Despite specific therapy now available for anemia in CKD, clinical data accumulated in the last 2 decades suggests that there is a continued need for RBCT, which, we surmise, is due to underutilization of Erythropoietin Stimulating Agents (ESA) or clinical settings such as active bleed, bone marrow resistance such as myelofibrosis or infections where ESAs are ineffective.
There are various causes of renal anemia such as decreased production of erythropoietin, resistance to erythropoietin, shortened survival of red blood cells, and bone marrow fibrosis.
For the current study, the authors explored the relation between specific cytogenetic clones and JAK2(V617F) mutational status in patients with MMM and the effects on treatment response to erythropoietin (Epo).
Here we report that expression of TEL-JAK2, a constitutively active variant of the JAK2 kinase, in lineage-depleted human umbilical cord blood cells results in erythropoietin-independent erythroid differentiation in vitro and induces the rapid development of myelofibrosis in an in vivo NOD/SCID xenotransplantation assay.