Colin Geddes

The reliable measurement of renal excretory function is of great importance in clinical practice and in research. The introduction of routine reporting of estimated glomerular filtration rate and a new definition of chronic kidney disease has renewed interest in methods of measuring renal function. Coupled with this is the fact that several countries are moving towards population screening for renal impairment to try to reduce the associated increased cardiovascular risk. Accurate measurement is methodologically difficult so surrogate measures such as serum creatinine levels and prediction formulas (based on factors such as the patient's age, sex, and serum creatinine level) are more commonly used in routine practice. We describe routine and more specialised methods of assessing renal function and discuss estimated glomerular filtration rate. The kidney has several interlinked functions (box). These depend on glomerular filtration rate, the unit measure of kidney function. Glomerular filtration rate can be defined as the volume of plasma cleared of an ideal substance per unit of time (usually expressed as ml/min). The ideal substance is one that is freely filtered at the glomerulus and neither secreted nor reabsorbed by the renal tubules. Creatinine is the closest to an ideal endogenous substance for measuring glomerular filtration rate.w1 Plasma creatinine is almost exclusively a product of the metabolism of creatine and phosphocreatine in skeletal muscle, although ingestion of meat may also contribute slightly.w2 w3 In patients with stable renal function, serum creatinine levels are usually constant, with variability daily of about only 8%.w4 w5 Creatinine is freely filtered at the glomerulus and is not reabsorbed, but up to 15% is actively secreted by the tubules.w6 In advanced renal failure, excretion of creatinine through the gastrointestinal tract increases.w7 Measuring the creatinine clearance using serum creatinine level and a timed urine collection gives an …

There is a trend to start dialysis earlier in patients with chronic renal failure. Studies that suggest improved survival from earlier initiation of dialysis are flawed in that they have measured survival from start of dialysis rather than from a time point before dialysis, when patients have the same renal function. This flaw is termed lead-time bias. Using the electronic patient record at the renal unit of Glasgow Royal Infirmary, all patients were identified who had received dialysis for chronic renal failure and who had sufficient data to calculate the time point at which they reached an estimated creatinine clearance (eC(Cr)) of 20 ml/min (n = 275). This date was used to time survival. The patients were divided into early and late start groups by the median eC(Cr) for all patients at initiation of dialysis, which was 8.3 ml/min. There was no significant benefit in patient survival from earlier initiation of dialysis. A Cox proportional hazards model demonstrated a significant inverse relationship between eC(Cr) at start of dialysis and survival (hazard ratio, 1.1; P = 0.02), i.e., patients who started dialysis with a lower eC(Cr) tended to survive longer. This relationship retained significance when gender, age, weight, presence of diabetes, mode of first dialysis, initial dialysis access, hemoglobin, serum albumin, blood leukocyte count, Wright/Khan index, and eC(Cr) at the start of dialysis were taken into account. This study fails to support a policy of earlier initiation of dialysis for patients with end-stage renal failure.