Severe primary graft dysfunction is characterized by a failure to restore cellular energy metabolism, reflected by coordinated upstream substrate accumulation and a distinct temporal pattern of succinate elevation. As an established metabolic signature of ischaemia-reperfusion injury, the succinate trajectory provides a biologically plausible link between impaired energetic recovery and downstream oxidative stress signaling. Although exploratory, these findings support a coherent metabolic framework distinguishing recovery from persistent energetic stress in severe primary graft dysfunction.
Rust et al. (Sat,) studied this question.