Implementing the Kidney Disease

Hoste, Eric; Corte, Wouter De

doi:10.1097/mcc.0000000000000039

Cited by 18 publications

(11 citation statements)

References 87 publications

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“…We calculated the duration of delirium as the cumulative number of days during which at least one assessment diagnosed delirium [30]. Secondary outcomes were: mortality within 30 and 90 postoperative days; duration of mechanical ventilation, ICU and hospital stay; hypotension (<30% of baseline blood pressure) during and after trial drug infusion; ventricular arrhythmias; and acute kidney injury [31].…”

Section: Methodsmentioning

confidence: 99%

A randomised controlled trial of dexmedetomidine for delirium in adults undergoing heart valve surgery

Jia

Zhang

et al. 2023

Anaesthesia

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Dexmedetomidine might reduce delirium after cardiac surgery. We allocated 326 participants to an infusion of dexmedetomidine at a rate of 0.6 lg kg À1 for 10 min and then at 0.4 lg.kg À1 .h À1 until the end of surgery; 326 control participants received comparable volumes of saline. We detected delirium in 98/652 (15%) participants during the first seven postoperative days: 47/326 after dexmedetomidine vs. 51/326 after placebo, p = 0.62, adjusted relative risk (95%CI) 0.86 (0.56-1.33), p = 0.51. Postoperative renal impairment (Kidney Disease Improving Global Outcomes stages 1, 2 and 3) was detected in 46, 9 and 2 participants after dexmedetomidine and 25, 7 and 4 control participants, p = 0.040. Intra-operative dexmedetomidine infusion did not reduce the incidence of delirium after cardiac valve surgery but might impair renal function.

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Section: Methodsmentioning

confidence: 99%

A randomised controlled trial of dexmedetomidine for delirium in adults undergoing heart valve surgery

Jia

Zhang

et al. 2023

Anaesthesia

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“…He observed large vacuoles in tubular epithelial cells following hypertonic sucrose infusion in rabbits [113] and humans [114, 115] and interpreted the vacuolization as the result of an osmotic gradient between the tubular lumen and tubular cells [116]. Hydropic vacuolization develops after intravenous injection of substances eliminated by the kidney, such as RCM [72, 114], polyethylene-glycol- (PEG-) conjugated proteins [117], hydroxy-ethyl-starch (HES) [118–120], dextran [121, 122], sucrose [43], mannitol [123], glucose [124], glycerol [125], sorbitol [126], inulin [127], or sugar (sucrose [128–130] or maltose [131]) stabilized intravenous immunoglobulin (IVIG) solutions. According to our experience (Figures 3(c) and 3(d)) different concentrations and repeated intraperitoneal doses of sucrose or maltose induced tubular vacuolization dose dependently.…”

Section: Characteristic Histopathological Changes In Ci-akimentioning

confidence: 99%

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Kiss

Hamar

2016

BioMed Research International

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Contrast-induced acute kidney injury (CI-AKI) can occur in 3–25% of patients receiving radiocontrast material (RCM) despite appropriate preventive measures. Often patients with an atherosclerotic vasculature have to receive large doses of RCM. Thus, animal studies to uncover the exact pathomechanism of CI-AKI are needed. Sensitive and specific histologic end-points are lacking; thus in the present review we summarize the histologic appearance of different rodent models of CI-AKI. Single injection of RCM causes overt renal damage only in rabbits. Rats and mice need an additional insult to the kidney to establish a clinically manifest CI-AKI. In this review we demonstrate that the concentrating ability of the kidney may be responsible for species differences in sensitivity to CI-AKI. The most commonly held theory about the pathomechanism of CI-AKI is tubular cell injury due to medullary hypoxia. Thus, the most common additional insult in rats and mice is some kind of ischemia. The histologic appearance is tubular epithelial cell (TEC) damage; however severe TEC damage is only seen if RCM is combined by additional ischemia. TEC vacuolization is the first sign of CI-AKI, as it is a consequence of RCM pinocytosis and lysosomal fusion; however it is not sensitive as it does not correlate with renal function and is not specific as other forms of TEC damage also cause vacuolization. In conclusion, histopathology alone is insufficient and functional parameters and molecular biomarkers are needed to closely monitor CI-AKI in rodent experiments.

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“…Despite novel drugs and improvements in critical care including renal replacement therapy, the outcomes for critically ill acute kidney injury (AKI) patients remains poor and its incidence during hospitalization keeps increasing [ 1 – 6 ]. Acute kidney ischemia-reperfusion (KIR) that causes AKI is frequently observed during contrast-media induced nephropathy [ 5 ], post-resuscitation shock [ 7 ], kidney transplantation [ 8 ] and chemical or drug toxicity.…”

Section: Introductionmentioning

confidence: 99%

DPP-4 enzyme deficiency protects kidney from acute ischemia-reperfusion injury: role for remote intermittent bowel ischemia-reperfusion preconditioning

et al. 2017

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We analyzed the effects of acute ischemia-reperfusion (KIR) injury on the status of kidney function and architecture in dipeptidyl peptidase4-difficient (DPP4D) rats and the effect of remote small bowel ischemia-reperfusion (BIR) preconditioning. DPP4-deficient (DPP4D) and normal Fischer344 (F344) rats were divided into 6 groups: (1) sham-F344, (2) sham-DPP4D, (3) KIR-F344 (4) KIR-DPP4D, (5) DPP4D-KIR-extendin-9-39 and (6) BIR-KIR-F344. Blood creatinine and urea nitrogen levels and the urinary protein-to-creatinine ratio was higher in KIR-F344 rats than BIR-KIR-F344 or KIR-DPP4D rats 72 h after acute KIR. Conversely, the circulating glucagon-like peptide 1 (GLP-1) levels were higher in BIR-KIR-F344 and KIR-DPP4D than KIR-F344 rats after acute KIR. KIR-F344 rats showed greater inflammation, oxidative stress, apoptosis, DNA damage and kidney injury than other rat groups. Damage to the kidney architecture in KIR-F344 rats was greater than in BIR-KIR-F344 or KIR-DPP4D rats. Expression of antioxidant proteins and GLP-1 receptor was higher in kidneys from KIR-DPP4D and BIR-KIR-F344 than KIR-F344 rats, which suggests better intrinsic responses. We therefore suggest that elevated circulating GLP-1 levels due to DPP4 deficiency and BIR preconditioning protect kidney function and architecture during acute IR injury.

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Implementing the Kidney Disease

Abstract: The KDIGO guidelines as presented in 2012 provide guidelines on the domain of definition of AKI, prevention and treatment, contrast-induced AKI and dialysis interventions for AKI. Especially, early application of a set of measures, the AKI bundle, may prevent AKI and improve outcome.

Cited by 18 publications

References 87 publications

A randomised controlled trial of dexmedetomidine for delirium in adults undergoing heart valve surgery

A randomised controlled trial of dexmedetomidine for delirium in adults undergoing heart valve surgery

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

DPP-4 enzyme deficiency protects kidney from acute ischemia-reperfusion injury: role for remote intermittent bowel ischemia-reperfusion preconditioning

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