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Creatinine versus cystatin C to estimate glomerular filtration rate in adults with congenital heart disease: Results of the Boston Adult Congenital Heart Disease Biobank - 14/07/19

Doi : 10.1016/j.ahj.2019.04.018 
Alexander R. Opotowsky, MD, MMSc a, b, , Matthew Carazo, MD a, b, Michael N. Singh, MD a, b, Konstantinos Dimopoulos, MD, MSc, PhD c, David A. Cardona-Estrada, MD d, Ahmed Elantably, MD d, Sushrut S. Waikar, MD, MPH b, Finnian R. Mc Causland, MBBCh, MMSc b, Gruschen Veldtman, MD e, Jasmine Grewal, MD f, Catherine Gray, BS a, Brittani N. Loukas, PA-C a, Saurabh Rajpal, MBBS, MD g
a Department of Cardiology, Boston Children's Hospital, Boston, MA, United States 
b Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA 
c Adult Congenital Heart Centre and Centre for Pulmonary Hypertension, Royal Brompton Hospital and National Heart and Lung Institute, Imperial College of Science and Medicine, London, United Kingdom 
d Department of Medicine, North Shore Medical Center, Salem, MA, USA 
e Adolescent and Adult Congenital Heart Disease Program, Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA 
f Pacific Adult Congenital Heart Disease Clinic, Division of Cardiology, St. Paul's Hospital, University of British Columbia, Vancouver, British Columbia, Canada 
g Ohio State University Division of Cardiovascular Medicine and Nationwide Children's Hospital Heart Center, Columbus, OH, USA 

Reprint requests: Alexander R. Opotowsky, Boston Children's Hospital and Brigham and Women's Hospital, 300 Longwood Ave, Department of Cardiology, Boston, MA 02115Boston Children's Hospital and Brigham and Women's HospitalDepartment of Cardiology300 Longwood AveBostonMA02115

Abstract

Background

Glomerular filtration rate is a key physiologic variable with a central role in clinical decision making and a strong association with prognosis in diverse populations. Reduced estimated glomerular filtration rate (eGFR) is common among adults with congenital heart disease (ACHD).

Methods

We conducted a prospective cohort study of outpatient ACHD ≥18 years old seen in 2012-2017. Creatinine and cystatin C were measured; eGFR was calculated using either the creatinine or cystatin C Chronic Kidney Disease–Epidemiology Collaboration equation (CKD-EPICr and CKD-EPICysC, respectively). Survival analysis was performed to define the relationship between eGFR and both all-cause mortality and a composite outcome of death or nonelective cardiovascular hospitalization.

Results

Our cohort included 911 ACHD (39 ± 14 years old, 49% female). Mean CKD-EPICr and CKD-EPICysC were similar (101 ± 20 vs 100 ± 23 mL/min/1.73 m2), but CKD-EPICr estimates were higher for patients with a Fontan circulation (n = 131, +10 ± 19 mL/min/1.73 m2). After mean follow-up of 659 days, 128 patients (14.1%) experienced the composite outcome and 31 (3.4%) died. CKD-EPICysC more strongly predicted all-cause mortality (eGFR <60 vs >90 mL/min/1.73 m2: CKD-EPICysC unadjusted HR = 20.2 [95% CI 7.6-53.1], C-statistic = 0.797; CKD-EPICr unadjusted HR = 4.6 [1.7-12.7], C-statistic = 0.620). CKD-EPICysC independently predicted the composite outcome, whereas CKD-EPICr did not (CKD-EPICysC adjusted HR = 3.0 [1.7-5.3]; CKD-EPICr adjusted HR = 1.5 [0.8-3.1]).

Patients reclassified to a lower eGFR category by CKD-EPICysC, compared with CKD-EPICr, were at increased risk for the composite outcome (HR = 2.9 [2.0-4.3], P < .0001); those reclassified to a higher eGFR class were at lower risk (HR = 0.5 [0.3-0.9], P = .03).

Conclusions

Cystatin C–based eGFR more strongly predicts clinical events than creatinine-based eGFR in ACHD. Creatinine-based methods appear particularly questionable in the Fontan circulation.

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Plan


 Funding sources: This work was conducted with support from Harvard Catalyst | The Harvard Clinical and Translational Science Center (National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health Award UL1 TR001102) and financial contributions from Harvard University and its affiliated academic health care centers. The content is solely the responsibility of the authors and does not necessarily represent the official views of Harvard Catalyst, Harvard University and its affiliated academic health care centers, or the National Institutes of Health. This work was also supported by an investigator-initiated study research grant from Roche Diagnostics (Indianapolis, IN). A. R. O. and M. S. are supported by the Dunlevie Family Fund.


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Vol 214

P. 142-155 - août 2019 Retour au numéro
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