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40
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Text
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URL Address
<a href="http://doi.org/10.14740/cr553w" target="_blank" rel="noreferrer noopener">http://doi.org/10.14740/cr553w</a>
Pages
87–95
Issue
3
Volume
8
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Cardiorenal Syndrome: Role of Arginine Vasopressin and Vaptans in Heart Failure.
Publisher
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Cardiology research
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-06
Subject
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Arginine vasopressin; Cardiorenal syndrome; Conivaptan; Heart failure; Tolvaptan; Vaptans; Vasopressin receptor antagonists
Creator
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Vinod Poornima; Krishnappa Vinod; Chauvin Abigail M; Khare Anshika; Raina Rupesh
Description
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Heart and kidney failure continued to be of increasing prevalence in today's society, and their comorbidity has synergistic effect on the morbidity and mortality of patients. Cardiorenal syndrome (CRS) is a complex disease with multifactorial pathophysiology. Better understanding of this pathophysiological network is crucial for the successful intervention to prevent advancement of the disease process. One of the major factors in this process is neurohormonal activation, predominantly involving renin-angiotensin-aldosterone system (RAAS) and arginine vasopressin (AVP). Heart failure causes reduced cardiac output/cardiac index (CO/CI) and fall in renal perfusion pressures resulting in activation of baroreceptors and RAAS, respectively. Activated baroreceptors and RAAS stimulate the release of AVP (non-osmotic pathway), which acts on V2 receptors located in the renal collecting ducts, causing fluid retention and deterioration of heart failure. Effective blockade of AVP action on V2 receptors has emerged as a potential treatment option in volume overload conditions especially in the setting of hyponatremia. Vasopressin receptor antagonists (VRAs), such as vaptans, are potent aquaretics causing electrolyte-free water diuresis without significant electrolyte abnormalities. Vaptans are useful in hypervolemic hyponatremic conditions like heart failure and liver cirrhosis, and euvolemic hyponatremic conditions like syndrome of inappropriate anti-diuretic hormone secretion. Tolvaptan and conivaptan are pharmaceutical agents that are available for the treatment of these conditions.
Identifier
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<a href="http://doi.org/10.14740/cr553w" target="_blank" rel="noreferrer noopener">10.14740/cr553w</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Arginine vasopressin
Cardiology research
Cardiorenal syndrome
Chauvin Abigail M
Conivaptan
Department of Internal Medicine
Heart failure
Khare Anshika
Krishnappa Vinod
NEOMED College of Graduate Studies Student
NEOMED College of Medicine
Raina Rupesh
Tolvaptan
Vaptans
Vasopressin receptor antagonists
Vinod Poornima
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.5414/cn109598" target="_blank" rel="noreferrer noopener">http://doi.org/10.5414/cn109598</a>
Pages
370–379
Issue
6
Volume
91
ISSN
0301-0430
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Endothelin-1 as a therapeutic target in autosomal dominant polycystic kidney disease
Publisher
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Clinical Nephrology
Date
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2019
2019-06
Subject
The topic of the resource
proliferation; hypertension; receptor; expression; Urology & Nephrology; growth-factor; renal damage; endothelin-1; excretion; polycystic kidney disease; chronic kidney disease; ADPKD; endothelin-1 antagonists; autosomal dominant; tolvaptan; urinary endothelin-1; water permeability
Creator
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Raina R; Chauvin A; Vajapey R; Khare A; Krishnappa V
Description
An account of the resource
Aims: Endothelin-1 (ET-1) is associated with the pathophysiology of autosomal dominant polycystic kidney disease (ADPKD) via cyst progression. Elevated concentrations of ET-1 in ADPKD correlate with many phenotypic changes in the kidney such as renal cyst development, interstitial fibrosis, and glomerulosclerosis. In addition, an imbalance between renal ETA and ETB receptors possibly leads to more severe disease progression. The objective of this review is to determine whether evaluating the efficacy of these drugs in treatment of cystic kidney disease may be a worthwhile aim, as determined by results from animal and human models. Materials and methods: PubMed/Medline, Embase, and Google Scholar databases were searched using the key words "endothelin, endothelin-1 antagonists, and autosomal dominant polycystic kidney disease". All animal and human studies describing the effects of endothelin and endothelin-1 antagonists in ADPKD subjects were included in the review. Results: Urinary ET-1 concentrations could serve as a noninvasive surrogate biomarker for kidney ET-1 levels, as it is inversely associated with eGFR, independent of age, sex, and blood pressure. Elevated urinary excretion of ET-1 may be a biomarker for early renal injury. Antagonization of ET-1 may hopefully be a novel therapy for slowing progression of kidney damage in ADPKD. Conclusion: Based on the literature reviewed in this manuscript, it is proposed that further research evaluating the efficacy of endothelin antagonists in treatment of cystic kidney disease is warranted. More human studies need to be performed with larger sample sizes. Therefore, the recommendation for treatment is inconclusive at this time.
Identifier
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<a href="http://doi.org/10.5414/cn109598" target="_blank" rel="noreferrer noopener">10.5414/cn109598</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2019
ADPKD
Autosomal Dominant
Chauvin A
Chronic kidney disease
Clinical nephrology
Department of Internal Medicine
endothelin-1
endothelin-1 antagonists
excretion
expression
growth-factor
Hypertension
June 2019 Update
Khare A
Krishnappa V
NEOMED College of Graduate Studies Student
NEOMED College of Medicine
NEOMED College of Medicine Student
NEOMED Student Publications
polycystic kidney disease
proliferation
Raina R
Receptor
renal damage
Tolvaptan
urinary endothelin-1
Urology & Nephrology
Vajapey R
water permeability