![]() ![]() It reflects absolute or relative hypovolemia, with vasoconstriction and sodium retention as a consequence of activation of the sympathoadrenal, renin-angiotensin-aldosterone, and antidiuretic hormone systems. With two very important exceptions (sepsis and liver failure), it is reversed by restoration of normal renal hemodynamics. In contrast, when postoperative ATN occurs, it is often a culmination of multiple lesser insults in a protected milieu, resulting in nonoliguric renal failure, defined as ARF with urine flow 15 to 80 mL/hour. In summary, oliguria is common but seldom implies ARF, but the presence of a normal urine flow rate does not exclude it. When ARF does ensue, loss of renal solute clearance begins to result in the buildup of serum concentrations of electrolytes, urea, water, and other osmotic elements (azotemia). Blood urea nitrogen and S Cr are the most commonly used indicators of renal function. Urea depends on tubular excretion but may be a misleading surrogate for tubular function because its blood level is affected by nonrenal pathology, such as gastrointestinal hemorrhage and protein catabolism (abnormally increased) or malnutrition and end-stage liver disease (abnormally decreased). ![]() S Cr reflects the balance between creatinine production and excretion. These come into equilibrium when renal function is in a steady state. Therefore, S Cr is a reliable surrogate for GFR. ![]() However, the relationship between S Cr and GFR is not direct it is exponentially inverse. That is, a doubling of S Cr implies a halving of GFR. Thus, a “trivial” increase in S Cr from 0.6 to 1.2 mg/dL implies a 50% decrease in GFR. In cachectic patients with low creatinine production, S Cr may be “normal” with a GFR as low as 30 mL/minute.Ĭreatinine clearance = ) × Weight × 1.73 m 2 × 0.85* ] 72 × S Cr × Body Surface area * Moreover, S Cr does not increase above normal limits until GFR has decreased below 50 mL/minute. ![]()
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