Azotemia is distinguished by abnormal levels of nitrogen containing compounds, such as creatinine, urea, various body waste compounds, and other nitrogen rich compounds in the blood. There are three types of Azotemia, they are classified based on its causative origin, but all three types share a few common features.
All types of azotemia are distinguished by a decrease in the glomerular filtration rate or GFR of the kidneys and increases in creatinine serum concentrations and BUN. The BUN-to-creatinine ratio is a valuable measure in determining the type of azotemia. Normally BUN-to-creatinine ratio is less than 15.
Postrenal azotemia is the blockage of urine flow in an area below the kidneys. It can be developed by congenital abnormalities such as pregnancy, vesicoureteral reflux, blockage of the ureters by kidney stones, prostatic hyperplasia, compression of the ureters by cancer, or blockage of the urethra by kidney or bladder stones. Like in prerenal azotemia, there is no underlying renal disease.
The increased resistance to urine flow can develop support into the kidneys, leading to hydronephrosis. The BUN-to-creatinine ratio in postrenal azotemia is generally greater than 15. The increased nephron tubular pressure is the reason for increased reabsorption of BUN, raising it abnormally relative to creatinine.
Prerenal azotemia is caused by a reduction in cardiac output, ensuing in inadequate blood supply to the kidneys. There is no fundamental renal disease. It can also develop from shock, hemorrhage, congestive heart failure and volume depletion.
Due to the mechanism of filtration of BUN and creatinine the BUN-to-creatinine ratio in prerenal azotemia is greater than 20. GFR levels are reduced due to hypoperfusion, leading to an increase in BUN and creatinine levels. Since some of the filtered BUN is resorbed from the proximal tubules of the kidney back into the blood, at the same time very little of the filtered creatinine is, more BUN builds up in the blood relative to creatinine.
Renal azotemia usually leads to uremia. It is an inborn disease of the kidney, usually the result of renal parenchymal damage. Its causes include, glomerulonephritis, renal failure, acute tubular necrosis or any other types of renal disease. The BUN-to-creatinine ratio in renal azotemia is usually normal less than 15.
Although the GFR is reduced and both BUN and creatinine levels are increased in the blood, because of the destroyed proximal tubules, no BUN is reabsorbed from the filtrate. Thus, BUN is destroyed into the urine just like creatinine, preserving the normal ratio.