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Prerenal azotemia

Alternative names

Azotemia - prerenal; Uremia; Renal underperfusion


Prerenal azotemia is an abnormally high level of nitrogen-type wastes in the bloodstream, caused by conditions that reduce blood flow to the kidneys.

Causes, incidence, and risk factors

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, forcing it under pressure through the glomeruli (structures in the kidneys).

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 in prerenal azotemia. This is because of the difference in size of these molecules. Urea molecules are small, and they more readily return to the bloodstream when the rate of filtration in the glomeruli is slow. Creatinine molecules are larger, 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)
Additional symptoms that may be associated with this disease:
  • Urination, excessive at night
  • Abdominal pain

Signs and tests

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, mucous membranes may be dry. 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.
Blood lab tests show a rapid accumulation of nitrogen wastes:
  • Increased BUN
  • Increased creatine
  • Increased BUN/creatinine ratio


The main goal of treatment is to rapidly correct the cause of the prerenal azotemia before damage occurs to the internal kidney structures. Hospitalization is often required, and may involve treatment in an intensive care unit. Treatment may include hemodialysis or peritoneal dialysis.

Intravenous fluids, including blood or blood products, may be used to increase blood volume. After blood volume has been restored, medications may be used to increase blood pressure and cardiac output. These may include dopamine , dobutamine, and similar cardiac medications. The cause of the decreased blood volume or blood pressure should be identified and treated as appropriate.

If other symptoms of acute renal failure are present, treatment for it should continue, including medications, dietary restrictions, or dialysis.

Expectations (prognosis)

Prerenal azotemia is reversible if the cause can be identified and corrected within 24 hours. However, if the cause is not corrected quickly, damage may occur to the internal structures of the kidney ( acute tubular necrosis ).


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

Calling your health care provider

Go to the emergency room or call the local emergency number (such as 911), if symptoms indicating prerenal azotemia may be present.


Prompt treatment of any condition that reduces the volume or force of blood flow through the kidneys may help to prevent prerenal azotemia from developing.

Update Date: 1/19/2004

Irfan A. Agha, M.D., Department of Medicine, St. Louis University, St. Louis, MO. Review provided by VeriMed Healthcare Network.

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Last updated: Tue, 06 Jan 2009 00:20:03 GMT