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Juan Carlos Q. Velez

Researcher at Ochsner Health System

Publications -  68
Citations -  2203

Juan Carlos Q. Velez is an academic researcher from Ochsner Health System. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 21, co-authored 48 publications receiving 1545 citations. Previous affiliations of Juan Carlos Q. Velez include University of Queensland & Veterans Health Administration.

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Factors Associated With Death in Critically Ill Patients With Coronavirus Disease 2019 in the US

TL;DR: This study identified demographic, clinical, and hospital-level risk factors that may be associated with death in critically ill patients with COVID-19 and can facilitate the identification of medications and supportive therapies to improve outcomes.
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Acute Kidney Injury Associated with Coronavirus Disease 2019 in Urban New Orleans

TL;DR: Higher BMI and inflammatory marker levels are associated with AKI as well as withAKI-RRT, and CoV-AKI is associated with high rates of RRT and death.
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Therapeutic Response to Vasoconstrictors in Hepatorenal Syndrome Parallels Increase in Mean Arterial Pressure: A Pooled Analysis of Clinical Trials

TL;DR: An increase in MAP during vasoconstrictor therapy in patients with HRS is associated with improvement in kidney function across the spectrum of drugs tested to date, and support consideration for a goal-directed approach to the treatment of HRS.
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The importance of the intrarenal renin–angiotensin system

TL;DR: The kidney RAS appears to be of critical importance for the regulation of blood pressure and salt balance and a better understanding of the autocrine and paracrine mechanisms involved in the renal RAS and other local RASs might direct future organ-specific therapy.
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Characterization of renin-angiotensin system enzyme activities in cultured mouse podocytes.

TL;DR: It is demonstrated that POD express a functional intrinsic renin-angiotensin system characterized by neprilysin, aminopeptidase A, ACE2, and renin activities, which predominantly lead to ANG-(1-7) and ANG-1-9) formation, as well as ANG II degradation.