Internal Medicine II Practice Test

When prerenal AKI is caused by hypoperfusion, the kidneys are structurally intact but not receiving enough blood flow. The priority is to restore renal perfusion and fix the underlying cause of the reduced forward flow. This is best achieved with volume repletion using appropriate IV fluids (often isotonic crystalloids) and by addressing factors driving the low effective circulating volume or low blood pressure (such as dehydration, hemorrhage, sepsis, or heart failure with poor forward flow). As kidney perfusion improves, GFR increases and creatinine and azotemia typically improve. Dialysis is not the first step in this scenario; it’s reserved for situations where AKI persists despite restoration of perfusion or for life-threatening complications (severe hyperkalemia, acidosis, uremia, or refractory fluid overload). Diuretics do not correct the underlying perfusion problem and are not the primary treatment for prerenal azotemia, though they may be used later if volume overload becomes an issue after perfusion is restored. Helpful context: prerenal azotemia often shows a low urine sodium and a high BUN/creatinine ratio, reflecting preserved tubular function and avid reabsorption due to reduced perfusion. These signs typically improve with successful volume resuscitation and correction of the underlying cause.