Pharmacology & TherapeuticsPending review

Lithium Toxicity

Lithium is handled by the kidney like sodium and has a narrow therapeutic index, so anything that promotes sodium and volume conservation drives lithium retention and pushes levels into a self-perpetuating, neurotoxic range.

In a nutshell

Lithium shares the proximal tubule's sodium reabsorption pathway, so dehydration, NSAIDs, ACE inhibitors/ARBs and diuretics all raise levels by promoting sodium (and lithium) retention. Toxicity then causes a nephrogenic diabetes insipidus that worsens dehydration further, creating a self-perpetuating cycle that severe cases break with dialysis.

Classic presentation

A patient established on lithium who develops coarse tremor, ataxia and confusion after an intercurrent illness, dehydration, or a newly started NSAID or ACE inhibitor/ARB.

Key points

Dehydration, NSAIDs, ACE inhibitors/ARBs and diuretics are the classic precipitants because they all increase proximal renal reabsorption of lithium.

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Educational content pending clinical review. Not medical advice.