Table 1 Summary of mechanisms associated with cerebral dysfunction during acute kidney injury

Impaired blood–brain barrier integrity

Alteration of essential amino acid concentrations, inflammatory mediators and organic osmolyte in the brain

Neurotransmitter derangement

Decreased cerebral norepinephrine, epinephrine and dopamine may lead to impaired locomotor activity

Trigger inflammatory cascade

Three waves of danger signalling unleashing uric acid, Weibel–Palade bodies and high mobility group box 1 protein

Acid–base disturbance

Activation of acid-sensing ion channels leading to cellular injury

Local vasodilatory effects as a result of cerebral oedema

Organic osmolyte and brain water disturbance

Increased intracellular idiogenic osmoles and brain water

Alteration of drug pharmacokinetics

Downregulation of organic acid transporters and organic cation transporters

Alteration of protein binding of drug

Impaired renal and hepatic clearance of drug