GFR Estimating Equations

Rule, Andrew D.; Glassock, Richard J.

doi:10.2215/cjn.01240213

Cited by 63 publications

(56 citation statements)

References 54 publications

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“…2 The CKDEpidemiology Collaboration formula was used in all association models because it is considered the best way to estimate GFR in general population-cohort studies. 31 We also estimated GFR with the MDRD 175 study equation to facilitate comparisons with other surveys.…”

Section: Definitionsmentioning

confidence: 99%

Prevalence of CKD and Its Relationship to eGFR-Related Genetic Loci and Clinical Risk Factors in the SardiNIA Study Cohort

Pani

Bragg‐Gresham

Masala

et al. 2014

Journal of the American Society of Nephrology

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The prevalence of CKD and of renal failure vary worldwide, yet parallel increases in leading risk factors explain only part of the differential prevalence. We measured CKD prevalence and eGFR, and their relationship with traditional and additional risk factors, in a Sardinian founder population cohort. The eGFR was calculated using equations from the CKD Epidemiology Collaboration and Modification of Diet in Renal Disease studies. With use of the Kidney Disease Improving Global Outcomes guidelines, a cross-sectional analysis of 4842 individuals showed that CKD prevalence was 15.1%, including 3.6% of patients in the high-risk and 0.46% in the very-high-risk categories. Longitudinal analyses performed on 4074 of these individuals who completed three visits with an average follow-up of 7 years revealed that, consistent with other populations, average eGFR slope was 20.79 ml/min per 1.73 m 2 per year, but 11.4% of the participants had an eGFR decline .2.3 ml/min per 1.73 m 2 per year (fast decline). A genetic score was generated from 13 reported eGFR-and CKDrelated loci, and univariable and multivariable analyses were applied to assess the relationship between clinical, ultrasonographic, and genetic variables with three outcomes: CKD, change in eGFR, and fast eGFR decline. Genetic risk score, older age, and female sex independently correlated with each outcome. Diabetes was associated with CKD prevalence, whereas hypertension and hyperuricemia correlated more strongly with fast eGFR decline. Diabetes, hypertension, hyperuricemia, and high baseline eGFR were associated with a decline of eGFR. Along with differential health practices, population variations in this spectrum of risk factors probably contributes to the variable CKD prevalence worldwide.

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Section: Definitionsmentioning

confidence: 99%

Prevalence of CKD and Its Relationship to eGFR-Related Genetic Loci and Clinical Risk Factors in the SardiNIA Study Cohort

Pani

Bragg‐Gresham

Masala

et al. 2014

Journal of the American Society of Nephrology

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“…16 The superior performance of cystatin C or the combination of creatinine and cystatin C versus creatinine alone to estimate GFR and predict CKD outcomes has been repeatedly demonstrated. 15,[23][24][25] Furthermore, reduced values for eGFR cys and eGFR creat-cys have a consistent linear association with increased risk of death for all eGFR levels below approximately 85 ml/min per 1.73 m 2 , which is well above the threshold of 60 ml/min per 1.73 m 2 for the detection of CKD with a creatinine-based eGFR. 16,26,27 However, cystatin C-based eGFR has limitations for an association with CKD risk factors as such and outcomes similar to that of measured GFR.…”

Section: Ert In Fdmentioning

confidence: 68%

“…16,26,27 However, cystatin C-based eGFR has limitations for an association with CKD risk factors as such and outcomes similar to that of measured GFR. 25 Furthermore, already Inker et al mentioned that unmeasured and largely unknown non-GFR determinants of cystatin C are similar in magnitude to those of creatinine. 15 In this respect, the equation that combines creatinine and cystatin C provides the Values are given as n (%) or as otherwise indicated.…”

Section: Ert In Fdmentioning

confidence: 99%

“…In that respect, Perkins and colleagues demonstrated the accuracy of the cystatin C-based GFR equation to detect eGFR decline over time, especially in patients with diabetes with normal or even high GFR values 28 ; however, the use of cystatin C in patients with hyperfiltration is controversially discussed. 25 Indeed, the primary goal of our study was to assess effects of the change or reduction of ERT on renal function between baseline and the 2-year follow-up visit and the discrimination of clinical outcomes. In this respect, we determined eGFR by the CKD-EPI formula on the basis of creatinine, cystatin C, and the combination of both.…”

