Rupal Mehta1, Hongyan Ning2, Nisha Bansal3, Jordana Cohen4, Anand Srivastava5, Mirela Dobre6, Erin D Michos7, Mahboob Rahman6, Raymond Townsend4, Stephen Seliger8, James P Lash9, Tamara Isakova5, Donald M Lloyd-Jones10, Sadiya S Khan10. 1. Division of Nephrology and Hypertension, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois; Center for Translational Metabolism and Health, Institute for Public Health and Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois; Jesse Brown Veterans Administration Medical Center; Chicago, Illinois. Electronic address: rupal.mehta@northwestern.edu. 2. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois. 3. Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington. 4. Division of Nephrology, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. 5. Division of Nephrology and Hypertension, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois; Center for Translational Metabolism and Health, Institute for Public Health and Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois. 6. Division of Nephrology and Hypertension, Department of Medicine, University Hospitals Cleveland Medical Center, Case Western Reserve University, Cleveland, Ohio. 7. Division of Cardiology, Department of Medicine, John Hopkins School of Medicine, Baltimore, Maryland. 8. Division of Nephrology, Department of Medicine, University of Maryland Medical Center, Baltimore, Maryland. 9. Division of Nephrology, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois. 10. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Abstract
BACKGROUND: Heart failure (HF) is a leading contributor to cardiovascular morbidity and mortality in the population with chronic kidney disease (CKD). HF risk prediction tools that use readily available clinical parameters to risk-stratify individuals with CKD are needed. METHODS: We included Black and White participants aged 30-79 years with CKD stages 2-4 who were enrolled in the Chronic Renal Insufficiency Cohort (CRIC) study and were without self-reported cardiovascular disease. We assessed model performance of the Pooled Cohort Equations to Prevent Heart Failure (PCP-HF) to predict incident hospitalizations due to HF and refit the PCP-HF in the population with CKD by using CRIC data-derived coefficients and survival from CRIC study participants in the CKD population (PCP-HFCKD). We investigated the improvement in HF prediction with inclusion of estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) into the PCP-HFCKD equations by change in C-statistic, net reclassification improvement (NRI), and integrated discrimination improvement index (IDI). We validated the PCP-HFCKD with and without eGFR and UACR in Multi-Ethnic Study of Atherosclerosis (MESA) participants with CKD. RESULTS: Among 2328 CRIC Study participants, 340 incident HF hospitalizations occurred over a mean follow-up of 9.5 years. The PCP-HF equations did not perform well in most participants with CKD and had inadequate discrimination and insufficient calibration (C-statistic 0.64-0.71, Greenwood-Nam-D'Agostino (GND) chi-square statistic P value < 0.05), with modest improvement and good calibration after being refit (PCP-HFCKD: C-statistic 0.61-0.78), GND chi-square statistic P value > 0.05). Addition of UACR, but not eGFR, to the refit PCP-HFCKD improved model performance in all race-sex groups (C-statistic [0.73-0.81], GND chi-square statistic P value > 0.05, delta C-statistic ranging from 0.03-0.11 and NRI and IDI P values < 0.01). External validation of the PCP-HFCKD in MESA demonstrated good discrimination and calibration. CONCLUSIONS: Routinely available clinical data that include UACR in patients with CKD can reliably identify individuals at risk of HF hospitalizations.
BACKGROUND: Heart failure (HF) is a leading contributor to cardiovascular morbidity and mortality in the population with chronic kidney disease (CKD). HF risk prediction tools that use readily available clinical parameters to risk-stratify individuals with CKD are needed. METHODS: We included Black and White participants aged 30-79 years with CKD stages 2-4 who were enrolled in the Chronic Renal Insufficiency Cohort (CRIC) study and were without self-reported cardiovascular disease. We assessed model performance of the Pooled Cohort Equations to Prevent Heart Failure (PCP-HF) to predict incident hospitalizations due to HF and refit the PCP-HF in the population with CKD by using CRIC data-derived coefficients and survival from CRIC study participants in the CKD population (PCP-HFCKD). We investigated the improvement in HF prediction with inclusion of estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) into the PCP-HFCKD equations by change in C-statistic, net reclassification improvement (NRI), and integrated discrimination improvement index (IDI). We validated the PCP-HFCKD with and without eGFR and UACR in Multi-Ethnic Study of Atherosclerosis (MESA) participants with CKD. RESULTS: Among 2328 CRIC Study participants, 340 incident HF hospitalizations occurred over a mean follow-up of 9.5 years. The PCP-HF equations did not perform well in most participants with CKD and had inadequate discrimination and insufficient calibration (C-statistic 0.64-0.71, Greenwood-Nam-D'Agostino (GND) chi-square statistic P value < 0.05), with modest improvement and good calibration after being refit (PCP-HFCKD: C-statistic 0.61-0.78), GND chi-square statistic P value > 0.05). Addition of UACR, but not eGFR, to the refit PCP-HFCKD improved model performance in all race-sex groups (C-statistic [0.73-0.81], GND chi-square statistic P value > 0.05, delta C-statistic ranging from 0.03-0.11 and NRI and IDI P values < 0.01). External validation of the PCP-HFCKD in MESA demonstrated good discrimination and calibration. CONCLUSIONS: Routinely available clinical data that include UACR in patients with CKD can reliably identify individuals at risk of HF hospitalizations.
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