| Pre Renal Azotemia | |
|---|---|
| Classification and external resources | |
| ICD-10 | R79.8 |
| ICD-9 | 790.6 |
| DiseasesDB | 26060 |
| MeSH | D053099 |
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.[1]
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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 serum creatinine 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]
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.
Renal azotemia (acute renal failure) 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.[2]
The BUN:Cr in renal azotemia is less than 15. 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]
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.[1] 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.[2]
The BUN:Cr in postrenal azotemia is >15.[3] The increased nephron tubular pressure causes increased reabsorption of urea, elevating it abnormally relative to creatinine.[2]
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.
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