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Article ; Online: Therapeutic options for chronic kidney disease-associated pulmonary hypertension.

Edmonston, Daniel L / Sparks, Matthew A

Current opinion in nephrology and hypertension

2020 Volume 29, Issue 5, Page(s) 497–507

Abstract: Purpose of review: Pulmonary hypertension is a common and devastating complication of chronic kidney disease (CKD). Traditionally considered a consequence of volume overload, recent findings now expand this paradigm. These novel mechanisms herald new ... ...

Abstract	Purpose of review: Pulmonary hypertension is a common and devastating complication of chronic kidney disease (CKD). Traditionally considered a consequence of volume overload, recent findings now expand this paradigm. These novel mechanisms herald new treatment options. This review summarizes the current evidence to provide a theoretical model of the contributing factors for CKD-associated pulmonary hypertension. Along this framework, we highlight current and emerging therapeutic strategies for each putative factor. Recent findings: A series of retrospective studies of right heart catheterization data provide insights into the potential hemodynamic profile of CKD-associated pulmonary hypertension. These studies suggest that elevated pulmonary vascular resistance may commonly contribute to pulmonary hypertension. In addition, preclinical models implicate an increasing array of CKD-associated factors which influence pulmonary vascular biology. Many of these factors also adversely affect kidney function and CKD progression. Clinical trial and other prospective data for treatments of CKD-associated pulmonary hypertension remain limited. Summary: Volume overload and left-ventricular dysfunction are the predominant focus of CKD-associated pulmonary hypertension treatment for most patients. However, new findings suggest that treatments targeting pulmonary vascular vasoconstriction and remodeling may be promising treatment options for select patients. Clinical trials are needed for all therapeutic strategies for CKD-associated pulmonary hypertension.
MeSH term(s)	Hemodynamics ; Humans ; Hypertension, Pulmonary/drug therapy ; Hypertension, Pulmonary/physiopathology ; Renal Insufficiency, Chronic/complications
Language	English
Publishing date	2020-07-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000624
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Zs.A 3686: Show issues

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Article ; Online: Clinical progress note: Indications for and management of sodium-glucose cotransporter-2 (SGLT-2) inhibitors in hospitalized patients.

Sata, Suchita Shah / Spratt, Susan E / Edmonston, Daniel L / Pagidipati, Neha

Journal of hospital medicine

2022 Volume 17, Issue 5, Page(s) 360–363

MeSH term(s)	Diabetes Mellitus, Type 2 ; Glucose ; Humans ; Hypoglycemic Agents/therapeutic use ; Sodium
Chemical Substances	Hypoglycemic Agents ; Sodium (9NEZ333N27) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2233783-0
ISSN	1553-5606 ; 1553-5592
ISSN (online)	1553-5606
ISSN	1553-5592
DOI	10.1002/jhm.12798
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Zs.A 6276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Coronary artery disease in chronic kidney disease: highlights from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference.

Edmonston, Daniel L / Pun, Patrick H

Kidney international

2019 Volume 97, Issue 4, Page(s) 642–644

MeSH term(s)	Coronary Artery Disease ; Humans ; Kidney ; Renal Insufficiency, Chronic
Language	English
Publishing date	2019-12-28
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2019.12.010
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Zs.A 797: Show issues

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Article ; Online: Hypoxia signaling in renal pericytes-is it safe to activate?

Herbek, Savannah / Edmonston, Daniel L / Souma, Tomokazu

Kidney international

2021 Volume 99, Issue 6, Page(s) 1267–1269

Abstract: While excitement has grown for the use of hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitors for treating renal anemia, multiple preclinical studies have shown the complex and cell-type-dependent roles of HIFs in kidney disease pathogenesis, ... ...

Abstract	While excitement has grown for the use of hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitors for treating renal anemia, multiple preclinical studies have shown the complex and cell-type-dependent roles of HIFs in kidney disease pathogenesis, including renal fibrosis. Pan et al. now clearly show that activating the HIF signaling in the Gli1-lineage myofibroblasts restores erythropoietin production while not adversely affecting matrix production, mitigating the concerns of exacerbated fibrosis by HIF prolyl hydroxylase inhibitors.
MeSH term(s)	Erythropoiesis ; Fibrosis ; Humans ; Hypoxia ; Hypoxia-Inducible Factor-Proline Dioxygenases ; Kidney ; Pericytes ; Prolyl-Hydroxylase Inhibitors ; Renal Insufficiency, Chronic
Chemical Substances	Prolyl-Hydroxylase Inhibitors ; Hypoxia-Inducible Factor-Proline Dioxygenases (EC 1.14.11.29)
Language	English
Publishing date	2021-01-30
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2021.02.014
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Article ; Online: Echocardiography to Screen for Pulmonary Hypertension in CKD.

