Finally, there are consistent data showing that some urine biomarkers, particularly NGAL (neutrophil gelatinase-associated lipocalin), may be useful in daily clinical practice for the differential diagnosis of the cause of AKI in cirrhosis.
The INK4a-ARF (CDKN2A) locus on chromosome 9p21 encodes two tumour suppressor proteins, p16(INK4a) and p14(ARF), which act as upstream regulators of the Rb-CDK4 and p53 pathways.
p14(ARF) tumor suppressor protein regulates p53 by interfering with mdm2-p53 interaction. p14(ARF) is activated in response to oncogenic stimuli but little is known of the responses of endogenous p14(ARF) to different types of cellular stress or DNA damage.
Therefore, in this study, we evaluated myo-inositol oxygenase (MIOX), neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C in terms of their applicability in the diagnosis of AKI.
One-year mortality was 32%.Risk factors and their weights were: acute kidney injury (2), American Society of Anesthesiology class greater than or equal to 4 (2), Charlson Comorbidity Index greater than or equal to 4 (1), albumin less than 3.5 mg/dL (1), and body mass index (less than 18.5 kg/m<sup>2</sup> [1]; 18.5 to 29.9 kg/m<sup>2</sup> [0]; ≥30 kg/m<sup>2</sup> [-1]).
Multivariable logistic regression analysis showed that male sex (OR, 4.45; 95% CI, 1.80-11.82; P = 0.002), preoperative use of beta-blockers (OR, 4.81; 95% CI, 1.24-16.50; P = 0.016), low preoperative serum albumin levels (OR, 0.29; 95% CI, 0.11-0.76; P = 0.011), and colloid administration (OR, 5.18; 95% CI, 1.42-18.15; P = 0.011) were associated with postoperative AKI.
The patients with AKI had significantly higher mean value of CRP and CAR (0.29 [0.16-0.50] vs. 0.55 [0.37-1.05]; p<0.001) and lower mean levels of albumin than those without AKI.
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.
Urinary IGFBP-7 level was predictive of severe AKI and achieved the AUC of 0.79 (P = 0.001), but was not better than serum (AUC = 0.89, P < 0.001) and urinary (AUC = 0.88, P < 0.001) CysC in predicting severe AKI.
Although serum cystatin C and creatinine are used as practical markers of renal function, the discrepancy between them in postrenal acute kidney injury (AKI) cases was reported.
In summary, we documented that TLR2 plays a protective role in cisplatin-induced AKI progression, in part, by a mechanism associated with autophagy up-regulation, considering that its interplay with HO-1 can promote renal tissue recover.
However, the uNGAL/uCreatinine ratio and bNGAL concentrations were significantly higher after 18 hours in the AKI group (no-AKI 1.69 (0.91 - 2.47) <i>vs</i> AKI 3.2 (2.08 - 5.92) ng/mg for uNGAL/uCreatinine ratio, P = 0.036; and no-AKI 83 (59 - 131) vs AKI 164 (126 - 263) ng/mL for bNGAL, P = 0.029).
The p14(ARF) tumor-suppressor gene product specifically interacts with human double minute 2, leading to the subsequent stabilization of p53 and G(1) arrest.
Logistic regression analysis was performed to obtain the odds ratio of AKI for various admission albumin strata using the albumin 3.5 to 3.9 mg/dL (lowest incidence of AKI) as the reference group.
We measured the ability of neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), liver type fatty-acid binding protein (L-FABP), kidney injury molecule-1 (KIM-1), tissue inhibitor of metalloproteinase-2 (TIMP-2), and insulin-like growth factor binding protein 7 (IGFBP7), to predict AKI (≥50% increase in serum creatinine from baseline).
(1) AKI diagnosed by change in Scr concentration during donor hospitalization and (2) concentrations of urinary biomarkers (neutrophil gelatinase-associated lipocalin [NGAL], liver-type fatty acid-binding protein [L-FABP], interleukin 18 [IL-18], and kidney injury molecule 1 [KIM-1]) measured at organ procurement.
Serum cystatin C and serum or urine NGAL have been shown to predict or diagnose AKI in AP; however, this evidence come from the single center studies of low number of patients.
We defined AKI as glomerular filtration rate (GFR) < 60 mL/min/1.73 m<sup>2</sup>; measured urine NGAL, CysC, TIMP-2, and protein; and explored AKI incidence, risk factors, and associations with mortality using Cox proportional hazards models.
Internal translational initiation of the mRNA encoding the Arf tumor suppressor yields an N-terminally truncated small Arf protein (smArf) that lacks amino acid residues required for Mdm2 binding and p53 activation.
Postoperative plasma biomarkers including NGAL, h-FABP, CK-MB, hsTNT, NT-proBNP, IL-6, IL-10 and VEGF were analyzed using group-based method among 426 patients with AKI after cardiac surgery.
Serum creatinine and cystatin C provide conflicting evidence of acute kidney injury following acute ingestion of potassium permanganate and oxalic acid.