Thanks for the link. I'm struggling a bit to reconcile the analysis on the easy-immune-health site with the results on the paper that I linked.
They both indicate that it is the PLP in the blood plasma that is normally used to assess the level of B6. OK. But the research paper says that the anomaly occurs only with the measured pyridoxine, not with the measured PLP. It was the pyridoxine that accumulated with repeated supplementation. I think I have that right.
Beware, layman speculating:
Perhaps the accumulation is because there is insufficient cellular PLP and therefore the body's control system thinks there is not enough B6 and so cuts down on the excretion of the excess pyridoxine. Hmmmm. But then the question arises, is the nerve damage due to the excess pyridoxine or to the PLP deficiency in the cells? The fact that very high doses of pyridoxine can induce neuropathy seems to favour the former explanation. If the neuropathy in this case were due to a PLP deficiency then high doses of pyridoxine would have no effect.

I think that my problem with the the easy-immune-health analysis is that they seem to be saying that if you have too high levels of PLP in your plasma then the solution is to take more PLP which will (somehow?) reduce the toxic level of PLP in your plasma. It really only makes sense if they were measuring the plasma pyridoxine instead. Perhaps the plasma measurement of B6 was actually of PLP plus pyridoxine?