In a cohort of patients diagnosed with acute kidney injury after cardiopulmonary bypass surgery, the decreased TG and cholesterol negatively correlated with increased EPO in serum.
The patients were monitored with serum neutrophil gelatinase-associated lipocalin (NGAL), blood urea and serum creatinine for assessing the degree of acute kidney injury.
SIRT1 activation and p53 deacetylation might be identified as potential targets for attenuating premature renal senescence and retarding the progression of CKD post AKI.
Measurement of the plasma NGAL level at the time ED presentation might improve the prediction of long-term neurological outcomes in patients who do not develop AKI after acute charcoal-burning CO poisoning.
In a typical at-risk population undergoing coronary and/or peripheral angiography, blood concentrations of KIM-1 may predict incident peri-procedural and non-procedural AKI, as well as progression to CKD.
Of these, neutrophil gelatinase-associated lipocalin is the most promising; however, significant overlap occurs among AKI phenotypes, with diagnostic values yet to be defined.
Both urinary biomarkers (Neutrophil Gelatinase Associated Lipocalin and Kidney Injury Molecule-1) of acute kidney injury (AKI) progressively increased during the race (p<0.05 vs baseline).
Together, these results suggested that NA attenuates sepsis-associated AKI through the downregulation of IL-6/sIL-6R axis activation-mediated renal PGC-1α suppression.
VEGF is known to play important roles in acute kidney injury (AKI), and the present study investigates the efficacy of SW for AKI by renal ischemia-reperfusion (I/R) injury.
Serum IL-24 was detected earlier than the elevation of serum creatinine levels and urinary IL-24 was detected as early as neutrophil gelatinase associated lipocalin (NGAL) in severe AKI (60 min of IRI).
Median levels of 5 biomarkers were significantly higher in AKI cases than controls at 1-3 days before AKI onset (all µg/mmol): clusterin [58(8-411) versus 7(3-17)], beta-2-microglobulin [1632(913-3823) versus 253(61-791)], KIM1 [0.16(0.13-0.76) versus 0.07(0.05-0.15)], MCP1 [0.40(0.16-1.90) versus 0.07(0.04-0.17)], and cystatin-C [33(27-2990) versus 11(7-19)], all p<0.05; their AUROC for AKI prediction were >0.80 (confidence intervals >0.50), with average accuracy highest for clusterin (86%), followed by beta-2-microglobulin, cystatin-C, MCP1, and KIM1 (57%) after cross-validation.
Among all biomarkers, urinary NGAL measured at day 3 had the greatest accuracy for differential diagnosis between ATN and other types of AKI (area under the receiver operating characteristic curve, 0.87; 95% confidence interval, 0.78-0.95).
Cisplatin treatment was associated with significantly greater severity of AKI in knockout compared with wild-type mice, as demonstrated by semiquantitative injury score (2.8 versus 1.89, P < 0.001), blood urea nitrogen (151.8 ± 17.2 mg/dL versus 97.8 ± 10.1 mg/dL, P < 0.05), and neutrophil gelatinase-associated lipocalin urine protein (55.6 ± 21.3 μg/mL versus 2.7 ± 0.53 μg/mL, P < 0.05).
We hypothesised that polymorphisms in 4 candidate genes, namely angiotensin-converting enzyme (ACE), apolipoprotein-E (ApoE), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-α) are associated with AKI.
Acute kidney injury is a frequent disorder that can be mimicked by the application of different nephrotoxic agents, including carbon tetrachloride (CCl<sub>4</sub>), where kidney injury marker-1 (KIM-1) has been recognized as a highly specific marker.
Ultra-high-performance liquid chromatography-mass spectrometry method for neutrophil gelatinase-associated lipocalin as a predictive biomarker in acute kidney injury.
Neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule 1 (KIM-1) are noninvasive urinary biomarkers that are believed to be highly sensitive to CNI-induced AKI.