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Hypogonadism in males with chronic kidney disease: another cause of resistance to erythropoiesis-stimulating agents?

Abstract
Anemia, inflammation, resistance to erythropoiesis-stimulating agents (ESA) and hypogonadism (testosterone deficiency) are highly prevalent conditions, which heralds poor prognosis, in chronic kidney disease (CKD). It has been speculated that testosterone stimulates erythropoiesis via production of hematopoietic growth factors and possibly improvement of iron bioavailability. Where as inflammation stimulates synthesis of the liver-derived iron regulatory protein hepcidin, a recent study suggests that testosterone inhibits hepcidin synthesis, thus offering a possible novel mechanism for testosterone-induced erythropoiesis. As any agent that lowers hepcidin may be an effective strategy to normalize iron homeostasis and overcome renal anemia, testosterone deficiency should be considered in this patient group. Indeed, a recent study in males with CKD showed that hypogonadism may be an additional cause of anemia and reduced ESA responsiveness. Thus, a randomized controlled trial is needed to test the possibility that restoration of testosterone levels in hypogonadal CKD males may translate into lower prevalence of anemia, better ESA responsiveness and better quality of life.
AuthorsPeter Stenvinkel, Peter Bárány
JournalContributions to nephrology (Contrib Nephrol) Vol. 178 Pg. 35-39 ( 2012) ISSN: 1662-2782 [Electronic] Switzerland
PMID22652713 (Publication Type: Journal Article)
CopyrightCopyright © 2012 S. Karger AG, Basel.
Chemical References
  • Hematinics
  • Testosterone
Topics
  • Chronic Disease
  • Drug Resistance
  • Erythropoiesis (drug effects)
  • Hematinics (pharmacology)
  • Humans
  • Hypogonadism (complications)
  • Kidney Diseases (complications)
  • Male
  • Renal Dialysis
  • Testosterone (pharmacology)

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