Patients with AKI were found to have a greater percentage rise of Cystatin C (118.7% v/s 81.8%, p = 0.005), IL-18 (59.0% v/s 25.5%, p = 0.004) and Uric acid (34.3% v/s 19.2%, p = 0.008) after 24 h. Absolute Uric acid level at day 1 was also significantly associated with AKI (5.18 ± 0.91 v/s 4.45 ± 0.86, p = 0.003).
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.
Serum creatinine and cystatin C provide conflicting evidence of acute kidney injury following acute ingestion of potassium permanganate and oxalic acid.
Compared with patients without AKI (1.01 ± 0.26 mg/L), the level of baseline serum cystatin C (CYS-C) was significantly higher in patients with AKI (3.64 ± 2.17 mg/L, <i>P</i> < 0.001).
Urinary kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and serum cystatin C (Cys C) are biomarkers of acute kidney injury (AKI).
Urinary neutrophil gelatinase-associated lipocalin (NGAL) and serum cystatin C measurements for early diagnosis of acute kidney injury in children admitted to PICU.
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.
Cystatin C has also been shown to outperform creatinine as an indicator of true GFR and to add information about the occurrence of acute kidney injury.
The anti-C5 antibody ameliorated the intra-renal complement activation (intra-renal C3 and C6), reduced systemic inflammation (C-reactive protein, and systemic C3), decreased intra-renal acute tubular necrosis damage and improved GFR (seen by the sensitive marker, serum cystatin C; 1.63 mg/L (I/R + placebo), 1.36 mg/L (I/R + low dose) and 1.21 mg/L (I/R + high dose), <i>p</i> = .08 and .03 compared with I/R + placebo).<b>Conclusion:</b> In I/R-induced AKI, the monoclonal anti-C5 complement factor ameliorates intra renal complement activation, decreases local and systemic inflammation and may improve GFR.
In addition, they reduced molecular biomarkers of kidney injury such as KIM-1 and Cystatin C, while increased the markers of proximal tubular epithelium such as AQP-1 and CK18 following cisplatin-induced AKI.
Overall area under the curve of serum cystatin C and urine cystatin C in prediction of AKI were 0.83 (95% CI: 0.80-0.86) and 0.85 (95% CI: 0.81-0.88), respectively.
The gold standard, serum creatinine, displays poor specificity and sensitivity with regard to identification of the incipient phase of AKI, and this is also true for cystatin C. We aimed to review novel biomarkers of AKI in urine and serum which have now progressed to the clinical phase.
These data were correlated to following preoperative parameters of kidney function: cystatin C, creatinine, FGF-23 and estimated glomerular filtration rate (eGFR), and outcome data (death, acute renal failure) using linear and logistic regressions, as well as nonparametric tests.
The best combined sensitivity/specificity for percent CysC rise to predict stage 1 SCr-AKI was with a 44 % CysC rise (sensitivity = 65 %, specificity = 83 %).
Overall, 26% of the total cohort had an eGFR <90 mL/min/1.73 m<sup>2</sup> using serum cystatin C (35% of AKI subjects, 14% of no AKI subjects, p = 0.25).
Over the past decade, numerous clinical studies have evaluated the utility of several biomarkers (e.g. neutrophil gelatinase-associated lipocalin, interleukin-18, liver-type fatty acid binding protein and kidney injury molecule-1, cystatin C) in the early diagnosis and risk stratification of AKI.
Evaluation of neutrophil gelatinase-associated lipocalin and cystatin C as biomarkers of acute kidney injury after ST-segment elevation myocardial infarction treated by percutaneous coronary intervention.
The plasma and urine concentrations of neutrophil gelatinase-associated lipocalin and cystatin C were assessed on the second day after intensive care unit admission and were followed for seven days to monitor the development of acute kidney injury.
The discriminative and prognostic aptitudes of serum cystatin-C as well as N-acetylglucosaminidase (NAG) and Interleukin-18 (IL-18) were inspected for the estimation of AKI.