Plasma and urine neutrophil gelatinase-associated lipocalin in septic versus non-septic acute kidney injury in critical illness

Bagshaw, Sean M.; Bennett, Michael; Haase, Michael; Haase-Fielitz, Anja; Egi, Moritoki; Morimatsu, Hiroshi; D’Amico, Giuseppe; Goldsmith, Donna; Devarajan, Prasad; Bellomo, Rinaldo

doi:10.1007/s00134-009-1724-9

Cited by 293 publications

(229 citation statements)

References 43 publications

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“…This is in contrast to the findings reported by Bagshaw and colleagues in this edition of the journal [2] who examined the measurement of both plasma and urinary NGAL in 83 patients with septic and non-septic AKI. Plasma NGAL was determined using the same technique as Cruz et al [3], whereas urinary NGAL was measured by a chemiluminescent microparticle assay using the ARCHITECT platform (Abbott Diagnostics Inc., Abbott Park, IL).…”

contrasting

confidence: 99%

“…Bagshaw et al [2] found a modest predictive capacity for worsening AKI (AuROC 0.71; 95% CI 0.55-0.88) and for the need of RRT (AuROC 0.70; 95% CI 0.58-0.82). It must be borne in mind that only a small number of patients with AKI did progress (N = 20) or need RRT (N = 13).…”

mentioning

confidence: 99%

“…Also, a larger trial of 451 critically ill adults demonstrated that urine NGAL, though independently associated with AKI, yielded only very moderate discrimination at 48 h [12]. Consequently, and in lack of a non-AKI control group, the study by Bagshaw et al [2] does not answer the question whether NGAL (either pNGAL or uNGAL) could help to discriminate between two different pathophysiologic entities of AKI (septic versus non-septic) or simply reflects the presence or absence of sepsis in addition to AKI.…”

mentioning

confidence: 99%

“…This issue of Intensive Care Medicine includes three studies addressing the performance of two biomarkers, serum neutrophil gelatinase-associated lipocalin (NGAL) and Ang-2, addressing specific applications in AKI [2][3][4].…”

mentioning

confidence: 99%

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Biomarkers and acute kidney injury: dining with the Fisher King?

2009

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Biomarkers and acute kidney injury: dining with the Fisher King?

2009

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“…They are investigated in different clinical settings including cardiac surgery [10], contrast agent use [11], critically ill patients [12][13][14][15][16][17][18][19][20][21] and in emergency department [22].…”

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confidence: 99%

The Use of Plasma and Urine Neutrophil Gelatinase Associated Lipocalin (NGAL) and Cystatin C in Early Diagnosis of Septic Acute Kidney Injury in Critically Ill Patients

et al. 2013

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Abstract. AIM:To assess and compare the roles of plasma and urine concentrations of neutrophil gelatinase associated lipocalin (NGAL) and Cystatin C for early diagnosis of septic acute kidney injury (AKI) in adult critically ill patients. METHODS: Patients were divided into three groups as sepsis-non AKI, sepsis-AKI and non sepsis-non AKI. Plasma samples for NGAL and Cystatin C were determined on admission and on alternate days and urinary samples were collected for every day until ICU discharge. RESULTS: One hundred fifty one patients were studied; 66 in sepsis-non AKI, 63 in sepsis-AKI, 22 in non-sepsis-non-AKI groups. Although plasma NGAL performed less well (AUC 0.44), urinary NGAL showed significant discrimination for AKI diagnosis (AUC 0.80) with a threshold value of 29.5 ng/ml (88% sensitivity, 73% specificity). Both plasma and urine Cystatin C worked well for the diagnosis of AKI (AUC 0.82 and 0.86, thresholds 1.5 and 0.106 mg/L respectively). CONCLUSION: Plasma and urinary Cystatin C and urinary NGAL are useful markers in predicting AKI in septic critically ill patients. Plasma NGAL raises in patients with sepsis in the absence of AKI and should be used with caution as a marker of AKI in septic ICU patients.

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Visceral fat‐specific regulation of plasminogen activator inhibitor‐1 in aged septic mice

Bruno

Mukherjee

Stromberg

et al. 2021

Journal Cellular Physiology

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Elevated plasma levels of plasminogen activator inhibitor-1 (PAI-1) are documented in patients with sepsis and levels positively correlate with disease severity and mortality. Our previous work demonstrated that visceral adipose tissues (VAT) are a major source of PAI-1, especially in the aged (murine endotoxemia), that circulating PAI-1 protein levels match the trajectory of PAI-1 transcript levels in VAT (clinical sepsis), and that PAI-1 in both VAT and plasma are positively associated with acute kidney injury (AKI) in septic patients. In the current study utilizing preclinical sepsis models, PAI-1 tissue distribution was examined and cellular sources, as well as mechanisms mediating PAI-1 induction in VAT, were identified. In aged mice with sepsis, PAI-1 gene expression was significantly higher in VAT than in other major organs. VAT PAI-1 gene expression correlated with PAI-1 protein levels in both VAT and plasma. Moreover, VAT and plasma levels of PAI-1 were positively associated with AKI markers, modeling our previous clinical data. Using explant cultures of VAT, we determined that PAI-1 is secreted robustly in response to recombinant transforming growth factor β (TGFβ) and tumor necrosis factor α (TNFα) treatment; however, neutralization was effective only for TNFα indicating that TGFβ is not an endogenous modulator of PAI-1. Within VAT, TNFα was localized to neutrophils and macrophages. PAI-1 protein levels were fourfold higher in stromal vascular fraction (SVF) cells compared with mature adipocytes, and among SVF cells, both immune and nonimmune compartments expressed PAI-1 in a similar fashion. PAI-1 was localized predominantly to macrophages within the immune compartment and preadipocytes and endothelial cells within the nonimmune compartment. Collectively, these results indicate that induction and secretion of PAI-1 from VAT is facilitated by a complex interaction among immune and nonimmune cells. As circulating PAI-1 contributes to AKI in sepsis, understanding PAI-1 regulation in VAT could yield novel strategies for reducing systemic consequences of PAI-1 overproduction.

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Plasma and urine neutrophil gelatinase-associated lipocalin in septic versus non-septic acute kidney injury in critical illness

Abstract: Septic AKI patients have higher detectable plasma and urine NGAL compared with non-septic AKI patients. These differences in NGAL values in septic AKI may have diagnostic and clinical relevance as well as pathogenetic implications.

Cited by 293 publications

References 43 publications

Biomarkers and acute kidney injury: dining with the Fisher King?

Biomarkers and acute kidney injury: dining with the Fisher King?

The Use of Plasma and Urine Neutrophil Gelatinase Associated Lipocalin (NGAL) and Cystatin C in Early Diagnosis of Septic Acute Kidney Injury in Critically Ill Patients

Visceral fat‐specific regulation of plasminogen activator inhibitor‐1 in aged septic mice

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