Prerenal azotemia results from hypoperfusion of the kidneys; if untreated, it progresses to AKI. Renal hypoperfusion typically the result of decreased arte-rial perfusion pressure, markedly increased venous pressure, or renal vasoconstriction (Table 57–7). Decreased perfusion pressure is usually associated with the release of norepinephrine, angiotensin II, and arginine vasopressin (or antidiuretic hormone). These hormones constrict cutaneous muscle and splanchnic vasculature and promote salt and water retention. The synthesis of vasodilating prostaglan-dins (prostacyclin and PGE 2) and nitric oxide in the kidneys and the intrarenal action of angiotensin II
help maintain glomerular filtration. Use of cyclo-oxygenase inhibitors (eg, ketorolac for postopera-tive pain control) or ACE inhibitors in the setting of marked prerenal azotemia can precipitate AKI. The diagnosis of prerenal azotemia is usually suspected from the clinical setting and confirmed by urinary laboratory indices (Table 57–8). Treatment of prer-enal azotemia is directed at correcting intravascular volume deficits, improving cardiac function, restor-ing a normal blood pressure, and reversing increases in renal vascular resistance.
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