Literature DB >> 26510884

Renal Hemodynamics in AKI: In Search of New Treatment Targets.

Martin Matejovic1, Can Ince2, Lakhmir S Chawla3, Roland Blantz4, Bruce A Molitoris5, Mitchell H Rosner6, Mark D Okusa7, John A Kellum8, Claudio Ronco9.   

Abstract

Novel therapeutic interventions are required to prevent or treat AKI. To expedite progress in this regard, a consensus conference held by the Acute Dialysis Quality Initiative was convened in April of 2014 to develop recommendations for research priorities and future directions. Here, we highlight the concepts related to renal hemodynamics in AKI that are likely to reveal new treatment targets on investigation. Overall, we must better understand the interactions between systemic, total renal, and glomerular hemodynamics, including the role of tubuloglomerular feedback. Furthermore, the net consequences of therapeutic maneuvers aimed at restoring glomerular filtration need to be examined in relation to the nature, magnitude, and duration of the insult. Additionally, microvascular blood flow heterogeneity in AKI is now recognized as a common occurrence; timely interventions to preserve the renal microcirculatory flow may interrupt the downward spiral of injury toward progressive kidney failure and should, therefore, be investigated. Finally, development of techniques that permit an integrative physiologic approach, including direct visualization of renal microvasculature and measurement of oxygen kinetics and mitochondrial function in intact tissue in all nephron segments, may provide new insights into how the kidney responds to various injurious stimuli and allow evaluation of new therapeutic strategies.
Copyright © 2016 by the American Society of Nephrology.

Entities:  

Keywords:  acute renal failure; clinical nephrology; hemodynamics and vascular; regulation

Mesh:

Year:  2015        PMID: 26510884      PMCID: PMC4696587          DOI: 10.1681/ASN.2015030234

Source DB:  PubMed          Journal:  J Am Soc Nephrol        ISSN: 1046-6673            Impact factor:   10.121


  60 in total

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5.  A single nephron model of acute tubular injury: role of tubuloglomerular feedback.

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6.  Selective inducible nitric oxide synthase inhibition during long-term hyperdynamic porcine bacteremia.

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Authors:  Bruce A Molitoris; Timothy A Sutton
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Authors:  J R Lugon; M A Boim; O L Ramos; H Ajzen; N Schor
Journal:  Kidney Int       Date:  1989-10       Impact factor: 10.612

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7.  Long-term outcomes in mouse models of ischemia-reperfusion-induced acute kidney injury.

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Review 9.  Bridging translation for acute kidney injury with better preclinical modeling of human disease.

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10.  The role of adenosine 1a receptor signaling on GFR early after the induction of sepsis.

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