Acute Renal Failure and the Critically Ill Surgical Patient

Sykes, Eliot; Cosgrove, J. F.

doi:10.1308/003588407x155536

Cited by 22 publications

(12 citation statements)

References 47 publications

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“…A history of diabetes has been shown to predict greater susceptibility to or worse outcomes with acute renal failure and trauma (12, 13). In contrast to this, a large, prospective, multicenter study of patients with septic shock found diabetes to be protective against the development of ALI.…”

Section: Resultsmentioning

confidence: 99%

Diabetes, insulin, and development of acute lung injury

Honiden

Gong

2009

Critical Care Medicine

114

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Objectives-Recently, many studies have investigated the immunomodulatory effects of insulin and glucose control in critical illness. This review examines evidence regarding the relationship between diabetes and the development of acute lung injury/acute respiratory distress syndrome (ALI/ARDS), reviews studies of lung injury related to glycemic and nonglycemic metabolic features of diabetes, and examines the effect of diabetic therapies.Data Sources and Study Selection-A MEDLINE/PubMed search from inception to August 1, 2008, was conducted using the search terms acute lung injury, acute respiratory distress syndrome, hyperglycemia, diabetes mellitus, insulin, hydroxymethylglutaryl-CoA reductase inhibitors (statins), angiotensin-converting enzyme inhibitor, and peroxisome proliferatoractivated receptors, including combinations of these terms. Bibliographies of retrieved articles were manually reviewed.Data Extraction and Synthesis-Available studies were critically reviewed, and data were extracted with special attention to the human and animal studies that explored a) diabetes and ALI; b) hyperglycemia and ALI; c) metabolic nonhyperglycemic features of diabetes and ALI; and d) diabetic therapies and ALI.Conclusions-Clinical and experimental data indicate that diabetes is protective against the development of ALI/ARDS. The pathways involved are complex and likely include effects of hyperglycemia on the inflammatory response, metabolic abnormalities in diabetes, and the interactions of therapeutic agents given to diabetic patients. Multidisciplinary, multifaceted studies, involving both animal models and clinical and molecular epidemiology techniques, are essential. Keywordsacute respiratory distress syndrome; acute lung injury; hyperglycemia; diabetes mellitus; insulin Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a devastating condition defined by the American-European Consensus Committee on ARDS as an acute syndrome of lung inflammation and increased permeability associated with severe hypoxia and bilateral infiltrates on chest radiographs with no evidence of left heart failure (1). Decades of animal and clinical studies have identified several pathophysiologic mechanisms important in the development of ALI/ARDS. Acute inflammation is a key feature, as evidenced by the central role of neutrophil recruitment and activation and the increased expression and release of inflammatory mediators, such as proinflammatory and antiinflammatory cytokines and chemokines. Disturbances in surfactant function and edema Copyright © 2009 clearance are present, and ample evidence supports imbalances in oxidant/antioxidant activity (2), coagulation/fibrinolysis, and fibrosis/repair. The relative balance of these interacting pathways either exacerbates or ameliorates further lung injury (3,4).ALI/ARDS is a commonly encountered condition, with 190,600 cases of ALI per year in the United States and an associated 74,500 deaths and 3.6 million hospital days (5). Of the predisposing injuries for ALI/ARDS, ...

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Section: Resultsmentioning

confidence: 99%

Diabetes, insulin, and development of acute lung injury

Honiden

Gong

2009

Critical Care Medicine

114

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“…However, immediate fluid therapy for potential circulatory deficits, avoidance and minimizing the use of nephrotoxic agents and dosage adjustment of medication according to kidney function are sometimes effective for preventing worsening of the early stages of AKI. 20 Transplant physicians and nephrologists need to work together in the treatment of patients receiving SCT to identify early renal disease and also to examine small changes in serum creatinine concentration or promising new urinary biomarkers. 6,21 Further efforts will be required to decrease the frequency of life-threatening AKI, with initial focus on m-allo and nmallo transplants.…”

Section: Discussionmentioning

confidence: 99%

A comparative assessment of the RIFLE, AKIN and conventional criteria for acute kidney injury after hematopoietic SCT

