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  • 1
    Abstract: Background: Despite standard laboratory quality control, drift and day-to-day variability in cystatin C measurements can be observed. We investigated whether correction for drift and day-to-day variation in cystatin C measurements improves the association of estimated glomerular filtration rate (eGFR) with chronic kidney disease (CKD) risk factors and prognosis. Methods: Plasma samples of the PREVEND study (Dutch cohort study, n = 8592) were used to measure cystatin C (Gentian assay) on 243 random days. A correction factor was calculated for each measurement day. GFR was estimated with CKD-EPI equation using routinely measured cystatin C (eGFR(cysC)) and corrected cystatin C (eGFR(cysC corr)). Participants were categorized in six categories of eGFR(cysC) and eGFR(cysC corr) : 〉= 120, 90-119, 75-89, 60-74, 45-59 and 〈 45 mL/min/1.73m(2). Independent replication was performed in the ESTHER study (German cohort study, n = 9949). Results: Compared to non-reclassified participants, participants re-classified upward had significantly lower age, body mass index, blood pressure, cholesterol, glucose and albuminuria, whereas the opposite was true for participants reclassified downward. CKD risk factors explained more variance in eGFR cysC corr than in eGFR cysC (p 〈 0.001). Compared to non-reclassified participants, risk of incident cardiovascular events (n = 789, follow-up 9.3 +/- 2.7 years) tended to be higher in downward reclassified and lower in upward reclassified participants. Net reclassification improvement for incident cardiovascular events using eGFR(cysC corr) was positive (0.102, p = 0.019). The ESTHER study showed similar results. Conclusions: Correction for drift and day-to-day variation in cystatin C measurement improves eGFR using cystatin C for its association with CKD risk factors and incident cardiovascular events.
    Type of Publication: Journal article published
    PubMed ID: 25415637
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  • 2
    Abstract: Background Chronic kidney disease is characterised by low estimated glomerular fi ltration rate (eGFR) and high albuminuria, and is associated with adverse outcomes. Whether these risks are modifi ed by diabetes is unknown. Methods We did a meta-analysis of studies selected according to Chronic Kidney Disease Prognosis Consortium criteria. Data transfer and analyses were done between March, 2011, and June, 2012. We used Cox proportional hazards models to estimate the hazard ratios (HR) of mortality and end-stage renal disease (ESRD) associated with eGFR and albuminuria in individuals with and without diabetes. Findings We analysed data for 1 024 977 participants (128 505 with diabetes) from 30 general population and highrisk cardiovascular cohorts and 13 chronic kidney disease cohorts. In the combined general population and highrisk cohorts with data for all-cause mortality, 75 306 deaths occurred during a mean follow-up of 8.5 years (SD 5.0). In the 23 studies with data for cardiovascular mortality, 21 237 deaths occurred from cardiovascular disease during a mean follow-up of 9.2 years (SD 4.9). In the general and high-risk cohorts, mortality risks were 1.2-1.9 times higher for participants with diabetes than for those without diabetes across the ranges of eGFR and albumin-tocreatinine ratio (ACR). With fi xed eGFR and ACR reference points in the diabetes and no diabetes groups, HR of mortality outcomes according to lower eGFR and higher ACR were much the same in participants with and without diabetes (eg, for all-cause mortality at eGFR 45 mL/min per 1.73 m y [vs 95 mL/min per 1.73 m y], HR 1.35; 95% CI 1.18-1.55; vs 1.33; 1.19-1.48 and at ACR 30 mg/g [vs 5 mg/g], 1.50; 1.35-1.65 vs 1.52; 1.38-1.67). The overall interactions were not signifi cant. We identifi ed much the same fi ndings for ESRD in the chronic kidney disease cohorts. Interpretation Despite higher risks for mortality and ESRD in diabetes, the relative risks of these outcomes by eGFR and ACR are much the same irrespective of the presence or absence of diabetes, emphasising the importance of kidney disease as a predictor of clinical outcomes.
    Type of Publication: Journal article published
    PubMed ID: 23013602
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