Treatment for lithium-induced nephrogenic diabetes insipidus

Most patients taking long-term lithium therapy have lithium-induced nephrogenic diabetes insipidus. The condition is characterised by reduced ability of the kidneys to concentrate the urine due to relative resistance to arginine vasopressin (AVP) (also known as antidiuretic hormone). Patients have increased free water loss (obligatory water loss varying between 3 to 12 L/day) and dehydration. Dehydration potentiates lithium toxicity, particularly in patients with intercurrent illness.

Lithium-induced nephrogenic diabetes insipidus is suggested by:

  • excessive thirst (polydipsia), including at night; drinking more than 5 L/day
  • polyuria and nocturia.

Biochemical markers of lithium-induced nephrogenic diabetes insipidus include:

  • serum sodium concentration in the upper end of the normal range
  • low urinary osmolality compared with serum osmolality1.

Treatment of lithium-induced nephrogenic diabetes insipidus involves treating dehydration with intravenous fluid replacement.

1 Effective serum osmolality (mOsm/kg) = (2 × [serum sodium concentration + serum potassium concentration]) + blood glucose concentration + serum urea concentration (all concentration units in mmol/L).Return