Failure of the filtration function of the kidneys leads to the development of azotemia (an excess of nitrogenous compounds in the blood), which may be classified as prerenal, renal, postrenal, or of mixed origin. Prerenal azotemia develops whenever mean systemic arterial blood pressure declines to values <60 mmHg and/or when dehydration causes plasma protein concentration to increase. Conditions that may lead to development of prerenal azotemia include dehydration, congestive heart failure, and shock. Prerenal azotemia generally resolves with appropriate treatment, because kidney structure has not been altered, which allows normal function to resume once renal perfusion has been restored. Renal azotemia refers to a reduction in glomerular filtration rate (GFR) of ~75% during acute or chronic primary renal (or intrarenal) diseases. Postrenal azotemia develops when the integrity of the urinary tract is disrupted (eg, bladder rupture) or urine outflow is obstructed (eg, urethral or bilateral ureteral obstruction). Once adequate urine flow is restored, postrenal azotemia will resolve.