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Prerenal azotemia - Overview

Alternative Names

Azotemia - prerenal; Uremia; Renal underperfusion

Definition of Prerenal azotemia:

Prerenal azotemia is an abnormally high level of nitrogen-type wastes in the blood.

Causes, incidence, and risk factors:

Prerenal azotemia is somewhat 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, blood filtration also drops, and may not occur at all. Waste products stay in the blood and little or no urine is formed, even though the kidney itself is intact and working.

Lab tests show that nitrogen-type wastes, 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. The build-up of nitrogen waste products and excess fluid in the body cause most of the symptoms of prerenal azotemia and acute kidney failure.

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
  • Loss of blood volume (such as with dehydration)
  • Prolonged vomiting or diarrhea, bleeding

Conditions in which blood volume is not lost, but the heart cannot pump enough blood or the blood is pumped at low volume, also increase the risk for prerenal azotemia. These conditions include:

It also can be caused by conditions where the blood flow to the kidney is interrupted, such as:

  • Reviewed last on: 8/12/2009
  • Parul Patel, MD, Private Practice specializing in Nephrology and Kidney and Pancreas Transplantation, affiliated with California Pacific Medical Center, Department of Transplantation, San Francisco, CA. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

References

Goldman L, Ausiello D, eds. Goldman: Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap 121.
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