تويت
Normal level =15-45mg/dl.
Major nitrogenous end product of protein and amino acid catabolism
Produced by liver and distributed throughout intracellular and extracellular fluid.
Most all urea is filtered out of blood by glomerular function .some reabsorbed 40%with water but most is removed in urine.
Clinical significance:
A wide variety of renal diseases can cause azotemia(increased blood urea ),which is divided in pre renal azotemia and post renal azotemia.
Pre renal Azotemia:
Identifying by an increase of plasma urea without concomitant increase of plasma creatinine:
Mild dehydration.1
High protein diet .2
Muscle wasting .3
Post renal azotemia:
Has its cause in conditions that obstruct urine outflow through the ureters ,bladder , or urethra .
Examples of these conditions are;
Nephrolithiasis.1
Prostatism.2
Tumors of genitourinary tract.3
(plasma urea and creatinine both rise).
Decrease levels may be seen in:
Low protein and high carbohydrate diets.1
Late pregnancy .2
Sever liver damage.3
Major nitrogenous end product of protein and amino acid catabolism
Produced by liver and distributed throughout intracellular and extracellular fluid.
Most all urea is filtered out of blood by glomerular function .some reabsorbed 40%with water but most is removed in urine.
Clinical significance:
A wide variety of renal diseases can cause azotemia(increased blood urea ),which is divided in pre renal azotemia and post renal azotemia.
Pre renal Azotemia:
Identifying by an increase of plasma urea without concomitant increase of plasma creatinine:
Mild dehydration.1
High protein diet .2
Muscle wasting .3
Post renal azotemia:
Has its cause in conditions that obstruct urine outflow through the ureters ,bladder , or urethra .
Examples of these conditions are;
Nephrolithiasis.1
Prostatism.2
Tumors of genitourinary tract.3
(plasma urea and creatinine both rise).
Decrease levels may be seen in:
Low protein and high carbohydrate diets.1
Late pregnancy .2
Sever liver damage.3
تعليق