M
Matthew A. Sparks
Researcher at Duke University
Publications - 113
Citations - 4404
Matthew A. Sparks is an academic researcher from Duke University. The author has contributed to research in topics: Angiotensin II & Renin–angiotensin system. The author has an hindex of 30, co-authored 96 publications receiving 3289 citations. Previous affiliations of Matthew A. Sparks include University of Virginia & Veterans Health Administration.
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Journal ArticleDOI
Acute Kidney Injury in COVID-19: Emerging Evidence of a Distinct Pathophysiology.
Daniel Batlle,María José Soler,Matthew A. Sparks,Matthew A. Sparks,Swapnil Hiremath,Andrew M South,Paul A. Welling,Sundararaman Swaminathan,Covid +8 more
TL;DR: This work presents a novel and scalable approach to regenerative medicine that combines traditional and regenerative approaches to treat central giant cell granuloma, a leading cause of cancer in women.
OtherDOI
Classical Renin‐Angiotensin System in Kidney Physiology
Matthew A. Sparks,Steven D. Crowley,Steven D. Crowley,Susan B. Gurley,Susan B. Gurley,Maria Mirotsou,Thomas M. Coffman,Thomas M. Coffman,Thomas M. Coffman +8 more
TL;DR: The physiological role of components of the "classical" renin-angiotensin system is reviewed, with an emphasis on new developments and modern concepts.
Journal ArticleDOI
AT1A Angiotensin Receptors in the Renal Proximal Tubule Regulate Blood Pressure
Susan B. Gurley,Anne Riquier-Brison,Jurgen Schnermann,Matthew A. Sparks,Andrew M. Allen,Volker H. Haase,John N. Snouwaert,Thu H. Le,Alicia A. McDonough,Beverley H. Koller,Thomas M. Coffman,Thomas M. Coffman +11 more
TL;DR: It is demonstrated that RAS actions in the epithelium of the proximal tubule have a critical and nonredundant role in determining the level of BP and effectively targeting epithelial functions of the proxy tubule of the kidney should be a useful therapeutic strategy in hypertension.
Journal ArticleDOI
Controversies of renin-angiotensin system inhibition during the COVID-19 pandemic.
TL;DR: The current COVID-19 pandemic is associated with unprecedented morbidity and mortality, highlighting the need to understand the relationship between the virus and the renin–angiotensin system (RAS) and how this might be affected by RAS inhibitors.
Journal ArticleDOI
Rare hereditary COL4A3/COL4A4 variants may be mistaken for familial focal segmental glomerulosclerosis.
Andrew F. Malone,Andrew F. Malone,Paul J. Phelan,Paul J. Phelan,Gentzon Hall,Gentzon Hall,Umran Cetincelik,Alison Homstad,Alison Homstad,Andrea S. Alonso,Andrea S. Alonso,Ruiji Jiang,Ruiji Jiang,Thomas Lindsey,Guanghong Wu,Matthew A. Sparks,Stephen R. Smith,Nicholas J. A. Webb,Philip A. Kalra,Adebowale Adeyemo,Andrey S. Shaw,Peter J. Conlon,J. Charles Jennette,David N. Howell,Michelle P. Winn,Michelle P. Winn,Rasheed Gbadegesin,Rasheed Gbadegesin +27 more
TL;DR: This study illustrates the power of molecular genetic diagnostics in the clarification of renal phenotypes by presenting seven families with rare or novel variants in COL4A3 orCOL4A4 from a cohort of 70 families with a diagnosis of hereditary FSGS.