2 Acute Postrenal Azotemia : Etiology , Clinicopathology , and Pathophysiology

Prompt and accurate assessment of the origins of azotemia—pre­ renal, renal, and/or postrenal—is essential to the proper management of azotemic patients. Prerenal azotemia occurs when decreased renal perfusion results in a diminished glomerular filtra­ tion rate (GFR); common causes of pre­ renal azotemia include volume depletion, vascular collapse, thrombotic diseases, and shock (cardiogenic, hemorrhagic, hy po volemic, or septic). Renal azotemia occurs when nephrons are directly dam­ aged, most frequently by toxic, infectious, in flammatory, ischemic, or neoplastic pro ­ cesses. Postrenal azotemia is caused by urinary tract breach or obstruction. Any process distal to the renal tubules that interferes with the collection, contain­ ment, or excretion of urine can result in azotemia by preventing elimination of waste ma terial in the urine, which can rapidly result in life­threatening fluid, electrolyte, and acid–base imbalances. Conditions causing prerenal and postrenal azotemia can also result in intrinsic renal damage if not identified and corrected. Postrenal azotemia can be acute or chron ic; this article addresses acute az o te­ mia. Because causes of postrenal az o temia interfere with normal urine collection and elimination from the body, their identifi­ cation is critical not only to determining definitive therapeutic strategies but also to developing appropriate stabilization and treatment plans.