Abstract
BackgroundOur hypothesis was that both the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) and Modification of Diet in Renal Disease (MDRD) equations would underestimate directly measured GFR (mGFR) to a similar extent in people with diabetes and preserved renal function.MethodsIn a cross-sectional study, bias (eGFR – mGFR) was compared for the CKD-EPI and MDRD equations, after stratification for mGFR levels. We also examined the ability of the CKD-EPI compared with the MDRD equation to correctly classify subjects to various CKD stages. In a longitudinal study of subjects with an early decline in GFR i.e., initial mGFR >60 ml/min/1.73 m2 and rate of decline in GFR (ΔmGFR) > 3.3 ml/min/1.73 m2 per year, ΔmGFR (based on initial and final values) was compared with ΔeGFR by the CKD-EPI and MDRD equations over a mean of 9 years.ResultsIn the cross-sectional study, mGFR for the whole group was 80 ± 2.2 ml/min/1.73 m2 (n = 199, 75 % type 2 diabetes). For subjects with mGFR >90 ml/min/1.73 m2 (mGFR: 112 ± 2.0, n = 76), both equations significantly underestimated mGFR to a similar extent: bias for CKD-EPI: -12 ± 1.4 ml/min/1.73 m2 (p < 0.001) and for MDRD: -11 ± 2.1 ml/min/1.73 m2 (p < 0.001). Using the CKD-EPI compared with the MDRD equation did not improve the number of subjects that were correctly classified to a CKD-stage. No biochemical or clinical patient characteristics were identified to account for the under estimation of mGFR values in the normal to high range by the CKD-EPI equation. In the longitudinal study (n = 30, 66 % type 1 diabetes), initial and final mGFR values were 102.8 ± 6 and 54.6 ± 6.0 ml/min/1.73 m2, respectively. Mean ΔGFR (ml/min/1.73 m2 per year) was 6.0 by mGFR compared with only 3.0 by MDRD and 3.2 by CKD-EPI (both p < 0.05 vs mGFR)ConclusionsBoth the CKD-EPI and MDRD equations underestimate reference GFR values >90 ml/min/1.73 m2 as well as an early decline in GFR to a similar extent in people with diabetes. There is scope to improve methods for estimating an early decline in GFR.
Highlights
Our hypothesis was that both the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) and Modification of Diet in Renal Disease (MDRD) equations would underestimate directly measured GFR to a similar extent in people with diabetes and preserved renal function
Overall there was an excellent agreement between measured GFR (mGFR) and estimated gomerular filtration rate (eGFR) derived from the MDRD or CKD-EPI equations as assessed by the concordance correlation coefficient as shown in Fig. 1a and b (MDRD: rho_c =0.841, 95 % CI 0.801-0.881 and CKD-EPI: rho_c =0.864, 95 % CI 0.832-0.828)
body mass index (BMI) Body Mass Index, mGFR measured Glomerular Filtration Rate, MDRD Modification of Diet in Renal Disease, CKD-EPI Chronic Kidney Disease-Epidemiology Collaboration, albumin excretion rate (AER) Albumin Excretion Rate, Normo Normoalbuminuria, Micro Microalbuminuria, Macro Macroalbuminuria, Glycated haemoglobin (HbA1c) Glycated Haemoglobin, ACE Angiotensin Converting Enzyme, IHD Ischaemic Heart Disease, cerebrovascular disease (CVD) Cerebrovascular Disease, PVD Peripheral Vascular Disease to 30.9 between an eGFR derived from the MDRD equation and mGFR
Summary
Our hypothesis was that both the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) and Modification of Diet in Renal Disease (MDRD) equations would underestimate directly measured GFR (mGFR) to a similar extent in people with diabetes and preserved renal function. It has been reported to reduce bias compared to the MDRD equation for GFR > 60 ml/ min/1.73 m2 in various study populations [2, 3] This reduction in bias has been attributed to the characteristics of the populations from which the CKD-EPI and the MDRD equations were derived, with the mean measured GFR levels being 68 and 40 ml/min/1.73 m2 in these respective populations [1, 4]. The reasons for the apparent lack of improvement in the underestimation of reference GFR levels when an eGFR is derived from the CKD-EPI compared with the MDRD equation remain unclear
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