Measuring glomerular filtration rate in the intensive care unit: no substitutes please

Abstract

Acute kidney injury (AKI), due to its increasing incidence, associated morbidity and mortality, and potential for development of chronic kidney disease with acceleration to end-stage renal disease, has become of major interest to nephrologists and critical care physicians. The development of biomarkers to diagnose AKI, quantify risk and predict prognosis is receiving considerable attention. Yet techniques to accurately assess functional changes within patients still rely on the use of an insensitive marker (creatinine), creatinine-based estimating equations and unreliable urinary tests. Therefore, it is critical that functional tests be developed and used in combination with biomarkers, thus allowing improved care in AKI and chronic kidney disease patient populations.

Figure 1

Serum creatinine is an insensitive marker of the glomerular filtration rate. With loss of the glomerular filtration rate (GFR) the renal reserve may be first lost, reducing the maximally stimulated GFR. Thereafter, as the GFR is lost the serum creatinine (SCr) does not rise until the GFR is reduced to around 50 to 60 ml/minute/1.73 m². Therefore, up to two-thirds of the patient’s original GFR has been lost before changes in SCr occur.