The impact of experimental hypoperfusion on subsequent kidney function

Saotome, Takao; Ishikawa, Ken; May, Clive N.; Birchall, Ian; Bellomo, Rinaldo

doi:10.1007/s00134-009-1740-9

Cited by 47 publications

(27 citation statements)

References 20 publications

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“…However, studies in large mammals, including humans, suggest that global renal hypoperfusion cannot be invoked as the sole etiology of AKI. [2][3][4][5] The causative contribution of renal blood flow (RBF) to kidney dysfunction is particularly puzzling in sepsis, and there is widespread disagreement as to whether RBF is reduced, normal, or even increased. 2,3,[6][7][8] In the few large animal and clinical studies, the patterns of RBF in AKI and its relation with systemic hemodynamics are highly variable.…”

Section: Total Renal Blood Flow In Akimentioning

confidence: 99%

Renal Hemodynamics in AKI

Matějovič

İnce

Chawla

et al. 2016

Journal of the American Society of Nephrology

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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.

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Section: Total Renal Blood Flow In Akimentioning

confidence: 99%

Renal Hemodynamics in AKI

Matějovič

İnce

Chawla

et al. 2016

Journal of the American Society of Nephrology

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“…15 Although complete cessation of renal blood flow is associated with AKI in animals and humans, in experimental animals, 80% reduction of renal blood flow for 2 hours is transiently associated with a decrease in renal function; however, recovery is rapid, and there is no morphologic evidence of acute tubular necrosis 5 days after occlusion. 16 Thus, despite significant hypoperfusion, there was minimal injury. Workgroup 1 emphasizes that the heterogeneity of microcirculatory blood flow is critical in determining the pathogenesis of AKI.…”

Section: Hemodynamics (Workgroup 1)mentioning

confidence: 97%

Therapeutic Targets of Human AKI

Okusa

Rosner

Kellum

et al. 2016

Journal of the American Society of Nephrology

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The opportunity to make advances in the prevention and treatment of AKI has never been greater than it is today. Major advances have been made in the understanding of the biology of AKI, the design of clinical trials, and the use of diagnostic and prognostic biomarkers. These advances have been supplemented by the coordinated effort of societies, federal agencies, and industry, such that we are poised in the ensuing years to positively address the unrelenting harm that this disorder has created. Over the past decade, major advances have been made in understanding the pathophysiology of AKI, mainly through the study of small animal models. However, translating these findings to human AKI remains a barrier, which is typified by the absence of effective therapeutic agents. The purpose of the Acute Dialysis Quality Initiative (ADQI) XIII was to harmonize human and animal studies and determine what is known about potential therapeutic targets and what gaps in knowledge remain. A series of invited reviews will distill key concepts from this initiative that focus on different pathogenic features of AKI, including hemodynamics, immunity and inflammation, cellular and molecular pathways, progression, and regeneration and repair. This series will convey the status of our knowledge of the pathophysiology of human AKI and propose therapeutic targets for further investigation.

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“…Intent to maintain or increase renal oxygen delivery by administration of fluids may also be questioned, because in AKI the metabolic activity is decreased with decreasing GFR, although both animal [14] and clinical data [15] suggest that sodium reabsorption becomes less metabolically efficient in AKI. Moreover, the causal relationship between periodic ischaemia and development of new AKI has been rejected [16].…”

Section: Physiological Rationale For Fluid Management In Akimentioning

confidence: 99%

Fluid management in acute kidney injury

et al. 2017

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Acute kidney injury (AKI) and fluids are closely linked through oliguria, which is a marker of the former and a trigger for administration of the latter. Recent progress in this field has challenged the physiological and clinical rational of using oliguria as a trigger for the administration of fluid and brought attention to the delicate balance between benefits and harms of different aspects of fluid management in critically ill patients, in particular those with AKI. This narrative review addresses various aspects of fluid management in AKI outlining physiological aspects, the effects of crystalloids and colloids on kidney function and the effect of various resuscitation and de-resuscitation strategies on the course and outcome of AKI.

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The impact of experimental hypoperfusion on subsequent kidney function

Cited by 47 publications

References 20 publications

Renal Hemodynamics in AKI

Renal Hemodynamics in AKI

Therapeutic Targets of Human AKI

Fluid management in acute kidney injury

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