Urea is a by-product of amino acid catabolism which occurs in the liver. Urea is filtered by the glomerulus. The glomerular filtrate flows through the proximal tubule and urea is re-absorbed and returned to the blood stream. Blood urea levels are sensitive indicators of renal disease.
Elevated blood urea nitrogen (BUN) is termed Azotemia. Azotemia results from either protein catabolism or impaired kidney function. Elevated protein catabolism may result from the following; consumption of a high proteinous meal, upper gastro-intestinal tract bleeding in which case blood is being digested and absorbed. Azotemia can be pre-renal, renal and post-renal respectively.
Pre-renal azotemia results from underperfusion of the kidney and this is as a result of dehydration, mild glomerulonephritis, hemorrhagic shock and so on. These factors compromises renal blood flow with respect to tubular function. Urine sodium is normally low because the kidney responds to low blood flow by trying to retain all the sodium it can accommodate.
Renal azotemia usually results from acute tubular necrosis, chronic interstitial nephritis and chronic glomerulonephritis. Such patients may develop a disease condition called Isosthenuria.
Post-renal azotemia occurs as a result of obstruction of urinary flow as observed in prostate problems, kidney stones, tumours and carcinomas.
In acute renal failure, blood urea nitrogen increases around 20mg/dl each day.(Normal BUN is 8-25mg/dl or 2.9-8.9mmol).Decreased levels of blood urea nitrogen (BUN) may appear as a result of the following; lack of protein as seen in Celiac disease and in some patients with Nephrotic syndrome, severe liver disease such as cirrhosis, hepatitis, enzyme dysfunction and paracetamol toxicity.
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