Expressing the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) Cystatin C Equations for Estimating GFR With Standardized Serum Cystatin C Values
Available from: PubMed Central
- "m2) = [127.7 × cystatin C−1.17 (mg/l) × age−0.13 × 0.91 (if female) × 1.06 (if African-American)] (27,28). "
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ABSTRACT: The aim of the present study was to explore the association between the cystatin C-based estimated glomerular filtration rate (eGFRcys) and the SYNTAX score (SXscore) in patients with diabetes. To the best of our knowledge, this correlation has not been reported previously. The eGFRcys and SXscore from 612 consecutive patients with diabetes were retrospectively included in this study. The patients were angiographically diagnosed with coronary artery disease (CAD) between July 2010 and March 2012 at the Department of Endocrinology. The SXscore was calculated using a previously described SXscore algorithm. Pearson correlations were used to analyze the correlation between eGFRcys and SXscore. Patients with renal dysfunction were older, more often female and more likely to have a history of hypertension when compared with those with normal renal function. The eGFRcys values were significantly lower and the cystatin C levels were significantly higher in the highest SXscore group than those in other groups (P<0.001). Correlation analysis indicated that eGFRcys was negatively correlated with the SXscore (r=-0.7918, P<0.001). In addition, a significantly positive correlation was identified between levels of cystatin C and the SXscore (r=0.8891, P<0.001). In conclusion, eGFRcys is an independent predictor of SXscore in patients with diabetes. The eGFRcys-estimating method may be considered important in the assessment of the SXscore in patients with diabetes.
Available from: Gijs Van Pottelbergh
- "The assay displayed total coefficient of variation from 2.3% to 4.3% (0.8 to 7.1 mg/L). The assay was run according to the manufacturer’s instructions and standards provided and met the new cystatin C International Federation of Clinical Chemistry and Laboratory Medicine standardization . "
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ABSTRACT: The prevalence of chronic kidney disease (CKD) increases with age, and new glomerular filtration rate-estimating equations have recently been validated. The epidemiology of CKD in older individuals and the relationship between a low estimated glomerular filtration rate as calculated by these equations and adverse outcomes remains unknown.
Data from the BELFRAIL study, a prospective, population-based cohort study of 539 individuals aged 80 years and older, were used. For every participant, five equations were used to calculate estimated glomerular filtration rate based on serum creatinine and/or cystatin C values: MDRD, CKD-EPIcreat, CKD-EPIcyst, CKD-EPIcreatcyst, and BIS equations. The outcomes analyzed included mortality combined with the necessity of new renal replacement therapy, severe cardiovascular events, and hospitalization.
During the follow-up period, which was an average of 2.9 years, 124 participants died, 7 required renal replacement therapy, 271 were hospitalized, and 73 had a severe cardiovascular event. The prevalence of estimated glomerular filtration rate values <60 mL/min/1.73 m2 differed depending on the equation used as follows: 44% (MDRD), 45% (CKD-EPIcreat), 75% (CKD-EPIcyst), 65% (CKD-EPIcreatcyst), and 80% (BIS). All of the glomerular filtration rate-estimating equations revealed that higher cardiovascular mortality was associated with lower estimated glomerular filtration rates and that higher probabilities of hospitalization were associated with estimated glomerular filtration rates <30 mL/min/1.73 m2. A lower estimated glomerular filtration rate did not predict a higher probability of severe cardiovascular events, except when using the CKD-EPIcyst equation. By calculating the net reclassification improvement, CKD-EPIcyst and CKD-EPIcreatcyst were shown to predict mortality (+25% and +18%) and severe cardiovascular events (+7% and +9%) with the highest accuracy. The BIS equation was less accurate in predicting mortality (-12%).
Higher prevalence of CKD were found using the CKD-EPIcyst, CKD-EPIcreatcyst, and BIS equations compared with the MDRD and CKD-EPIcreat equations. The new CKD-EPIcreatcyst and CKD-EPIcyst equations appear to be better predictors of mortality and severe cardiovascular events.
Available from: Jeffrey R Schelling
- "× age−0.203 × 0.742 (if female) × 1.212 (if African American) prior to May 20, 2007 , or eGFRcreat (mL/min/1.73 m2) = 175 × creatinine (mg/dL)−1.154 "
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Diabetic nephropathy is a growing clinical problem, and the cause for >40% of incident ESRD cases. Unfortunately, few modifiable risk factors are known. The objective is to examine if albuminuria and history of diabetic nephropathy (DN) in a sibling are associated with early DN progression or mortality.
In this longitudinal study of adults >18 yrs with diabetes monitored for up to 9 yrs (mean 4.6 ± 1.7 yrs), 435 subjects at high risk (DN family history) and 400 at low risk (diabetes >10 yrs, normoalbuminuria, no DN family history) for DN progression were evaluated for rate of eGFR change using the linear mixed effects model and progression to ESRD. All-cause mortality was evaluated by Kaplan-Meier analyses while controlling for baseline covariates in a Cox proportional hazards model. Covariates included baseline eGFR, age, gender, race, diabetes duration, blood pressure, hemoglobin A1c and urine albumin:creatinine ratio. Propensity score matching was used to identify high and low risk group pairs with balanced covariates. Sensitivity analyses were employed to test for residual confounding.
Mean baseline eGFR was 74 ml/min/1.73 m2 (86% of cohort >60 ml/min/1.73 m2). Thirty high risk and no low risk subjects developed ESRD. eGFR decline was significantly greater in high compared to low risk subjects. After controlling for confounders, change in eGFR remained significantly different between groups, suggesting that DN family history independently regulates GFR progression. Mortality was also significantly greater in high versus low risk subjects, but after controlling for baseline covariates, no significant difference was observed between groups, indicating that factors other than DN family history more strongly affect mortality. Analyses of the matched pairs confirmed change in eGFR and mortality findings. Sensitivity analyses demonstrated that the eGFR results were not due to residual confounding by unmeasured covariates of a moderate effect size in the propensity matching.
Diabetic subjects with albuminuria and family history of DN are vulnerable for early GFR decline, whereas subjects with diabetes for longer than 10 years, normoalbuminuria and negative family history, experience slower eGFR decline, and are extremely unlikely to require dialysis. Although we would not recommend that patients with low risk characteristics be neglected, scarce resources would be more sensibly devoted to vulnerable patients, such as the high risk cases in our study, and preferably prior to the onset of albuminuria or GFR decline.
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