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.

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.

scholarly journals Noninvasive Urine Oxygen Monitoring and the Risk of Acute Kidney Injury in Cardiac Surgery

2021 ◽  
Author(s):  
Natalie A. Silverton ◽  
Lars R. Lofgren ◽  
Isaac E. Hall ◽  
Gregory J. Stoddard ◽  
Natalia P. Melendez ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Oxygen Partial Pressure ◽  
Partial Pressure ◽  
Multivariable Analysis ◽  
Kidney Injury ◽  
Subsequent Development ◽  
Urine Flow ◽  
Pressure Measurements ◽  
Novel Device

Background Acute kidney injury (AKI) is a common complication of cardiac surgery. An intraoperative monitor of kidney perfusion is needed to identify patients at risk for AKI. The authors created a noninvasive urinary oximeter that provides continuous measurements of urinary oxygen partial pressure and instantaneous urine flow. They hypothesized that intraoperative urinary oxygen partial pressure measurements are feasible with this prototype device and that low urinary oxygen partial pressure during cardiac surgery is associated with the subsequent development of AKI. Methods This was a prospective observational pilot study. Continuous urinary oxygen partial pressure and instantaneous urine flow were measured in 91 patients undergoing cardiac surgery using a novel device placed between the urinary catheter and collecting bag. Data were collected throughout the surgery and for 24 h postoperatively. Clinicians were blinded to the intraoperative urinary oxygen partial pressure and instantaneous flow data. Patients were then followed postoperatively, and the incidence of AKI was compared to urinary oxygen partial pressure measurements. Results Intraoperative urinary oxygen partial pressure measurements were feasible in 86/91 (95%) of patients. When urinary oxygen partial pressure data were filtered for valid urine flows greater than 0.5 ml · kg–1 · h–1, then 70/86 (81%) and 77/86 (90%) of patients in the cardiopulmonary bypass (CPB) and post-CPB periods, respectively, were included in the analysis. Mean urinary oxygen partial pressure in the post-CPB period was significantly lower in patients who subsequently developed AKI than in those who did not (mean difference, 6 mmHg; 95% CI, 0 to 11; P = 0.038). In a multivariable analysis, mean urinary oxygen partial pressure during the post-CPB period remained an independent risk factor for AKI (relative risk, 0.82; 95% CI, 0.71 to 0.95; P = 0.009 for every 10-mmHg increase in mean urinary oxygen partial pressure). Conclusions Low urinary oxygen partial pressures after CPB may be associated with the subsequent development of AKI after cardiac surgery. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

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