Treating secondary hyperparathyroidism (SHPT) may also improve control of anemia in hemodialysis patients, according to the authors of a new review article published in

Motoko Tanaka, MD, of Akebono Clinic in Japan, and colleagues discussed evidence supporting parathyroid hormone (PTH), a uremic toxin, as a cause of renal anemia. Experimental studies suggest elevated PTH concentrations may inhibit erythropoietin synthesis, shorten red blood cell survival, and promote myelofibrosis that decreases hematopoiesis. It is also possible that fibroblast growth factor 23 (FGF23) interferes with erythropoiesis.

Recent clinical studies further show that SHPT treatment with vitamin D receptor activators, calcimimetics, or parathyroidectomy relieves renal anemia. “Future clinical trials should determine the effect of PTH-lowering therapy on hemoglobin levels or ESA doses as a primary endpoint,” Dr Tanaka and his collaborators stated.

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The investigators noted that there are several possible mechanisms by which cinacalcet could improve renal anemia. The most plausible mechanism is that cinacalcet-related decreases in PTH attenuate the multiple inhibitory effects of PTH on erythropoiesis, they stated. In addition, because cinacalcet also inhibits FGF23 secretion, cinacalcet-induced reduction in FGF23 levels may contribute to improved renal anemia.

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Tanaka M, Komaba H, and Fukagawa M. Emerging association between parathyroid hormone and anemia in hemodialysis patients. Therap Apheresis Dial 2018. doi: 10.1111/1744-9987.12685