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1. ARenal impairment increases hepatic metabolism of lithium, generating a toxic metabolite that crosses the blood-brain barrier
2. BRenal impairment causes hyponatraemia, which has no bearing on lithium handling but coincidentally produces an identical clinical picture
3. CRenal impairment reduces protein binding of lithium, increasing the free fraction available to act at GABA receptors
4. DReduced renal clearance allows lithium to accumulate, and because its therapeutic and toxic concentrations are close together
5. ELithium is primarily metabolised by the kidney itself, so renal impairment directly slows its inactivation in the renal tubule