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Azotemia is a medical condition characterized by abnormally high 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.
Types

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 blood urea nitrogen (BUN) and serumcreatinine 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.[2]
[edit]Prerenal

azotemia

Prerenal azotemia is caused by a decrease in blood flow (hypoperfusion) to the kidneys. However, there is no inherent kidney disease. It can occur following hemorrhage, shock, volume depletion, congestive heart failure, and narrowing of the renal artery among other things.[1] The BUN:Cr in prerenal azotemia is greater than 20. 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 greater increase in BUN than creatinine. Since the kidney is functioning correctly, the response to decreased GFR is to increase reabsorption rates. The increased reabsorption of Na leads to increased water and urea reabsorption from the proximal tubules of the kidney back into the blood. In contrast, creatinine is actually secreted in the proximal tubule. This generally leads to a BUN:Cr ratio > 20 and a fractional excretion of Na of < 1% and an elevated urine osmolarity. [edit]Renal

azotemia

Renal azotemia (acute renal failure) typically leads to uremia. It is an intrinsic disease of the kidney, generally the result of renal parenchymaldamage. Causes include renal failure, glomerulonephritis, acute tubular necrosis, or any other kind of renal disease.[2] The BUN:Cr in renal azotemia is less than 15.[citation needed] In cases of renal disease, glomerular filtration rate decreases. So nothing gets filtered as well as it normally would. However, in addition to not being normally filtered, what urea does get filtered is not reabsorbed by the proximal tubule as it normally would be. This results in lower levels of urea in the blood and higher levels of urea in the urine. Creatinine filtration decreases, leading to higher amount of creatinine in the blood. Third spacing of fluids such as peritonitis, osmotic diuresis, or low aldosterone states such as Addisons Disease.[2] [edit]Postrenal

azotemia

Blockage of urine flow in an area below the kidneys results in postrenal azotemia. It can be caused by congenital abnormalities such asvesicoureteral 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.
[1]

Like in prerenal azotemia, there is no inherent renal disease.


[2]

The increased resistance to urine flow can cause back up into the kidneys, leading to hydronephrosis.
[3]

The BUN:Cr in postrenal azotemia is >15. The increased nephron tubular pressure causes increased reabsorption of urea, elevating it abnormally relative to creatinine.
[2]

s/sx
Decreased or absent urine output (oliguria or anuria). Fatigue Asterixis 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.

Race
In the 2008 annual report of the United States Renal Data System (USRDS), more than 500,000 patients with end-stage renal disease were receiving dialysis or a kidney transplant in the United States. Racial distribution was reported as Asian/Pacific Islander (4.7%), black (32.0%), white (61.0%), American Indian (1.3%), and other/unknown (0.6%).

Sex
Of the patients reported in the 2008 annual report of the USRDS, male frequency is 56.0% and female frequency is 44.0%.

Age
Of the patients reported in the 2008 annual report of the USRDS, frequencies for patients aged 0-19 years is 1.5%; aged 20-44 years, 19.1%; aged 45-64 years, 44.0%; aged 65-74 years, 19.6%; and older than 75 years, 15.7%.

http://emedicine.medscape.com/article/238545-clinical

Azotemia
Azotemia is a condition where the patient's blood contains uncommon levels of urea, creatinine, and other compounds rich in nitrogen. Azotemia is also one clinical characteristic of a wider condition known as uremia, which includes other conditions such as acidosis, anemia, hyperkalemia, hypertension, hypocalcemia, etc. Causes The underlying cause of azotemia is typically that the kidneys' blood filtering is not sufficient. Direct causes may include: certain antiviral medications, congestive heart failure, extended diarrhea or vomiting, kidney trauma, liver failure, severe burns, or shock. Azotemia may be labeled based upon its cause: Prerenal azotemia: The kidneys do not receive proper blood supply. Postrenal azotemia: There is a blockage in the urinary outflow tract.

Some forms of azotemia are actually caused directly by diseases within the kidneys.

Symptoms Symptoms of prerenal azotemia may include: Confusion Decreased urine output (possibly even absent) Decreased level of alertness Dry mouth Fatigue Orthostatic hypotension Pale skin Rapid pulse (tachycardia) Swelling Thirst

Treatment Speedy treatment of some azotemias may offer restoration of kidney function, while a delay in treatment may lead to permanent loss of function. Some treatment options include hemodialysis, peritoneal dialysis, medications, and treatment for the underlying condition

http://www.azotemia.net/prerenal.php

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