| disease | Prerenal Renal Failure |
"Prerenal" indicates renal hypoperfusion caused by intravascular volume depletion, leading to renal failure due to insufficient renal blood flow.
bubble_chart Etiology
The common causes of acute prerenal renal failure include renal or extrarenal dehydration induced by diarrhea, vomiting, and excessive use of diuretics; rare causes include septic shock, acute pancreatitis, and large doses of antihypertensive drugs. These lead to relative or absolute hypovolemia. In heart failure, decreased cardiac output also results in insufficient effective renal blood flow. Careful clinical evaluation helps differentiate the primary diseases causing acute renal failure.
Cirrhosis (hepatorenal syndrome), cyclosporine, nonsteroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors can also cause a sharp decline in glomerular filtration rate. These factors appear to induce abrupt failure of glomerular capillary function through intrarenal physiological changes regulated by prostaglandins and the renin-angiotensin system. Urinalysis results closely resemble those of prerenal renal failure, but clinical evaluation may not necessarily confirm the presence of true prerenal renal failure. Discontinuing the aforementioned medications, aggressive treatment of liver disease, or liver transplantation often leads to improvement in glomerular filtration rate.
bubble_chart Clinical Manifestations
(1) Except for a few patients with prerenal renal failure caused by heart failure, other patients usually have symptoms such as thirst and orthostatic dizziness, along with a history of fluid loss. Sudden weight loss often reflects the degree of dehydration.
(2) Physical examination may reveal poor skin elasticity, collapsed veins, dry mucous membranes and armpits, with the most important sign being orthostatic or postural hypotension and a thready, rapid pulse.bubble_chart Auxiliary Examination
(1) Urine: Urine output is usually reduced. Indwelling catheterization can accurately measure hourly urine output and also rule out lower urinary tract obstruction. Urine specific gravity and urine osmolality are elevated (>1.025 and >600mosm/kg respectively). Routine urinalysis is generally of little value.
(2) Urine and blood chemistry analysis: The normal ratio of blood urea nitrogen to creatinine is 10:1, which is increased in patients with prerenal acute renal failure. Mannitol and other diuretics can disrupt renal tubular secretion and reabsorption of urea, sodium, and creatinine, thus affecting the interpretation of test results.
(3) Central venous pressure: Decreased central venous pressure usually indicates hypovolemia, which may be caused by blood loss or dehydration. However, if the primary cause of prerenal acute renal failure is severe heart failure, cardiac output decreases while central venous pressure increases.
(4) Fluid challenge test: The fluid challenge test has both diagnostic and therapeutic value for prerenal acute renal failure. If urine output increases after cautious fluid administration, prerenal acute renal failure can be diagnosed. The test begins with rapid intravenous infusion of 300-500ml of normal saline or 125ml of 20% mannitol. Urine output is measured after 1-3 hours. If hourly urine output exceeds 50ml, the treatment is effective, and intravenous normal saline should be continued to expand blood volume and correct dehydration. If urine output does not increase, the blood and urine analysis results should be carefully reviewed, the patient's fluid status reassessed, and physical examination repeated to determine whether another fluid challenge test (with or without furosemide) is needed.
In cases of dehydration, prerenal oliguria is primarily caused by fluid loss, and rapid fluid replacement is necessary. Insufficient fluid can further worsen renal hemodynamics, ultimately leading to tubular degeneration (acute tubular necrosis). When fluid has been adequately replenished but oliguria persists, vasopressors should be used to treat hypotension caused by septic shock or cardiogenic shock. Vasopressors that maintain blood pressure while preserving renal blood flow and function should be selected. Administering dopamine at 1–5 μg/kg per minute can increase renal blood flow without altering systemic blood pressure. However, if hypotension persists despite adequate fluid replacement, a higher dose of dopamine (5–20 μg/kg) is required. Sometimes, simply discontinuing antihypertensive medications or diuretics can reverse significant prerenal renal failure.
