The preoperative serum albumin level was associated with postoperative AKI (odds ratio [OR] 0.506, 95% confidence interval [CI] 0.325-0.788; P = 0.003).
We report here that NO induces the accumulation of transcriptionally active p53 in a variety of cell types and that NO signaling to p53 does not require ataxia telangiectasia-mutated (ATM), poly(ADP-ribose) polymerase 1, or the ARF tumor suppressor protein.
To explore the role of ASPP2 in the progression of AKI, we prepared an AKI mouse model induced by ischaemia reperfusion (I/R) in wild-type (ASPP2<sup>+/+</sup> ) mice and ASPP2 haploinsufficient (ASPP2<sup>+/-</sup> ) mice.
These findings indicate that farrerol can effectively activate Nrf2 and can serve as a therapeutic target in the treatment of acute kidney injury (AKI).
Increased biomarker levels of acute kidney injury (AKI) in HK-2 cells, including kidney injury molecule-1, neutrophil gelatinase-associated lipocalin and cystatin C, decrease the mitochondrial membrane potential in HK-2 cells, and cause mitochondrial dysfunction, it also reduced the ratio of mitochondria-associated apoptotic protein Bax/Bcl-2, leading to cell apoptosis.
Both plasma and urinary KIM-1 expression levels were significantly higher in AKI and chronic kidney disease (CKD) patients than in healthy volunteers, and urinary KIM-1 expression was significantly higher in CKD patients than in AKI patients.
There was an increase in kidney expression of pro-inflammatory cytokines CXCL1 and TNF-α, known mediators of cisplatin-induced AKI, in IL-33-deficient mice.
Urinary L-type fatty acid-binding protein (L-FABP), neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), N-acetyl-β-D-glucosaminidase (NAG), and albumin in patients with prerenal AKI showed modest but significantly higher concentrations than in patients with non-AKI.
Urinary KIM-1 and NGAL could efficiently discriminate patients with or without vancomycin-associated AKI earlier than Scr, and the combined urinary biomarkers showed fair discrimination compared with the individual biomarkers.
Insight into the pathophysiology of acute kidney injury is gleaned from the temporal change markers of renal injury (urine neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, calbindin), followed by a marker of cell cycle arrest (urine insulin-like growth factor-binding protein 7) and, finally, by functional markers of filtration (serum creatinine and cystatin C).
We have examined how disease progression correlates with changes in expression of the p14ARF (ARF) tumour suppressor, a key regulator of the p53 tumour suppressor pathway that is silenced in some 30% of cancers overall, but for which a role in oesophageal cancer is unclear.
This study investigated the possible renoprotective effect of telluric acid (TEL) against lipopolysaccharide (LPS)-induced acute kidney injury (AKI) in mice, targeting toll-like receptor 4 (TLR4), phosphoinositide 3-kinase (PI3K)/Akt, and nuclear factor-erythroid 2-related factor-2 (Nrf2) pathways as possible mechanistic contributors to TEL's effect.AKI was induced by LPS (2 mg/kg).TEL (60 μg/kg; i.p.) was administered once daily for seven consecutive days before LPS injection.
The neutrophil gelatinase-associated lipocalin (NGAL) has been emerging as a novel biomarker of acute kidney injury while its value in lupus nephritis is uncertain.
We will describe the presumed pathophysiological role and diagnostic value of sepsis markers that are used even more widely in the clinical practice (i.e. procalcitonin, IL-6), summarize the data regarding the sepsis marker candidates that are investigated in some initial study (i.e. matrix metalloproteinases, microRNA fingerprints), and we will discuss substances that may be specific markers for certain organ failures related to sepsis (i.e. neutrophil gelatinase-derived lipocalin in acute renal failure).
Hence, we studied this AKI model to determine whether p53 activation corresponds with p21 gene induction and/or whether alternative mechanism(s) might be involved.
S-nitrosoglutathione attenuates the severity of LPS-induced AKI by inhibiting the TLR4-NF-κB signalling pathway and may act as a protective agent for septic AKI.
Control patients were healthy children enrolled from the emergency department with no history of UTI or renal dysfunction, normal urinalysis at the time of enrollment, and presenting no diagnosis associated with increased NGAL levels, such as acute kidney injury or infection.NGAL was measured by immunoblot.
Multivariable logistic regression analysis indicated that presence of tumors, higher serum albumin, and AKI stage 1 were associated with failure to timely diagnose AKI, whereas presence of chronic kidney disease, oliguria, higher blood urea nitrogen, and greater number of organ failures correlated with earlier diagnosis.
Poor cardiac function (left ventricular ejection fraction < 35%) prior to surgery was a significant contributing factor associated with the onset of AKI [odds ratio (OR) 5.55, 95% confidential interval (CI) 1.39-22.13; P = 0.015], while a longer duration from diagnosis to surgical repair (OR 0.97, 95% CI 0.95-1.00; P = 0.049) and a higher preoperative albumin level (OR 0.83, 95% CI 0.70-0.99; P = 0.041) were found to lower the risk of AKI.
Neutrophil gelatinase-associated lipocalin (NGAL) is a predictive biomarker of acute kidney injury and may increase after cardiopulmonary bypass (CPB).
Although the importance of the ARF tumor suppressor in p53 regulation is well established, numerous studies indicate that ARF also suppresses cell growth in a p53/Mdm2-independent manner.