body waste


[az-uh-tee-mee-uh, ey-zuh-]
Azotemia is a medical condition characterized by abnormal levels of nitrogen-containing compounds, such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds in the blood. It is largely related to insufficient filtering of blood by the kidneys.


Azotemia has three classifications, depending on its causative origin, but all three types share a few common features. All forms of azotemia are characterized by a decrease in the glomerular filtration rate (GFR) of the kidneys and increases in BUN and creatinine serum concentrations. The BUN-to-creatinine ratio (BUN:Cr) is a useful measure in determining the type of azotemia. A normal BUN:Cr is less than 15.

Prerenal azotemia

Prerenal azotemia is caused by a decrease in cardiac output, resulting in inadequate blood supply to the kidneys. There is no inherent kidney disease. It can occur from hemorrhage, shock, volume depletion, and congestive heart failure; among other things.

The BUN:Cr in prerenal azotemia is greater than 15. The reason for this lies in the mechanism of filtration of BUN and creatinine. GFR levels are decreased due to hypoperfusion, leading to a general increase in BUN and creatinine levels. However, since some of the filtered BUN is reabsorbed from the proximal tubules of the kidney back into the blood, whereas very little of the filtered creatinine is, more BUN builds up in the blood relative to creatinine.

Renal azotemia

Renal azotemia typically leads to uremia. It is an intrinsic disease of the kidney, generally the result of renal parenchymal damage. Causes include renal failure, glomerulonephritis, acute tubular necrosis, or any other kind of renal disease.

The BUN:Cr in renal azotemia is normal--less than 15. Although the GFR is decreased and both BUN and creatinine levels are increased in the blood, because of the damaged proximal tubules, no BUN is reabsorbed from the filtrate. Thus, BUN is lost into the urine just like creatinine, preserving the normal ratio.

Postrenal azotemia

Blockage of urine flow in an area below the kidneys results in postrenal azotemia. It can be caused by congenital abnormalities such as vesicoureteral reflux, blockage of the ureters by kidney stones, pregnancy, compression of the ureters by cancer, prostatic hyperplasia, or blockage of the urethra by kidney or bladder stones. Like in prerenal azotemia, there is no inherent renal disease. The increased resistance to urine flow can cause back up into the kidneys, leading to hydronephrosis.

The BUN:Cr in postrenal azotemia is greater than 15. The increased nephron tubular pressure causes increased reabsorption of BUN, elevating it abnormally relative to creatinine.

Signs and symptoms (prerenal azotemia)

  • Decreased or absent urine output (oliguria or anuria).
  • Fatigue
  • Decreased alertness
  • Confusion
  • Pale skin color
  • Tachycardia (rapid pulse)
  • Dry mouth (xerostomia)
  • Thirst, swelling (edema, anasarca)
  • Orthostatic blood pressure (rises or falls, significantly depending on position)
  • Uremic frost, a condition when urea and urea derivatives are secreted through the skin in sweat, which evaporates away to leave solid uric compounds, resembling a frost.

A urinalysis will typically show a decreased urine sodium level, a high urine creatinine-to-serum creatinine ratio, a high urine urea-to-serum urea ratio, and concentrated urine (determined by osmolality and specific gravity). None of these is particularly useful in diagnosis.

In pre-renal and post-renal azotemias, elevation of the BUN exceeds that of the creatinine (i.e., BUN>12*creatinine). This is because BUN is readily absorbed while creatinine is not. In congestive heart failure (a cause of pre-renal azotemia) or any other condition that causes poor perfusion of kidneys, the sluggish flow of glomerular filtrate results in excessive absorption of BUN and elevation of its value in blood. Creatinine, however, is not absorbable and therefore does not rise significantly. Stasis of urine in post-renal azotemia has the same effect.

Prompt treatment of some causes of azotemia can result in restoration of kidney function; delayed treatment may result in permanent loss of renal function. Treatment may include hemodialysis or peritoneal dialysis, medications to increase cardiac output and increase blood pressure, and the treatment of the condition that caused the azotemia.

See also


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