Serum cystatin C in mouse models: a reliable and precise marker for renal function and superior to serum creatinine

Song, Su Hyun; Meyer, Marko; Türk, Tobias R.; Wilde, Benjamin; Feldkamp, Thorsten; Assert, Roland; Wu, Kun; Kribben, Andreas; Witzke, Oliver

doi:10.1093/ndt/gfn626

Cited by 88 publications

(64 citation statements)

References 29 publications

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“…Mouse serum cystatin C has been reported as a reliable marker for renal function in mouse AKI models that could be better than serum creatinine levels. 28,29 B cell-transferred MT mice showed a tendency toward increased serum cystatin C level compared with MT mice (control versus MT mice versus B celltransferred MT mice, 961.1 Ϯ 40.6 versus 944.3 Ϯ 22.6 versus 1072.0 Ϯ 57.9 ng/ml; P ϭ 0.083 between MT mice and B celltransferred MT mice). MR16-1-treated mice had lower serum cystatin C level than control IgG-treated mice (control IgG versus MR16-1-treated mice, 1222.4 Ϯ 109.4 versus 876.2 Ϯ 77.8 ng/ml; P Ͻ 0.05; Figure 9).…”

Section: Anti-mouse Cd126 Antibody-treated Mice Had Less Tubular Atromentioning

confidence: 95%

B Cells Limit Repair after Ischemic Acute Kidney Injury

Jang

Gandolfo

Ko³

et al. 2010

Journal of the American Society of Nephrology

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Section: Anti-mouse Cd126 Antibody-treated Mice Had Less Tubular Atromentioning

confidence: 95%

B Cells Limit Repair after Ischemic Acute Kidney Injury

Jang

Gandolfo

Ko³

et al. 2010

Journal of the American Society of Nephrology

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“…Relative to the above confusing results, using biomarkers to assess hypothermia treatment appears to be more clarity and reliable. Both NGAL and CysC are sensitive for the prediction of moderate-to-severe kidney injury in the early stage after ROSC [20][21][22] .NGAL is expressed in epithelial cells in different organs, and is considered to be an inflammatory mediator whose expression is upregulated in tubular injury. In CA patients, NGAL measured in blood within 4h after ROSC is a predictor of AKI…”

Section: ■ Discussionmentioning

confidence: 99%

Effect of mild hypothermia on renal ischemia/reperfusion injury after cardiopulmonary resuscitation in a swine model

Yuan

Zhao

et al. 2017

Acta Cir. Bras.

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Purpose: To investigate the effect of intravascular cooling on renal function after resuscitation. Methods: Twenty four pigs were randomized into three groups (n=8 in each group): therapeutic hypothermia group (TH group), normothermia group (NH group) and sham operation group (SHAM group). After 6 minutes of untreated VF, CPR was performed. Upon ROSC, the TH group received the intravascular cooling. The NH and SHAM group did not undergo therapeutic hypothermia. Haemodynamic parameters were recorded. The bloods were analyzed for serum creatinine (sCr), CysC and NGAL. The kidney was surgically removed observe pathologic changes under a light microscope. Results: The sCr increased in both TH and NH groups after ROSC, compared to baseline. Between two groups, the sCr and creatinine clearance (Cc) showed lower level in the TH group. The urine volume per hour in the TH group were higher during cooling. After resuscitation, NGAL and CysC in the NH group were higher than in the TH group. Under the light microscope, compared with the TH group, the renal injury was prominent in the NH group. Conclusion: Mild hypothermia had a protection to renal ischemia reperfusion injury after resuscitation.

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“…Serum ALT concentration was determined using a DRI-CHEM 4000 Chemistry Analyzer System (Heska) (23). Renal function was determined by assaying serum for cystatin C [interassay coefficient of variability (CV): 2.8%] using an enzyme immunoassay kit (R&D) (55). Histology.…”

Section: Methodsmentioning

confidence: 99%

Blue light reduces organ injury from ischemia and reperfusion

Yuan

Collage

Huang

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Evidence suggests that light and circadian rhythms profoundly influence the physiologic capacity with which an organism responds to stress. However, the ramifications of light spectrum on the course of critical illness remain to be determined. Here, we show that acute exposure to bright blue spectrum light reduces organ injury by comparison with bright red spectrum or ambient white fluorescent light in two murine models of sterile insult: warm liver ischemia/reperfusion (I/R) and unilateral renal I/R. Exposure to bright blue light before I/R reduced hepatocellular injury and necrosis and reduced acute kidney injury and necrosis. In both models, blue light reduced neutrophil influx, as evidenced by reduced myeloperoxidase (MPO) within each organ, and reduced the release of high-mobility group box 1 (HMGB1), a neutrophil chemotactant and key mediator in the pathogenesis of I/R injury. The protective mechanism appeared to involve an optic pathway and was mediated, in part, by a sympathetic (β3 adrenergic) pathway that functioned independent of significant alterations in melatonin or corticosterone concentrations to regulate neutrophil recruitment. These data suggest that modifying the spectrum of light may offer therapeutic utility in sterile forms of cellular injury.

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Serum cystatin C in mouse models: a reliable and precise marker for renal function and superior to serum creatinine

Cited by 88 publications

References 29 publications

B Cells Limit Repair after Ischemic Acute Kidney Injury

B Cells Limit Repair after Ischemic Acute Kidney Injury

Effect of mild hypothermia on renal ischemia/reperfusion injury after cardiopulmonary resuscitation in a swine model

Blue light reduces organ injury from ischemia and reperfusion

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