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The glomerular filtration rate (GFR) is widely accepted as the best overall index of kidney function in health and disease. However, GFR is difficult to measure and is commonly estimated from the serum level of endogenous filtration markers, such as creatinine. Recently, Chertow et al.1 found that an increase of serum creatinine (SCr) of > 0.3 mg/dl ( > 26.5 µmol/l) was independently associated with mortality. Similarly, Lassnigg et al.3 saw, in a cohort of patients who underwent cardiac surgery, that either an increase of SCr ≥ 0.5 mg/dl ( ≥ 44.2 µmol/l) or a decrease > 0.3 mg/dl ( > 26.5 µmol/l) was associated with worse survival. The reasons why small alterations in SCr lead to increases in hospital mortality are not entirely clear. Possible explanations include the untoward effects of decreased kidney function such as volume overload, retention of uremic compounds, acidosis, electrolyte disorders, increased risk for infection, and anemia.6 Although, these changes in SCr could simply be colinear with unmeasured variables that lead to increased mortality, multiple attempts to control for known clinical variables has led to the consistent conclusion that decreased kidney function is independently associated with outcome. Furthermore, more severe reductions in kidney function tend to be associated with even worse outcome as compared to milder reductions.
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