03178nas a2200169   4500000000100000008004100001100001300042700001500055700002000070700001400090245026000104250001500364300001100379490000700390520256500397020004602962       2010                            d1 aWhite S.1 aChadban S.1 aPolkinghorne K.1 aAtkins R.00aComparison of the prevalence and mortality risk of CKD in Australia using the CKD Epidemiology Collaboration (CKD-EPI) and Modification of Diet in Renal Disease (MDRD) Study GFR estimating equations: the AusDiab (Australian Diabetes, Obesity and Lifestyle  a2010/02/09  a660-700 v553 a<p>
BACKGROUND: The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) is more accurate than the Modification of Diet in Renal Disease (MDRD) Study equation. We applied both equations in a cohort representative of the Australian adult population. STUDY DESIGN: Population-based cohort study. SETTING &amp; PARTICIPANTS: 11,247 randomly selected noninstitutionalized Australians aged &gt;or= 25 years who attended a physical examination during the baseline AusDiab (Australian Diabetes, Obesity and Lifestyle) Study survey. PREDICTORS &amp; OUTCOMES: Glomerular filtration rate (GFR) was estimated using the MDRD Study and CKD-EPI equations. Kidney damage was defined as urine albumin-creatinine ratio &gt;or= 2.5 mg/mmol in men and &gt;or= 3.5 mg/mmol in women or urine protein-creatinine ratio &gt;or= 0.20 mg/mg. Chronic kidney disease (CKD) was defined as estimated GFR (eGFR) &gt;or= 60 mL/min/1.73 m(2) or kidney damage. Participants were classified into 3 mutually exclusive subgroups: CKD according to both equations; CKD according to the MDRD Study equation, but no CKD according to the CKD-EPI equation; and no CKD according to both equations. All-cause mortality was examined in subgroups with and without CKD. MEASUREMENTS: Serum creatinine and urinary albumin, protein, and creatinine measured on a random spot morning urine sample. RESULTS: 266 participants identified as having CKD according to the MDRD Study equation were reclassified to no CKD according to the CKD-EPI equation (estimated prevalence, 1.9%; 95% CI, 1.4-2.6). All had an eGFR &gt;or= 45 mL/min/1.73 m(2) using the MDRD Study equation. Reclassified individuals were predominantly women with a favorable cardiovascular risk profile. The proportion of reclassified individuals with a Framingham-predicted 10-year cardiovascular risk &gt;or= 30% was 7.2% compared with 7.9% of the group with no CKD according to both equations and 45.3% of individuals retained in stage 3a using both equations. There was no evidence of increased all-cause mortality in the reclassified group (age- and sex-adjusted hazard ratio vs no CKD, 1.01; 95% CI, 0.62-1.97). Using the MDRD Study equation, the prevalence of CKD in the Australian population aged &gt;or= 25 years was 13.4% (95% CI, 11.1-16.1). Using the CKD-EPI equation, the prevalence was 11.5% (95% CI, 9.42-14.1). LIMITATIONS: Single measurements of serum creatinine and urinary markers. CONCLUSIONS: The lower estimated prevalence of CKD using the CKD-EPI equation is caused by reclassification of low-risk individuals.
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