Renal Pathophysiology



Blood Urea Nitrogen to Plasma Creatinine Ratio In most patients with renal injury, the decline in GFR raises both the BUN and plasma creatinine concentration in proportion. As a result, the ratio be tween these parameters remains at 10 to 15:1, similar to that seen in normal patients. Prerenal disease represents an exception. Renal hypoperfusion is associated with an appropriate increase in proximal sodium and water reab sorption that are mediated in part by increased release of angiotensin II. The reabsorption of water raises the tubular fluid urea concentration, thereby leading to an equivalent elevation in proximal urea reabsorption. The incre ment in urea reabsorption will raise the BUN out of proportion to any change in GFR, thereby increasing the BUN-to-plasma creatinine ratio. A ratio > 20:1 is generally indicative of prerenal disease in the absence of a high-protein diet, increased tissue breakdown, gastrointestinal bleeding, or administration of corticosteroids all of which raise the BUN independent of the GFR. A normal ratio, however, is less useful. It can be seen with ATN but may also be seen in prerenal disease when urea production is reduced due to de creased protein intake or hepatic disease. Urine Sodium Concentration and Fractional Excretion of Sodium Sodium retention is an appropriate response to renal hypoperfusion that is partially impaired in ATN. Thus, the urine sodium concentration is generally < 20 mEq/L in prerenal disease but > 40 mEq/L in ATN. There is, however, appreciable overlap that is due in part to the urine sodium concentration be ing influenced by the rate of reabsorption of water as well as that of sodium. The confounding effect of water transport can be removed and the diag nostic accuracy increased by calculating the fractional excretion of sodium (FENa), which is a direct measure of the reabsorption of filtered sodium. (The formula for calculating the FENa is derived in Chapter 8.) A FENa < 1% (indi cating that more than 99% of the filtered sodium has been reabsorbed) sug gests prerenal disease, whereas a value > 2% is usually due to ATN. However, recall that normally over 99% of filtered sodium is reabsorbed (Chapter 1), so this calculation is most useful in the context of AKI and reduced GFR. Urine Osmolality Marked volume depletion is a potent stimulus to the release of antidiuretic hormone (See Chapter 2 and Fig. 2.4). This should result in a highly concen trated urine (osmolality > 500 mOsm/kg) when tubular function is intact, as in prerenal disease. In comparison, concentrating ability is impaired early in ATN because the medullary cells in the thick ascending limb are among the cells that are first damaged by renal ischemia. As a result, the urine is relatively isosmotic to the plasma in ATN, with the urine osmolality being between 300 and 350 mOsm/kg in most cases. There is, however, substantial overlap, so that only a high value > 500 mOsm/kg is of diagnostic importance.

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