scholarly journals Volatile Anesthesia Activates Renal Sympathetic Nerves to Reduce Renal Excretory Function: Implications for Surgically-Induced Acute Kidney Injury

Function ◽  
2021 ◽  
Author(s):  
John W Osborn ◽  
Arthur De La Cruz-Lynch
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Sympathetic Nerves ◽  
Excretory Function ◽  
Volatile Anesthesia ◽  
Surgically Induced ◽  
Renal Excretory Function ◽  
Renal Sympathetic

Pathophysiology of Acute Kidney Injury

2017 ◽  
Author(s):  
Shalini Bumb ◽  
Andrew Malone ◽  
Matthew A. Sparks
Keyword(s):  
Acute Kidney Injury ◽  
Fluid Overload ◽  
Kidney Injury ◽  
Tissue Perfusion ◽  
Urinary Flow ◽  
Cellular Injury ◽  
Waste Products ◽  
Excretory Function ◽  
Tubular Necrosis ◽  
Vascular Compromise

Acute kidney injury (AKI) is defined as the abrupt loss of kidney excretory function with the accumulation of nitrogenous waste products and fluid overload. The etiologies of AKI are numerous and can largely be classified as prerenal, intrinsic, or postrenal. Complex pathways involving inflammatory mediators, vascular compromise, and direct cellular injury are triggered, and equally as complex pathways, including autophagy and fibrosis, are involved in the recovery. Prerenal azotemia is caused by a reduction in tissue perfusion with resulting AKI. Although acute tubular necrosis is the most common intrinsic etiology, other nephrotoxins and exposures can result in intrinsic injury as well. Postrenal AKI is due to obstruction of urinary flow. Herein, in further detail, the mechanisms, pathophysiology, and manifestations of these causes of AKI are discussed. Research into the mechanisms and development of markers and techniques to advance clinical practice is ongoing.

Acute kidney injury

2020 ◽  
pp. 4807-4829
Author(s):  
John D. Firth
Keyword(s):  
Acute Kidney Injury ◽  
Specific Treatment ◽  
Kidney Injury ◽  
Initial Assessment ◽  
Volume Depletion ◽  
Excretory Function ◽  
Tubular Necrosis ◽  
Life Threatening ◽  
Common Precipitant ◽  
General Aspects

Definition—for practical clinical purposes, acute kidney injury (AKI) is defined as a significant decline in renal excretory function occurring over hours or days, detected by either a fall in urinary output or a rise in the serum concentration of creatinine. Oliguria—defined (arbitrarily) as a urinary volume of less than 400 ml/day—is usually present, but not always. Clinical approach: diagnosis—all patients admitted to hospital with acute illness, but particularly older people and those with pre-existing chronic kidney disease, should be considered at risk of developing AKI. The most common precipitant is volume depletion. Serum creatinine and electrolytes should be measured on admission in all acutely ill patients, and repeated daily or on alternate days in those who remain so. Assessment—after treatment of life-threatening complications, the initial assessment of a patient who appears to have AKI must answer three questions: (1) is the kidney injury really acute? (2) Is urinary obstruction a possibility? And (3) is there a renal inflammatory cause? General aspects of management—the immediate management of a patient with renal impairment is directed towards three goals: (1) recognition and treatment of any life-threatening complications of AKI, (2) prompt diagnosis and treatment of hypovolaemia, and (3) specific treatment of the underlying condition—if this persists untreated then renal function will not improve. Specific causes of acute kidney injury—there are many possible causes of AKI, but in any given clinical context few of these are likely to require consideration. By far the most frequent are prerenal failure and acute tubular necrosis, which together account for 80 to 90% of cases of AKI seen by physicians.

Sex differences in ischemia/reperfusion-induced acute kidney injury are dependent on the renal sympathetic nervous system

2013 ◽  
Vol 714 (1-3) ◽  
pp. 397-404 ◽  
Author(s):  
Ryosuke Tanaka ◽  
Hidenobu Tsutsui ◽  
Mamoru Ohkita ◽  
Masanori Takaoka ◽  
Tokihito Yukimura ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Nervous System ◽  
Sex Differences ◽  
Sympathetic Nervous System ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

scholarly journals Functional Magnetic Resonance Imaging in Acute Kidney Injury: Present Status

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Hai Ying Zhou ◽  
Tian Wu Chen ◽  
Xiao Ming Zhang
Keyword(s):  
Acute Kidney Injury ◽  
Magnetic Resonance ◽  
Mr Imaging ◽  
Alternative Assessment ◽  
Assessment Tool ◽  
Kidney Injury ◽  
Subsequent Development ◽  
Blood Oxygen Level Dependent ◽  
Early Assessment ◽  
Excretory Function

Acute kidney injury (AKI) is a common complication of hospitalization that is characterized by a sudden loss of renal excretory function and associated with the subsequent development of chronic kidney disease, poor prognosis, and increased mortality. Although the pathophysiology of renal functional impairment in the setting of AKI remains poorly understood, previous studies have identified changes in renal hemodynamics, perfusion, and oxygenation as key factors in the development and progression of AKI. The early assessment of these changes remains a challenge. Many established approaches are not applicable to humans because of their invasiveness. Functional renal magnetic resonance (MR) imaging offers an alternative assessment tool that could be used to evaluate renal morphology and function noninvasively and simultaneously. Thus, the purpose of this review is to illustrate the principle, application, and role of the techniques of functional renal MR imaging, including blood oxygen level-dependent imaging, arterial spin labeling, and diffusion-weighted MR imaging, in the management of AKI. The use of gadolinium in MR imaging may exacerbate renal impairment and cause nephrogenic systemic fibrosis. Therefore, dynamic contrast-enhanced MR imaging will not be discussed in this paper.