Section: Ert In Fdmentioning

confidence: 99%

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Patients with Fabry Disease after Enzyme Replacement Therapy Dose Reduction and Switch–2-Year Follow-Up

Lenders¹,

Canaan–Kühl²,

Krämer

et al. 2016

Journal of the American Society of Nephrology

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Because of the shortage of agalsidase-b supply between 2009 and 2012, patients with Fabry disease either were treated with reduced doses or were switched to agalsidase-a. In this observational study, we assessed end organ damage and clinical symptoms with special focus on renal outcome after 2 years of dose-reduction and/or switch to agalsidase-a.Atotalof89adultpatientswithFabrydiseasewhohadreceivedagalsidase-b (1.0mg/kgbodywt)for.1 yearwerenonrandomlyassignedtocontinuethistreatmentregimen(regular-dosegroup,n=24),toreceiveareduced dose of 0.3-0.5 mg/kg and a subsequent switch to 0.2 mg/kg agalsidase-a (dose-reduction-switch group, n=28), or to directly switch to 0.2 mg/kg agalsidase-a (switch group, n=37) and were followed-up for 2 years. We assessed clinical events (death, myocardial infarction, severe arrhythmia, stroke, progression to ESRD), changes in cardiac and renal function, Fabry-related symptoms (pain, hypohidrosis, diarrhea), and disease severity scores. Determination of renal functionbycreatinineandcystatinC-basedeGFRrevealeddecreasingeGFRsinthedose-reduction-switchgroupand the switch group. The Mainz Severity Score Index increased significantly in these two groups (P=0.02 and P,0.001, respectively), and higher frequencies of gastrointestinal pain occurred during follow-up. In conclusion, after 2 years of observation,allgroupsshowedastableclinicaldiseasecoursewithrespecttoseriousclinicalevents.However,patients under agalsidase-b dose-reduction and switch or a direct switch to agalsidase-a showed a decline of renal function independent of the eGFR formula used.

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“…GFR-estimating equations have clearly been a major advance in detection of patients with CKD and the epidemiologic study of CKD and its outcomes, although concerns remain about their imperfections and risk of misdiagnosis (50)(51)(52)(53). However, they are just estimating equations; clinicians who use them should be familiar with their strengths and weaknesses and understand their potential for significant inaccuracy.…”

Section: Discussionmentioning

confidence: 99%

Clinical Decision Making in a Patient with Stage 5 CKD—Is eGFR Good Enough?

Berns

2015

Clinical Journal of the American Society of Nephrology

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The development and widespread use of serum creatinine concentration-based prediction equations to calculate eGFR have been major advances for detection of patients with CKD and the epidemiologic study of CKD and its outcomes. However, these equations as well as those that also incorporate serum cystatin C concentration provide GFR estimates that, although reasonably precise on average, can differ markedly and in clinically important ways from actual GFR. Thus, it is important that clinicians who use these equations for clinical decisionmaking be familiar with their strengths and weaknesses and have an appreciation of their potential for error. More precise knowledge of actual GFR is important in certain clinical circumstances, including, as presented in this Attending Rounds, patients with stage 5 CKD, in whom decisions regarding dialysis initiation are necessary. Nephrologists should have the ability to accurately determine GFR when needed if clinical circumstances suggest inaccuracy of the calculated eGFR reported by the clinical laboratory.

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GFR Estimating Equations

Cited by 63 publications

References 54 publications

Prevalence of CKD and Its Relationship to eGFR-Related Genetic Loci and Clinical Risk Factors in the SardiNIA Study Cohort

Prevalence of CKD and Its Relationship to eGFR-Related Genetic Loci and Clinical Risk Factors in the SardiNIA Study Cohort

Patients with Fabry Disease after Enzyme Replacement Therapy Dose Reduction and Switch–2-Year Follow-Up

Clinical Decision Making in a Patient with Stage 5 CKD—Is eGFR Good Enough?

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