How would you treat lithium induced nephrogenic DI?
When oral water intake is inadequate and hypernatraemia occurs, urinary losses should be replaced with dextrose, or another hypo-osmolar fluid.
Rapid correction of hypernatraemia should be avoided to reduce the risk of causing central pontine myelinosis (aim for a maximum reduction in serum sodium of 0.5mmol/L/hr).
The administration of dextrose containing fluid risks a glycaemic osmotic diuresis if given in high dose.
The psychiatric effects of stopping lithium must be considered.
Once stopped, established lithium induced DI may take several weeks/months to recover.
Treatment of concurrent electrolyte disturbances
Hypercalcaemia and hypokalaemia increase renal ADH resistance, so if present they should be corrected
Amiloride and thiazide diuretics are the most commonly used medications in the treatment of lithium induced DI.
Amiloride blocks the uptake of lithium by the distal convoluted tubule and collecting ducts, reducing the effects of lithium.
Several mechanisms have been proposed for thee paradoxical effect of thiazides in the treatment of DI; an initial renal loss of sodium causing extracellular volume contraction and subsequent salt and water absorption is thought to be the most likely mechanism. Caution is required however as serum lithium concentration may increase with thiazide therapy.
Indomethacin, high dose desmopressin and acetazolamide have also been used, although none are considered first line therapies.