Edmonston, Daniel L / Rajagopal, Sudarshan / Wolf, Myles

Kidney international reports

2020 Volume 5, Issue 12, Page(s) 2275–2283

Abstract: 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 ... ...

Abstract	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.
Language	English
Publishing date	2020-10-03
Publishing country	United States
Document type	Journal Article
ISSN	2468-0249
ISSN (online)	2468-0249
DOI	10.1016/j.ekir.2020.09.033
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Article ; Online: Coronavirus Disease 2019 and Hypertension: The Role of Angiotensin-Converting Enzyme 2 and the Renin-Angiotensin System.

Edmonston, Daniel L / South, Andrew M / Sparks, Matthew A / Cohen, Jordana B

Advances in chronic kidney disease

2020 Volume 27, Issue 5, Page(s) 404–411

Abstract: Hypertension emerged from early reports as a potential risk factor for worse outcomes for persons with coronavirus disease 2019 (COVID-19). Among the putative links between hypertension and COVID-19 is a key counter-regulatory component of the renin- ... ...

Abstract	Hypertension emerged from early reports as a potential risk factor for worse outcomes for persons with coronavirus disease 2019 (COVID-19). Among the putative links between hypertension and COVID-19 is a key counter-regulatory component of the renin-angiotensin system (RAS): angiotensin-converting enzyme 2 (ACE2). ACE2 facilitates entry of severe acute respiratory syndrome coronavirus 2, the virus responsible for COVID-19, into host cells. Because RAS inhibitors have been suggested to increase ACE2 expression, health-care providers and patients have grappled with the decision of whether to discontinue these medications during the COVID-19 pandemic. However, experimental models of analogous viral pneumonias suggest RAS inhibitors may exert protective effects against acute lung injury. We review how RAS and ACE2 biology may affect outcomes in COVID-19 through pulmonary and other systemic effects. In addition, we briefly detail the data for and against continuation of RAS inhibitors in persons with COVID-19 and summarize the current consensus recommendations from select specialty organizations.
MeSH term(s)	Acute Lung Injury/epidemiology ; Acute Lung Injury/immunology ; Acute Lung Injury/metabolism ; Angiotensin I/immunology ; Angiotensin I/metabolism ; Angiotensin II/immunology ; Angiotensin II/metabolism ; Angiotensin Receptor Antagonists/therapeutic use ; Angiotensin-Converting Enzyme 2/immunology ; Angiotensin-Converting Enzyme 2/metabolism ; Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; COVID-19/epidemiology ; COVID-19/immunology ; COVID-19/metabolism ; Comorbidity ; Humans ; Hypertension/drug therapy ; Hypertension/epidemiology ; Hypertension/metabolism ; JNK Mitogen-Activated Protein Kinases/immunology ; JNK Mitogen-Activated Protein Kinases/metabolism ; Lung/immunology ; Lung/metabolism ; MAP Kinase Signaling System ; Peptide Fragments/immunology ; Peptide Fragments/metabolism ; Protective Factors ; Receptors, Coronavirus/immunology ; Receptors, Coronavirus/metabolism ; Renin-Angiotensin System ; Risk Factors ; SARS-CoV-2 ; Up-Regulation
Chemical Substances	Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors ; Peptide Fragments ; Receptors, Coronavirus ; Angiotensin II (11128-99-7) ; Angiotensin I (9041-90-1) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; angiotensin I (1-7) (IJ3FUK8MOF)
Language	English
Publishing date	2020-07-04
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1548-5609 ; 1548-5595
ISSN (online)	1548-5609
ISSN	1548-5595
DOI	10.1053/j.ackd.2020.07.002
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Zs.A 4627: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Noninvasive Risk Score to Screen for Pulmonary Hypertension With Elevated Pulmonary Vascular Resistance in Diseases of Chronic Volume Overload.

Edmonston, Daniel L / Matsouaka, Roland / Shah, Svati H / Rajagopal, Sudarshan / Wolf, Myles

The American journal of cardiology

2021 Volume 159, Page(s) 113–120

Abstract: Volume overload promotes pulmonary hypertension (PH) through pulmonary venous hypertension. However, PH with elevated pulmonary vascular resistance (hereafter PH-PVR) may develop in patients with diseases of volume overload, such as heart failure or ... ...

