Abstract
Irradiation of cellular blood components is well established as a countermeasure against
transfusion-associated graft-versus-host disease (TA-GVHD). Unintended consequences
of ionizing radiation are also well established. The red cell “storage lesion” – a
progression of metabolic, functional, and morphological changes – may be exacerbated
by irradiation rates and doses typically used for TA-GVHD prophylaxis. With or without
irradiation, a storage lesion change of clinical concern is the accelerated egress
of intracellular potassium. ATP depletion during storage limits the activity of the
red cell membrane’s sodium-potassium pump (Na,K-ATPase), which normally maintains
intracellular potassium (K+) at levels 30–40 times higher than the extracellular milieu.
The natural diffusion of potassium down this concentration gradient proceeds faster
if the cell membrane is damaged, and oxidative damage to cellular membranes and membrane
proteins – including Na,K-ATPase – is an effect of ionizing radiation.
Preventing transfusion-related hyperkalemia is a reason for limiting the shelf life
of irradiated red cells. In the absence of specific measurements to assess storage
lesion in a particular unit of blood, and in the absence of specific interventions
at the time of transfusion to mitigate effects of storage lesion, it is consistent
with the precautionary principle to put conservative limits on a blood component’s
shelf life. On the other hand, both the safety and sufficiency of a nation’s blood
supply might be improved by interventions that benefit specific recipients when they
are transfused, and benefit future patients by extending the allowable shelf life
of blood components. Potassium filtration of irradiated red blood cell components
is one such intervention.
Keywords
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Published online: March 11, 2022
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