Protective effect of 17β-estradiol on ischemic acute kidney injury through the renal sympathetic nervous system

2012 ◽  
Vol 683 (1-3) ◽  
pp. 270-275 ◽  
Author(s):  
Ryosuke Tanaka ◽  
Hidenobu Tsutsui ◽  
Shuhei Kobuchi ◽  
Takahiro Sugiura ◽  
Masayo Yamagata ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Protective Effect ◽  
Kidney Injury ◽  
17Β Estradiol ◽  
Ischemic Acute Kidney Injury ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

scholarly journals Role of renal sympathetic nerve activity in volatile anesthesia's effect on renal excretory function

Function ◽  
2021 ◽  
Author(s):  
Micael Taavo ◽  
Mats Rundgren ◽  
Peter Frykholm ◽  
Anders Larsson ◽  
Stephanie Franzén ◽  
...  
Keyword(s):  
Blood Flow ◽  
Water Retention ◽  
Sympathetic Nerve Activity ◽  
Sevoflurane Anesthesia ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Excretory Function ◽  
Renal Excretory Function ◽  
Renal Sympathetic

Abstract Regulation of fluid balance is pivotal during surgery and anesthesia and affects patient morbidity, mortality and hospital length of stay. Retention of sodium and water is known to occur during surgery but the mechanisms are poorly defined. In this study, we explore how the volatile anesthetic sevoflurane influences renal function by affecting renal sympathetic nerve activity (RSNA). Our results demonstrate that sevoflurane induces renal sodium and water retention during pediatric anesthesia in association with elevated plasma concentration of renin but not arginine-vasopressin. The mechanisms are further explored in conscious and anesthetized ewes where we show that RSNA is increased by sevoflurane compared with when conscious. This is accompanied by renal sodium and water retention and decreased renal blood flow. Finally, we demonstrate that renal denervation normalizes renal excretory function and improves renal blood flow during sevoflurane anesthesia in sheep. Taken together this study describes a novel role of the renal sympathetic nerves in regulating renal function and blood flow during sevoflurane anesthesia.

Cofilin-1 as a potential biomarker to evaluate acute kidney injury

2018 ◽  
Vol 44 (1) ◽  
pp. 9-15
Author(s):  
Abdurrahman Coşkun ◽  
Yasemin Ucal ◽  
Ibrahim Berber ◽  
Ülkem Çakır ◽  
Mustafa Serteser ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Current Knowledge ◽  
Kidney Injury ◽  
Rapid Loss ◽  
Serum Samples ◽  
Preservation Solution ◽  
Kidney Preservation ◽  
Excretory Function ◽  
Potential Biomarker ◽  
New Biomarkers

Abstract Acute kidney injury (AKI) is a worldwide health problem and defined by rapid loss of excretory function of the kidney with the accumulation of metabolic end products. For effective treatment and prevent complications the early diagnosis of AKI is crucial. The current analytes used to diagnose AKI are not adequately sensitive and specific and therefore clinicians need new biomarkers. One of the new promising biomarker candidates of renal injury is cofilin-1. Previously, in our laboratory we isolated cofilin-1 in kidney preservation solution prior to transplantation and attempted to measure serum cofilin-1 in renal transplanted patients. However, cofilin-1 was not accurately measured in serum samples due to the methodological issues. In this mini-review, we summarized the current knowledge and concepts both in the literature and our experiences with cofilin-1 as a potential biomarker for the diagnosis and management of AKI.

scholarly journals Blunted natriuretic response to saline loading in sheep with hypertensive kidney disease following radiofrequency catheter-based renal denervation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Reetu R. Singh ◽  
Zoe McArdle ◽  
Harshil Singh ◽  
Lindsea C. Booth ◽  
Clive N. May ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Disease ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Sympathetic Nerves ◽  
Excretory Function ◽  
Load Following ◽  
Saline Loading ◽  
Renal Sympathetic

AbstractRenal sympathetic nerves contribute to renal excretory function during volume expansion. We hypothesized that intact renal innervation is required for excretion of a fluid/electrolyte load in hypertensive chronic kidney disease (CKD) and normotensive healthy settings. Blood pressure, kidney hemodynamic and excretory response to 180 min of isotonic saline loading (0.13 ml/kg/min) were examined in female normotensive (control) and hypertensive CKD sheep at 2 and 11 months after sham (control-intact, CKD-intact) or radiofrequency catheter-based RDN (control-RDN, CKD-RDN) procedure. Basal blood pressure was ~ 7 to 9 mmHg lower at 2, and 11 months in CKD-RDN compared with CKD-intact sheep. Saline loading did not alter glomerular filtration rate in any group. At 2 months, in response to saline loading, total urine and sodium excretion were ~ 40 to 50% less, in control-RDN and CKD-RDN than intact groups. At 11 months, the natriuretic and diuretic response to saline loading were similar between control-intact, control-RDN and CKD-intact groups but sodium excretion was ~ 42% less in CKD-RDN compared with CKD-intact at this time-point. These findings indicate that chronic withdrawal of basal renal sympathetic activity impairs fluid/electrolyte excretion during volume expansion. Clinically, a reduced ability to excrete a saline load following RDN may contribute to disturbances in body fluid balance in hypertensive CKD.

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