Eduardo R. Argaiz

ORCID: 0000-0002-5542-6098
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Hemodynamic Monitoring and Therapy
  • Ultrasound in Clinical Applications
  • Ion Transport and Channel Regulation
  • Liver Disease and Transplantation
  • Magnesium in Health and Disease
  • Renal function and acid-base balance
  • Potassium and Related Disorders
  • Cardiac, Anesthesia and Surgical Outcomes
  • Venous Thromboembolism Diagnosis and Management
  • Non-Invasive Vital Sign Monitoring
  • Radiology practices and education
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Sepsis Diagnosis and Treatment
  • Radiation Dose and Imaging
  • Hormonal Regulation and Hypertension
  • Healthcare Systems and Reforms
  • Ion channel regulation and function
  • Electrolyte and hormonal disorders
  • Pulmonary Hypertension Research and Treatments
  • Abdominal Surgery and Complications
  • Acute Kidney Injury Research
  • Sodium Intake and Health
  • Cerebrovascular and Carotid Artery Diseases
  • GABA and Rice Research
  • Phagocytosis and Immune Regulation

Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán
2015-2025

Tecnológico de Monterrey
2014-2025

Parque Tecnológico de la Salud
2024

Universidad Nacional Autónoma de México
2014-2021

The University of Texas MD Anderson Cancer Center
2010

Michael E. DeBakey VA Medical Center
2010

Baylor College of Medicine
2010

Abstract The importance of functional right ventricular failure and resultant splanchnic venous congestion has long been under-appreciated is difficult to assess by traditional physical examination standard diagnostic imaging. recent development the excess ultrasound score (VExUS) growth point-of-care in last decade made for a potentially very useful clinical tool. We review rationale its use several pathologies illustrate with cases where VExUS was pivotal management.

10.1186/s13089-021-00232-8 article EN cc-by The Ultrasound Journal 2021-06-19

It is widely recognized that the phenotype of familial hyperkalemic hypertension mainly a consequence increased activity renal Na + –Cl − cotransporter (NCC) because altered regulation by with no–lysine–kinase 1 (WNK1) or WNK4. The effect WNK4 on NCC, however, has been controversial both inhibition and activation have reported. recently shown long isoform WNK1 (L-WNK1) chloride-sensitive kinase activated low Cl - concentration. Therefore, we hypothesized effects NCC could be modulated...

10.1681/asn.2014050470 article EN cc-by Journal of the American Society of Nephrology 2014-12-27

Familial hyperkalemic hypertension (FHHt) is a monogenic disease resulting from mutations in genes encoding WNK kinases, the ubiquitin scaffold protein cullin 3 (CUL3), or substrate adaptor kelch-like (KLHL3). Disease-associated CUL3 abrogate kinase degradation cells, but it not clear how mutant forms of promote stability. Here, we demonstrated that an FHHt-causing (CUL3 Δ403–459) only retains ability to bind and ubiquitylate kinases KLHL3 also more heavily neddylated activated than WT CUL3....

10.1172/jci76126 article EN Journal of Clinical Investigation 2014-09-23

Systemic venous congestion is associated with an increased risk of acute kidney injury (AKI) in critically ill patients. Venous Excess Ultrasound Score (VExUS) has been proposed as a non-invasive score to assess systemic congestion. We aimed evaluate the association between VExUS and AKI patients coronary syndrome (ACS).This prospective study including diagnosis ACS (both ST elevation non-ST ACS). was performed during first 24 h hospital stay. Patients were classified according presence...

10.1093/ehjacc/zuad048 article EN European Heart Journal Acute Cardiovascular Care 2023-05-08

Stress-induced cardiomyopathy, triggered by acute catecholamine discharge, is a syndrome characterized transient, apical ballooning linked to heart failure and ventricular arrhythmias. Rats receiving an isoproterenol (ISO) overdose (OV) suffer cardiac apex ischemia-reperfusion damage arrhythmia, then undergo remodeling dysfunction. Nevertheless, the subcellular mechanisms underlying dysfunction after subsides are not thoroughly understood. To address this question, Wistar rats received...

10.1152/ajpheart.00734.2013 article EN AJP Heart and Circulatory Physiology 2014-12-20

STE20 (Sterile 20)/SPS-1 related proline/alanine-rich kinase (SPAK) and oxidative stress-response kinase-1 (OSR1) phosphorylate activate the renal Na(+) -K(+) -2Cl(-) cotransporter 2 (NKCC2) Cl(-) (NCC). Mouse models suggest that OSR1 mainly activates NKCC2-mediated sodium transport along thick ascending limb, while SPAK NCC distal convoluted tubule, but kinases may compensate for each other. We hypothesized disruption of both would lead to polyuria severe salt-wasting, generated SPAK/OSR1...

