T
Tara I. Chang
Researcher at Stanford University
Publications - 141
Citations - 5620
Tara I. Chang is an academic researcher from Stanford University. The author has contributed to research in topics: Kidney disease & Blood pressure. The author has an hindex of 32, co-authored 132 publications receiving 3813 citations. Previous affiliations of Tara I. Chang include University of California, San Francisco & Baylor College of Medicine.
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Journal ArticleDOI
Cardiorenal Syndrome: Classification, Pathophysiology, Diagnosis, and Treatment Strategies: A Scientific Statement From the American Heart Association.
Janani Rangaswami,Vivek Bhalla,John E.A. Blair,Tara I. Chang,Salvatore P. Costa,Krista L. Lentine,Edgar V. Lerma,Kenechukwu Mezue,Mark E. Molitch,Wilfried Mullens,Claudio Ronco,W.H. Wilson Tang,Peter A. McCullough +12 more
TL;DR: The mission of this scientific statement is to describe the epidemiology and pathogenesis of cardiorenal syndrome in the context of the continuously evolving nature of its clinicopathological description over the past decade.
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Contemporary Incidence, Predictors, and Outcomes of Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Interventions : Insights From the NCDR Cath-PCI Registry
Thomas T. Tsai,Thomas T. Tsai,Uptal D. Patel,Tara I. Chang,Kevin F. Kennedy,Frederick A. Masoudi,Michael E. Matheny,Mikhail Kosiborod,Amit P. Amin,John C. Messenger,John S. Rumsfeld,John A. Spertus +11 more
TL;DR: Almost 7% of patients undergoing a PCI experience AKI, which is strongly associated with in-hospital mortality, and strategies to minimize the risk of AKI in patients undergoing PCI are needed.
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KDIGO 2021 Clinical Practice Guideline for the Management of Blood Pressure in Chronic Kidney Disease
Alfred K. Cheung,Tara I. Chang,William C. Cushman,Susan L. Furth,Fan Fan Hou,Joachim H. Ix,Gregory A. Knoll,Paul Muntner,Roberto Pecoits-Filho,Mark J. Sarnak,Sheldon W. Tobe,Charles R.V. Tomson,Johannes F.E. Mann +12 more
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Effects of Intensive BP Control in CKD
Alfred K. Cheung,Mahboob Rahman,Mahboob Rahman,David M. Reboussin,Timothy E. Craven,Tom Greene,Paul L. Kimmel,William C. Cushman,Amret T. Hawfield,Karen C. Johnson,Cora E. Lewis,Suzanne Oparil,Michael V. Rocco,Kaycee M. Sink,Paul K. Whelton,Jackson T. Wright,Jan Basile,Jan Basile,Srinivasan Beddhu,Udayan Bhatt,Tara I. Chang,Glenn M. Chertow,Michel Chonchol,Barry I. Freedman,William E. Haley,Joachim H. Ix,Lois A. Katz,Lois A. Katz,Anthony A. Killeen,Vasilios Papademetriou,Ana C. Ricardo,Karen S. Servilla,Barry M. Wall,Barry M. Wall,Dawn F. Wolfgram,Jerry Yee +35 more
TL;DR: Among patients with CKD and hypertension without diabetes, targeting an SBP<120 mm Hg compared with <140mm Hg reduced rates of major cardiovascular events and all-cause death without evidence of effect modifications by CKD or deleterious effect on the main kidney outcome.
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Evidence that elevated glucose causes altered gene expression, apoptosis, and neural tube defects in a mouse model of diabetic pregnancy.
TL;DR: It is found that elevated glucose alone can cause the changes in Pax-3 expression observed during diabetic pregnancy and that the NTD rate rises with significant increases in blood glucose levels, suggesting that congenital malformations associated with diabetic pregnancy are caused by disruption of regulatory gene expression in the embryo in response to elevated glucose.