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.