Figure 123

Overview of blood urea nitrogen (BUN) and serum creatinine. Given the central role of BUN and serum creatinine in determining the presence of renal failure, an understanding of the metabolism of these substances is needed. Urea nitrogen derives from the breakdown of proteins that are delivered to the liver. Thus, the urea nitrogen production rate can vary with exogenous protein intake and endogenous protein catabolism. Urea nitrogen is a small, uncharged molecule that is not protein bound, and as such, it is readily filtered at the renal glomerulus. Urea nitrogen undergoes renal tubular reabsorption by specific transporters. This tubular reabsorption limits the value of BUN as a marker for glomerular filtration. However, the BUN usually correlates with the symptoms of uremia. By contrast, the production of creatinine is usually more constant unless there has been a marked reduction of skeletal muscle mass (eg, loss of a limb, prolonged starvation) or diffuse muscle injury. Although creatinine undergoes secretion into renal tubular fluid, this is very modest in degree. Thus, a steady-stable serum crea-tinine concentration is usually a relatively good marker of glomerular filtration rate as noted in Figure 12-5.

> 10

< 10

Increased protein intake

Starvation

Catabolic state

Advanced liver disease

Fever

Postdialysis state

Sepsis

Drugs that impair tubular secretion

Trauma

Cimetidine

Corticosteroids

Trimethoprim

Tissue necrosis

Rhabdomyolysis

Tetracyclines

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