Prerenal azotemia is not uncommon, especially in hospitalized patients. It is a result of conditions that impair blood flow to the kidney. The kidneys normally filter the blood as it is forced under pressure through the glomeruli.

When the volume or pressure of the blood flow through the kidney decreases, glomerular filtration is reduced drastically, and may not occur at all. Little or no urine is formed, and waste products remain in the bloodstream even though the internal structures of the kidney are intact and functional.

The glomeruli and tubules continue to filter wastes, but the rate of filtration is so slow that many of these wastes are reabsorbed into the blood, rather than being excreted in the urine.

The levels of urea rise faster than the levels of creatinine with prerenal azotemia. This is because of the difference in size of these molecules. Urea is small, and so more readily returns to the bloodstream when the rate of filtration in the glomeruli is slow. Creatinine is larger, so more of it is excreted, although its excretion is lower than normal.

Lab tests show accumulation of nitrogen-type wastes, such as creatinine and urea in the body (azotemia). Various waste products act as poisons when they accumulate in the body, damaging tissues and reducing the ability of organs to function. The build-up of nitrogen waste products and accumulation of excess fluid in the body are responsible for most of the symptoms of prerenal azotemia and acute renal failure.

Prerenal azotemia is the most common form of kidney failure seen in hospitalized patients. Any condition that reduces blood flow to the kidney may cause it. Risks for prerenal azotemia include loss of blood volume -- such as may occur with dehydration, prolonged vomiting or diarrhea, bleeding, burns, and other conditions that allow escape of fluid from the circulation.

Conditions where the volume is not lost, but where the heart cannot pump enough blood, or the blood is pumped at low volume, also increase risk for prerenal azotemia. These conditions include shock (such as septic shock), heart failure, and conditions where the blood flow to the kidney is interrupted, such as trauma to the kidney, surgery of various types, renal artery embolism, and other types of renal artery occlusion.

• Decreased or no urine produced
• Fatigue
• Decreased alertness
• Confusion
• Pale skin color
• Rapid pulse
• Dry mouth
• Thirst
• Swelling (edema, anasarca)

• Urination, excessive at night
• Abdominal pain

An examination may show signs of low cardiac output or signs of hypovolemia. The blood pressure may be low or may drop when the person stands up. The pulse pressure (difference between systolic blood pressure and diastolic blood pressure) may be reduced. The heart rate may be rapid.

Skin turgor may be poor, with dry mucous membranes. The neck veins may be collapsed. There may be little or no urine in the bladder even when drained by a catheter. If the condition is prolonged, other signs of acute renal failure may be present.

A urinalysis may show decreased kidney function preserving the ability of the tubules. Nitrogen wastes and electrolytes continue to be excreted, but at abnormally low rates.

• Urine sodium may be low, with fractional excretion at less than 1%.
• Urine creatinine to serum creatinine ratio is high.
• Urine urea to serum urea (BUN) ratio is high.
• Fractional excretion of urea is low.
• Osmolality and specific gravity show concentrated urine.

• Increased BUN
• Increased creatine
• Increased BUN/creatinine ratio

• Acute renal failure
• Acute tubular necrosis (tissue death)