Improving the clinical value of estimating glomerular filtration rate by reporting all values: a contrarian viewpoint.

The serious limitations of the estimating glomerular filtration rate (eGFR) appear related not to a shortcoming of the equation, but to the futility of trying to force agreement between two inherently different parameters: a blood marker of kidney function with a very stable concentration (creatinine) and a renal filtration parameter that fluctuates continually (glomerular filtration rate, GFR). Although GFR is regarded as the ultimate determinant of kidney function, it may be less ideal as an early clinical marker to detect declining kidney function. Another shortcoming of GFR is that it has significant overlap between health and kidney disease states categorized according to stage I, II, etc. Serum creatinine has a real and measurable increase as kidney function declines, but this is often masked when creatinine is plotted on a scale of 1.0 mg/dl (88 micromol/l), which is well above the detection limit of modern creatinine methods of about 0.05 mg/dl. A new equation to estimate GFR, the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) creatinine equation, modestly improves accuracy from 80.6% of the Modification of Diet in Renal Disease eGFRs being within 30% of the measured GFR, to 84.1% of the CKD-EPI eGFRs being within 30% of the measured GFR. Creatinine methods have recently been standardized to an isotope dilution mass stectrometry reference method. While this will lessen the systematic bias between methods, it will have no effect on either the imprecision of a particular creatinine method or on the inherent random differences between serum creatinine (or eGFR) and actual GFR. Finally, the eGFR is not recommended for reporting until it is well below a reference range for those with no kidney disease. However, if the eGFR were properly regarded as an age-, gender-, and race-adjusted serum creatinine, it could be reported at all values and become a more clinically useful parameter.

Duke Scholars

Author John Griffith Toffaletti Pathology