and animal models that have provided key insights into the molecular mechanisms governing iron homeostasis and its disturbance in CKD, and summarizes how these findings may yield advances in the care of this patient population.
Program in Anemia Signaling Research, Division of Nephrology, Program in Membrane Biology, Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Kimberly
K
Zumbrennen-Bullough
Jodie L
JL
Babitt
D018798:Anemia, Iron-Deficiency / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D004247:DNA / Q000235:genetics; D018450:Disease Progression; D005786:Gene Expression Regulation / Q000502:physiology; D020022:Genetic Predisposition to Disease; D064451:Hepcidins / Q000096:biosynthesis / Q000235:genetics; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007501:Iron / Q000378:metabolism*; D008962:Models, Theoretical; D051436:Renal Insufficiency, Chronic / Q000235:genetics / Q000378:metabolism*
D064451:Hepcidins; D004247:DNA; D007501:Iron
anemia; chronic kidney disease; hepcidin; iron; review