A 28-year-old woman comes to the clinic due to generalized weakness and frequent, high-volume urination. She has had no dysuria, hematuria, or abdominal pain. The patient's symptoms have been ongoing for several months, but she cannot recall exactly when they began. She has no other medical conditions. The patient is a single mother of a 2-year-old child, has little social support, and occasionally uses alcohol and marijuana "to cope with the stress." Vital signs and physical examination are normal. Blood glucose is 95 mg/dL and serum sodium is 132 mEq/L. Urinalysis shows no white or red blood cells. During further evaluation, urine osmolality is serially measured while fluid intake is restricted; vasopressin is subsequently administered 7 hours into the test. The results are shown below.
Show Explanatory Sources
Which of the following is the most appropriate long-term treatment for this patient?
Polyuria & polydipsia | |||
Water deprivation test | |||
Serum sodium | Urine osmolality after water deprivation | Urine osmolality with vasopressin injection | |
Normal | Normal | Increased | No additional increase |
Central diabetes insipidus | High | No change or mild increase | Large increase |
Nephrogenic diabetes insipidus | High | No change or mild increase | Mild increase |
Primary polydipsia | Low | Increased | No additional increase |
This patient has polyuria (urine output >3 L/day) with a low initial urine osmolality, which is indicative of water diuresis caused by one of the following conditions:
In patients with primary polydipsia, excessive water intake often leads to mild hyponatremia. In contrast, primary ADH deficiency in DI leads to free water loss often with ensuing hypernatremia. In certain patients, water deprivation testing may be helpful for differentiating PP from DI.
During a water deprivation test, drinking water is withheld and urine osmolality is monitored until it reaches a steady-state plateau (representing the maximal concentrating ability of the kidneys). Water deprivation in patients with PP stimulates ADH secretion and leads to a significant rise in urine concentration, whereas urine in patients with DI remains dilute. Once a plateau is reached, vasopressin is administered. In DI, exogenous vasopressin causes an increase in urine osmolality; in PP, urine concentration remains unchanged because at this point in the test, the endogenous ADH effect is already at maximum.
If PP is confirmed, long-term management includes restriction of free water intake.
(Choices A, B, and C) Central DI can be treated with desmopressin (synthetic ADH analog), while nephrogenic DI is typically treated with thiazide diuretics (induce mild hypovolemia that decreases polyuria) or NSAIDs (inhibit renal prostaglandins that act as ADH antagonists). However, during water deprivation, patients with central or nephrogenic DI typically have no change or only a mild increase in urine osmolality due to lack of adequate ADH effect; subsequent vasopressin administration would also be expected to cause an increase in urine osmolality.
(Choice D) Severe hyperglycemia in diabetes mellitus can overwhelm the ability of the kidneys to recover the filtered glucose load, leading to osmotic diuresis and polyuria. However, this typically occurs with blood glucose >180 mg/dL; this patient's glucose is normal.
Educational objective:
Primary (psychogenic) polydipsia is characterized by excessive intake of free water, leading to hyponatremia and production of large volumes of dilute urine. Water restriction normalizes serum sodium levels and increases urine osmolality.