Ando

Mori

Ohashi

et al. 2010

Bone Marrow Transplant

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An observational cohort study was conducted to compare the performance of the RIFLE (risk, injury, failure, loss and end-stage kidney disease), AKIN (acute kidney injury network) and conventional graded criteria to identify acute kidney injury (AKI) following SCT and to predict long-term mortality in 141 myeloablative allogeneic SCT (m-allo), 60 non-myeloablative allogeneic SCT (nm-allo) and 48 autologous SCT (auto) cases. The AKIN criteria had less ability to identify patients as having the lowest category, stage 1 (analogous to RIFLE risk): 33% (37%) in m-allo, 23% (32%) in nm-allo and 8.3% (16.7%) in auto. Cox regression showed that categories higher than the intermediate stage were independent predictors of mortality in all three definitions. The areas under receiver operating characteristic curves showed that both definition systems had similar and significant ability to predict mortality (0.643-0.649 in m-allo and 0.734-0.766 in nmallo, respectively). These abilities of the conventional graded criteria were comparable with those of the RIFLE criteria. The RIFLE criteria have greater sensitivity than the AKIN criteria to identify patients with AKI and therefore are more favorable as a uniform definition system for post-SCT AKI. However, the RIFLE criteria do not improve on the clinical relevance of the conventional graded criteria.

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“…NFAT5 is ubiquitously expressed in all tissues and cellular types and particularly in tissues that are often subjected to osmotic stress, such as kidney renal medulla, eyes and skin [14][15][16]. NFAT5 is also highly expressed in mouse, ovine and human placenta [17,18] and at late gestation throughout the whole mouse embryo suggesting its important role during embryonic development and fetal maturation [19].…”

Section: Introductionmentioning

confidence: 99%

NFAT5 Is Up-Regulated by Hypoxia: Possible Implications in Preeclampsia and Intrauterine Growth Restriction1

Dobierzewska

Palominos

Irarrázabal

et al. 2015

Biology of Reproduction

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During gestation, low oxygen environment is a major determinant of early placentation process, while persistent placental hypoxia leads to pregnancy-related complications such as preeclampsia (PE) and intrauterine growth restriction (IUGR). PE affects 5%-8% of all pregnancies worldwide and is a cause of maternal and fetal morbidity and mortality. During placental development, persistent hypoxia due to poor trophoblast invasion and reduced uteroplacental perfusion leads to maternal endothelial dysfunction and clinical manifestation of PE. Here we hypothesized that nuclear factor of activated T cells-5 (NFAT5), a well-known osmosensitive renal factor and recently characterized hypoxia-inducible protein, is also activated in vivo in placentas of PE and IUGR complications as well as in the in vitro model of trophoblast hypoxia. In JAR cells, low oxygen tension (1% O2) induced NFAT5 mRNA and increased its nuclear abundance, peaking at 16 h. This increase did not occur in parallel with the earlier HIF1A induction. Real-time PCR and Western blot analysis confirmed up-regulation of NFAT5 mRNA and NFAT5 nuclear content in human preeclamptic placentas and in rabbit placentas of an experimentally induced IUGR model, as compared with the control groups. In vitro lambda protein phosphatase (lambda PPase) treatment revealed that increased abundance of NFAT5 protein in nuclei of either JAR cells (16 h of hypoxia) or PE and IUGR placentas is at least partially due to NFAT5 phosphorylation. NFAT5 downstream targets aldose reductase (AR) and sodium-myo-inositol cotransporter (SMIT; official symbol SLC5A3) were not significantly up-regulated either in JAR cells exposed to hypoxia or in placentas of PE- and IUGR-complicated pregnancies, suggesting that hypoxia-dependent activation of NFAT5 serves as a separate function to its tonicity-dependent stimulation. In conclusion, we propose that NFAT5 may serve as a novel marker of placental hypoxia and ischemia independently of HIF1A.

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Acute Renal Failure and the Critically Ill Surgical Patient

Cited by 22 publications

References 47 publications

Diabetes, insulin, and development of acute lung injury

Diabetes, insulin, and development of acute lung injury

A comparative assessment of the RIFLE, AKIN and conventional criteria for acute kidney injury after hematopoietic SCT

NFAT5 Is Up-Regulated by Hypoxia: Possible Implications in Preeclampsia and Intrauterine Growth Restriction1

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