This refers to reduced urine output, usually defined as<400 mL/d. Oligoanuria refers to a more marked reduction in urine output, i.e., <100 mL/d. Anuria indicates the complete absence of urine output. Oliguria most often occurs in the setting of volume depletion and/or renal hypoperfusion, resulting in “prerenal azotemia” and acute renal failure (Chap. 141 Acute Renal Failure). Anuria can be caused by complete bilateral urinary tract obstruction; a vascular catastrophe (dissection or arterial occlusion); renal vein thrombosis; renal cortical necrosis; severe acute tubular necrosis; nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme (ACE) inhibitors, and/or angiotensin receptor blockers; and hypovolemic, cardiogenic, or septic shock. Oliguria is never normal, because at least 400 mL of maximally concentrated urine must be produced to excrete the obligate daily osmolar load.
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). Polyuria (Table 48-2 Major Causes of Polyuria) 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. 48-2. Approach to the Pt with Polyuria.