Echocardiography to Screen for Pulmonary Hypertension in CKD
© 2020 International Society of Nephrology Introduction: Pulmonary hypertension (PH) is a common yet incompletely understood complication of chronic kidney disease (CKD). Although transthoracic echocardiogram is commonly used to noninvasively estimate PH, it has not been validated in a CKD population. We investigated the utility of this diagnostic tool for CKD-associated PH in a large right heart catheterization (RHC) cohort. Methods: We reviewed RHC and echocardiography data in 4036 patients (1714 with CKD) obtained between 2011 and 2014 at a single center. We used multivariate regression to determine the associations of echocardiography measurements with PH, and evaluated whether estimated glomerular filtration rate (eGFR) modified these associations. Using internal validation, we sequentially added measurements to predictive models and analyzed the incremental predictive performance using the change in the area under the receiver operating characteristic curve (ΔAUC) and net reclassification improvement. Results: The echocardiography measurements most strongly associated with the diagnosis of PH included tricuspid regurgitant velocity (TRV), tricuspid annular plane systolic excursion (TAPSE), right atrial pressure, diastolic dysfunction, and right ventricular function. Among these measurements, eGFR significantly modified the associations of TAPSE and diastolic dysfunction with the diagnosis of PH. The model consisting of a combination of TRV, right atrial pressure, and TAPSE most accurately predicted the diagnosis of PH in a CKD population (AUC 0.82). Conclusions: The optimal model to predict PH diagnosis included TRV, right atrial pressure, and TAPSE. Since TAPSE more strongly associated with PH in the CKD population, these findings support a CKD-specific approach to the development of noninvasive screening algorithms for PH.
Published Version (Please cite this version)
Edmonston, Daniel L, Sudarshan Rajagopal and Myles Wolf (2020). Echocardiography to Screen for Pulmonary Hypertension in CKD. Kidney International Reports, 5(12). pp. 2275–2283. 10.1016/j.ekir.2020.09.033 Retrieved from https://hdl.handle.net/10161/22283.
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My primary research focus lies at the intersection of kidney and cardiovascular disease including pulmonary hypertension, heart failure, and atherosclerotic disease in patients with chronic kidney disease.
I am a physician-scientist with a research focus on G protein-coupled receptor signaling in inflammation and vascular disease and a clinical focus on pulmonary vascular disease, as I serve as Co-Director of the Duke Pulmonary Vascular Disease Center. My research spans the spectrum from clinical research in pulmonary vascular disease, to translational research in cardiovascular disease, to the basic science of receptor signaling.
Our basic science resesarch focuses on understanding and untapping the signaling potential of G protein-coupled receptors (GPCRs) to regulate inflammation in vascular disease. GPCRs are the most common transmembrane receptors in the human genome (over 800 members) and are some of the most successful targets for drug therapies. While it has been known for some time that these receptors signal through multiple downstream effectors (such as heterotrimeric G proteins and multifunctional beta arrestin adapter proteins), over the past decade it has been better appreciated that these receptors are capable of signaling with different efficacies to these effectors, a phenomenon referred to as “biased agonism”. Ligands can be biased, by activating different pathways from one another, and receptors can be biased, by signaling to a limited number of pathways that are normally available to them. Moreover, this phenomenon also appears to be common to other transmembrane and nuclear receptors. While a growing number of biased agonists acting at multiple receptors have been identified, there is still little known regarding the mechanisms underlying biased signaling and its physiologic impact.
Much of our research focuses on the chemokine system, which consists of approximately twenty receptors and fifty ligands that display considerable promiscuity with each other in the regulation of immune cell function in inflammatory diseases. Research from our group and others have shown that many of these ligands act as biased agonists when signaling through the same receptor. We use models of inflammation such as contact hypersensitivity and pulmonary arterial hypertension (PAH). PAH is a disease of the pulmonary arterioles that results in right heart failure and most of its treatments target signaling by GPCRs. We use multiple approaches to probe these signaling mechanisms, including in-house pharmacological assays, advanced phosphoproteomics and single cell RNA sequencing.
The focus of my research is disordered mineral metabolism across the spectrum of chronic kidney disease, including dialysis, kidney transplantation and earlier stages.
My research has been published in leading general medicine and subspecialty journals, including the New England Journal of Medicine, JAMA, the Journal of Clinical Investigation, Circulation, Cell Metabolism, Journal of the American Society of Nephrology, and Kidney International, among others.
My primary contributions have been in the area of hormonal regulation of phosphate homeostasis. I have helped to characterize the physiological role of fibroblast growth factor 23 in health and in chronic kidney disease, and the impact of elevated fibroblast growth factor 23 levels on adverse clinical outcomes in patients with kidney disease.
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