Renal Anemia, EPO Hyporesponsiveness, and Vitamin D Deficiency
Renal Anemia, EPO Hyporesponsiveness, and Vitamin D Deficiency
The hyperparathyroid state induces anaemia in patients with normal kidney function. In secondary hyperparathyroidism of CKD patients, the high levels of circulating PTH have multiple biological effects, including an unfavourable influence on the anaemia of CKD patients. Possible pathogenic mechanisms of this relationship may be PTH-direct effects on inhibition of early erythroid progenitors, endogenous EPO synthesis and RBC survival and loss. On the other side, the most acknowledged, indirect, negative effect of PTH on bone marrow cellularity is through the induction of fibrosis. In HD patients, the surgical and pharmacological suppression of PTH release an improvement in anaemia. Hyperphosphataemia and the increase in serum alkaline phosphatase are also associated with CKD anaemia and EPO hyporesponsiveness. Recent studies showing the association among vitamin D deficiency, low Hb levels and EPO resistance suggest a new pathophysiological co-factor of CKD anaemia ( Table 1 ).
CKD-MBD, Anaemia and EPO Resistance
The hyperparathyroid state induces anaemia in patients with normal kidney function. In secondary hyperparathyroidism of CKD patients, the high levels of circulating PTH have multiple biological effects, including an unfavourable influence on the anaemia of CKD patients. Possible pathogenic mechanisms of this relationship may be PTH-direct effects on inhibition of early erythroid progenitors, endogenous EPO synthesis and RBC survival and loss. On the other side, the most acknowledged, indirect, negative effect of PTH on bone marrow cellularity is through the induction of fibrosis. In HD patients, the surgical and pharmacological suppression of PTH release an improvement in anaemia. Hyperphosphataemia and the increase in serum alkaline phosphatase are also associated with CKD anaemia and EPO hyporesponsiveness. Recent studies showing the association among vitamin D deficiency, low Hb levels and EPO resistance suggest a new pathophysiological co-factor of CKD anaemia ( Table 1 ).