I remember reading papers on the subject. in the mouse seems to be straightforward: http://www.pnas.org/content/97/19/10526.full.pdf

however, bbb for primates seems to be much tigheter and epo does not cross in sgnificant amounts. engineered versions have been made available:http://jpet.aspetjournals.org/content/333/3/961.long

a number of effects of epo seems to be brought about at cerebral vascular level, but it is safe to assume that there is not much epo in the parenchima. I must stress that a lot of papers deal with epo neuroprotection after stroke in rats or mice and those findings may not be easily translated in primates (e.g., many epo trials failed).

Dear Dr. Roselli

Thank you for information. I agree with you. But some studies claimed after breakdown of the BBB during stroke, kidney-derived EPO gets access into the brain (Erythropoietin and the hypoxic brain, Hugo H. Marti, 2004). On the other hand, another study indicated plasma EPO level increases after focal cerebral ischemia in male rats (Transient Middle Cerebral Artery Occlusion Influence on Systemic Oxygen Homeostasis and Erythropoiesis in Wistar Rats, Gendron et al., 2004). So, does this mean that kidneys contribute to recovery after stroke?

How we can evaluate this?

Well, first it must be shown that epo does contribute to recovery: the paper reports that epo elevation is due to systemic hypoxiemia following the experimental stroke. So the question is not whether kidney contributes, but if there is a significant contribution at all. The exp would be simple: inject anti-epo antibody and see if there is a worsening of the outcome.