Profound Hyponatremia Resulting from a Thiazide-Induced Decrease in Urinary Diluting Capacity in a Patient with Primary Polydipsia

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Abstract
PRIMARY polydipsia, whether "psychogenic" or neurogenic, is seldom associated with clinical manifestations other than the resultant polyuria and, when they are present, symptoms of an underlying emotional disturbance. Despite an intake of water in excess of normal requirements clinical hyponatremia does not, as a rule, develop in these patients. However, if mechanisms for excreting water should become compromised by some intervening event, the continued ingestion of abnormally large amounts of water could exceed the reduced excretory capacity, and water retention and symptomatic hyponatremia would result. Thiazide diuretics are known to reduce urine volume and increase urinary osmolality during experimental water . . .