Polyuria is defined as a urine output >3 L/d. It is often accompanied by nocturia and urinary frequency and must be differentiated from other more common conditions associated with lower urinary tract pathology and urinary urgency or frequency (e.g., cystitis, prostatism). It is often accompanied by hypernatremia (Chap. 1. Electrolytes/Acid-Base Balance). Polyuria (Table 46-2) can occur as a response to a solute load (e.g., hyperglycemia) or to an abnormality in arginine vasopressin (AVP; also known as antidiuretic hormone [ADH]) action. Diabetes insipidus is termed central if due to the insufficient hypothalamic production of AVP and nephrogenic if the result of renal insensitivity to the action of AVP. Excess fluid intake can lead to polyuria, but primary polydipsia rarely results in changes in plasma osmolality unless urinary diluting capacity is impaired. Tubulointerstitial diseases, lithium therapy, and resolving acute tubular necrosis or urinary tract obstruction can be associated with nephrogenic diabetes insipidus, which is more rarely caused by mutations in the V2 AVP receptor, the aquaporin-1 water channel in the descending thin limb of the loop of Henle, and the AVP-regulated water channel in principal cells, aquaporin 2.

The approach to the pt with polyuria is shown in Fig. 46-2.