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Prerenal azotemia
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Prerenal azotemia

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Azotemia - prerenal; Uremia; Renal underperfusion

Prerenal azotemia is an abnormally high level of nitrogen waste products in the blood.

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  • Causes

    Prerenal azotemia is common, especially in people who are in the hospital.

    The kidneys normally filter the blood. When the volume or pressure of blood flow through the kidney drops, filtering of the blood also drops, or may not occur at all. Waste products stay in the blood and little or no urine is formed, even though the kidney itself is working.

    Nitrogen waste products, such as creatinine and urea, build up in the body (azotemia). These waste products act as poisons when they build up. They damage tissues and reduce the ability of the organs to function.

    Prerenal azotemia is the most common form of kidney failure in hospitalized patients. Any condition that reduces blood flow to the kidney may cause it, including:

    • Burns
    • Conditions that allow fluid to escape from the bloodstream
    • Long-term vomiting, diarrhea, or bleeding
    • Loss of blood volume (such as with dehydration)

    Conditions in which the heart cannot pump enough blood or pumps blood at a low volume also increase the risk for prerenal azotemia. These conditions include:

    • Heart failure
    • Shock (such as septic shock)

    It also can be caused by conditions that interrupt blood flow to the kidney, such as:

    • Certain types of surgery
    • Injury to the kidney
    • Renal artery embolism
    • Renal artery occlusion
  • Symptoms

    • Confusion
    • Decreased alertness
    • Decreased or no urine production
    • Dry mouth
    • Fast pulse
    • Fatigue
    • Pale skin color
    • Swelling
    • Thirst

    Other symptoms may include:

    • Excessive urination at night
    • Pain in the abdomen
  • Exams and Tests

    An examination may show:

    • Collapsed neck veins
    • Dry mucus membranes
    • Little or no urine in the bladder
    • Low blood pressure
    • Low heart function or hypovolemia
    • Poor skin turgor
    • Rapid heart rate
    • Reduced pulse pressure (difference between systolic blood pressure and diastolic blood pressure)
    • Signs of acute kidney failure

    The following tests may be done:

    • Blood creatinine
    • BUN
    • Urine osmolality and specific gravity
    • Urine tests to check sodium and creatinine levels and to monitor kidney function
  • Treatment

    The main goal of treatment is to quickly correct the cause before the kidney becomes damaged. People often need to stay in the hospital, and may need treatment in an intensive care unit.

    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 heart output. These may include dopamine, dobutamine, and other heart medications. The cause of the decreased blood volume or blood pressure should be diagnosed and treated.

    If the person has other symptoms of acute kidney failure, treatment for it should include:

    • Dialysis, including hemodialysis or dialysis inside the body (peritoneal dialysis)
    • Diet changes
    • Medication
  • Outlook (Prognosis)

    Prerenal azotemia can be reversed if the cause can be found and corrected within 24 hours. However, if the cause is not fixed quickly, damage may occur to the kidney (acute tubular necrosis).

  • Possible Complications

    • Acute kidney failure
    • Acute tubular necrosis (tissue death)
  • When to Contact a Medical Professional

    Go to the emergency room or call the local emergency number (such as 911) if you have symptoms of prerenal azotemia.

  • Prevention

    Quickly treating any condition that reduces the volume or force of blood flow through the kidneys may help prevent prerenal azotemia.

Related Information

  Septic shockHeart Failure Over...Acute arterial occ...     Heart failure

References

Yu ASL. Diseases of magnesium and phosphorous. In: Goldman L, Ausiello D, eds. Goldman: Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap 121.

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Review Date: 9/21/2011  

Reviewed By: Herbert Y. Lin, MD, PhD, Nephrologist, Massachusetts General Hospital; Associate Professor of Medicine, Harvard Medical School. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

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