10.1113/jp272311 article EN cc-by The Journal of Physiology 2016-04-12

Familial hyperkalemic hypertension (FHHt) can be mainly attributed to increased activity of the renal Na+:Cl- cotransporter (NCC), which is caused by altered expression and regulation with-no-lysine (K) 1 (WNK1) or WNK4 kinases. The WNK1 gene gives rise a kidney-specific isoform that lacks kinase domain (KS-WNK1), occurs primarily in distal convoluted tubule. role played KS-WNK1 modulation WNK/STE20-proline-alanine rich (SPAK)/NCC pathway remains elusive. In present study, we assessed effect...

10.1152/ajprenal.00145.2018 article EN cc-by AJP Renal Physiology 2018-05-31

Gain-of-function mutations in with no lysine (K) 1 (WNK1) and WNK4 genes are responsible for familial hyperkalemic hypertension (FHHt), a rare, inherited disorder characterized by arterial hyperkalemia metabolic acidosis. More recently, FHHt-causing the Kelch-like 3–Cullin 3 (KLHL3-CUL3) E3 ubiquitin ligase complex have shed light on importance of WNK's cellular degradation renal ion transport. Using full exome sequencing 4-generation family then targeted other suspected cases, we identified...

10.1172/jci94171 article EN Journal of Clinical Investigation 2020-08-13

<b><i>Introduction:</i></b> Optimal method for noninvasive assessment of venous congestion remains an unresolved issue. Portal vein (PV) and intrarenal flow alterations are markers abdominal have been associated with acute kidney injury (AKI) in cardiac surgery patients. It is currently unknown if portal (PVF) heart failure can be reversed diuretic treatment track decongestion. <b><i>Objective:</i></b> The aim this study to evaluate PVF...

10.1159/000511714 article EN cc-by-nc Cardiorenal Medicine 2021-01-01

We aimed to compare internal jugular vein and inferior vena cava ultrasonography as predictors of central venous pressure in cirrhotic patients. performed ultrasound assessments the (IJV) then invasively measured (CVP). compared their correlation with CVP area under receiver operating characteristic curves determine which had best sensitivity specificity. IJV cross-sectional collapsibility index at 30° correlated better ( r = −0.56, P < 0.001), an AP-CI ≤ 24.8% was predicting a ≥8 mm Hg,...

10.14309/ajg.0000000000002315 article EN The American Journal of Gastroenterology 2023-05-05

Introduction Venous congestion is a pathophysiological state where high venous pressures cause organ oedema and dysfunction. associated with worse outcomes, particularly acute kidney injury (AKI), for critically ill patients. can be measured by Doppler ultrasound at the bedside through interrogation of inferior vena cava (IVC), hepatic vein (HV), portal (PV) intrarenal veins (IRV). The objective this study to quantify association between identified need renal replacement therapy (RRT) or...

10.1136/bmjopen-2023-074843 article EN cc-by-nc BMJ Open 2023-07-01

Acute kidney injury (AKI) in patients with cirrhosis is a diagnostic challenge due to multiple and sometimes overlapping possible etiologies. Many times, diagnosis cannot be made based on case history, physical examination or laboratory data, especially when the nephrologist faced AKI hemodynamic basis, such as hepatorenal syndrome. In addition, guidelines still include generalized recommendations regarding withdrawal of diuretics plasma volume expansion albumin for 48 h, which may...

10.1093/ckj/sfae112 article EN cc-by Clinical Kidney Journal 2024-04-13

BACKGROUND: The exposure of phosphatidylserine occurs during platelet (PLT) activation and in vitro storage. Phosphatidylserine also apoptosis after the release mitochondrial cytochrome c . We have examined role release, membrane potential (ΔΨm), cyclophilin D (CypD) due to STUDY DESIGN AND METHODS: loss ΔΨm were determined a flow cytometer using fluorescein isothiocyanate–lactadherin JC‐1, lipophilic cationic reporter dye. CypD was with cyclosporin A CypD‐deficient murine PLTs. Cytochrome...

10.1111/j.1537-2995.2010.02676.x article EN Transfusion 2010-05-07

Chronic kidney disease (CKD) represents a substantial global burden of due to lack universal tests and misinterpretation biomarkers.

10.24875/gmm.m24000830 article EN cc-by-nc-nd Gaceta Médica de México 2024-02-19

Renal and liver congestion are associated with adverse outcomes in patients tricuspid regurgitation (TR). Currently, there no valid sonographic indicators of fluid status this population. Intra-renal venous Doppler (IRVD) is a novel method for quantifying renal but its interpretation can be challenging severe TR due to altered haemodynamics. This study explores the potential portal vein (PVD) as an alternative marker decongestion during volume removal TR. Forty-two undergoing decongestive...

10.1093/ehjacc/zuae057 article EN European Heart Journal Acute Cardiovascular Care 2024-05-12
Coming Soon ...