Abstract	Volume overload promotes pulmonary hypertension (PH) through pulmonary venous hypertension. However, PH with elevated pulmonary vascular resistance (hereafter PH-PVR) may develop in patients with diseases of volume overload, such as heart failure or chronic kidney disease (CKD). In such cases, volume management alone may be insufficient to slow PH progression. An accurate, noninvasive method to screen for PH-PVR in these diseases would facilitate early targeted therapy. We integrated invasive hemodynamic and echocardiography data collected from a single-center clinical cohort and identified patients with CKD or heart failure at the time of assessment. We applied penalized regression to derive a risk score of clinical parameters and echocardiography data associated with PH-PVR and categorized patients into low- (≤5 points), intermediate- (6-10 points), or high-risk (>10 points) groups. Using an internal validation strategy, we evaluated the ability of this risk score to predict PH-PVR and determined the association of this risk classification with 3-year all-cause mortality. Of 2422 patients, 42.4% had PH-PVR. In adjusted analyses, tricuspid regurgitant velocity, right ventricular function, BMI, heart rate, and hemoglobin most strongly associated with PH-PVR. The risk score significantly associated with PH-PVR (age-adjusted odds ratio 11.69 for the highest-risk group, 95% confidence interval [CI] 6.54-20.92). The high-risk group also associated with a significantly higher risk of 3-year all-cause mortality in adjusted analyses (hazard ratio 1.85, 95% CI 1.50-2.27). In conclusion, a noninvasive risk score derived from echocardiography and clinical parameters significantly associated with PH-PVR and all-cause mortality in a cohort of patients with CKD and heart failure.
MeSH term(s)	Aged ; Blood Volume ; Chronic Disease ; Cohort Studies ; Female ; Humans ; Hypertension, Pulmonary/epidemiology ; Hypertension, Pulmonary/physiopathology ; Male ; Middle Aged ; Risk Factors ; Vascular Resistance
Language	English
Publishing date	2021-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80014-4
ISSN	1879-1913 ; 0002-9149
ISSN (online)	1879-1913
ISSN	0002-9149
DOI	10.1016/j.amjcard.2021.08.016
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Article ; Online: Atrial fibrillation and kidney disease: stuck outside the CABANA.

Edmonston, Daniel L / Wyatt, Christina M / Al-Khatib, Sana M

Kidney international

2019 Volume 96, Issue 5, Page(s) 1054–1055

MeSH term(s)	Atrial Fibrillation ; Catheter Ablation ; Humans ; Kidney Diseases ; Quality of Life
Language	English
Publishing date	2019-06-05
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2019.05.023
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Article ; Online: Corrigendum to "Statins and atherosclerotic cardiovascular outcomes in patients on incident dialysis and with atherosclerotic heart disease" [Am Heart J (2021) 231:36-44].

Shavadia, Jay S / Wilson, Jonathan / Edmonston, Daniel / Platt, Alyssa / Ephraim, Patti / Hall, Rasheeda / Goldstein, Benjamin A / Boulware, L Ebony / Peterson, Eric / Pendergast, Jane / Scialla, Julia J

American heart journal

2022 Volume 253, Page(s) 99–100

Language	English
Publishing date	2022-08-05
Publishing country	United States
Document type	Published Erratum
ZDB-ID	80026-0
ISSN	1097-6744 ; 0002-8703
ISSN (online)	1097-6744
ISSN	0002-8703
DOI	10.1016/j.ahj.2022.06.009
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Article ; Online: COVID-19 and Hypertension: The Role of ACE2 and the Renin-Angiotensin System

Edmonston, Daniel L. / South, Andrew M. / Sparks, Matthew A. / Cohen, Jordana B.

Adv Chronic Kidney Dis

Abstract: ABSTRACT Hypertension emerged from early reports as a potential risk factor for worse outcomes for persons with coronavirus disease 2019 (COVID-19). Among the putative links between hypertension and COVID-19 is a key counter-regulatory component of the ... ...

Abstract	ABSTRACT Hypertension emerged from early reports as a potential risk factor for worse outcomes for persons with coronavirus disease 2019 (COVID-19). Among the putative links between hypertension and COVID-19 is a key counter-regulatory component of the renin-angiotensin system (RAS): angiotensin-converting enzyme 2 (ACE2). ACE2 facilitates entry of SARS-CoV-2, the virus responsible for COVID-19, into host cells. Since RAS inhibitors have been suggested to increase ACE2 expression, healthcare providers and patients have grappled with the decision of whether to discontinue these medications during the COVID-19 pandemic. However, experimental models of analogous viral pneumonias suggest RAS inhibitors may exert protective effects against acute lung injury. We review how RAS and ACE2 biology may affect outcomes in COVID-19 through pulmonary and other systemic effects. In addition, we briefly detail the data for and against continuation of RAS inhibitors in persons with COVID-19 and summarize the current consensus recommendations from select specialty organizations.
Keywords	covid19
Publisher	Elsevier; PMC
Document type	Article ; Online
DOI	10.1053/j.ackd.2020.07.002
Database	COVID19

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