• KIM-1
• SDF-1
• Withania somnifera
• mercuric chloride
• oxidative stress
• renal toxicity

• experimental renal insufficiency
• hyperuricaemia
• kidney morphology
• oxonic acid

• Mammary human cells lines
• Mercury
• Metallomics
• Toxicity

• Cell Line
• Chromatography, High Pressure Liquid
• Humans
• Mammary Glands, Human/cytology
• Mercury/toxicity
• Metals/metabolism
• Protein Binding/drug effects
• Proteins/metabolism
• Proteomics

• P20 GM103443 NIGMS NIH HHS
• P20 RR016479 NCRR NIH HHS

The aim of this study was to determine whether elevated serum level of uric acid (sUA) could predict renal outcome after contrast-enhanced computerized tomography (CCT). We used a historical cohort of 58,106 non-dialysis adult patients who received non-ionic iso-osmolar CCT from 1 June 2008 to 31 March 2015 to evaluate the association of sUA and renal outcome. The exclusion criteria were patients with pre-existing acute kidney injury (AKI), multiple exposure, non-standard volume of contrast, and missing data for analysis. A total of 1440 patients were enrolled. Post-contrast-AKI (PC-AKI), defined by the increase in serum creatinine ≥ 0.3 mg/dL within 48 h or ≥50% within seven days after CCT, occurred in 180 (12.5%) patients and the need of hemodialysis within 30 days developed in 90 (6.3%) patients, both incidences were increased in patients with higher sUA. sUA ≥ 8.0 mg/dL was associated with an increased risk of PC-AKI (odds ratio (OR) of 2.62; 95% confidence interval (CI), 1.27~5.38, p = 0.009) and the need of hemodialysis (OR, 5.40; 95% CI, 1.39~21.04, p = 0.015). Comparing with sUA < 8.0 mg/dL, patients with sUA ≥ 8.0 mg/dL had higher incidence of PC-AKI (16.7% vs. 11.1%, p = 0.012) and higher incidence of hemodialysis (12.1% vs. 4.3%, p < 0.001). We concluded that sUA ≥ 8.0 mg/dL is associated with worse renal outcome after CCT. We suggest that hyperuricemia may have potential as an independent risk factor for PC-AKI in patients receiving contrast-enhanced image study.

• acute kidney injury
• chronic kidney disease
• contrast media
• hemodialysis
• uric acid

The association between elevated admission serum uric acid (SUA) and risk of in-hospital acute kidney injury (AKI) is limited. The aim of this study was to assess the risk of developing AKI in all hospitalized patients with various admission SUA levels.

This is a single-center retrospective study conducted at a tertiary referral hospital. All hospitalized adult patients who had admission SUA available from January 2011 through December 2013 were analyzed in this study. Admission SUA was categorized based on its distribution into six groups (<3.4, 3.4–4.5, 4.5–5.8, 5.8–7.6, 7.6–9.4 and >9.4 mg/dL). The primary outcome was in-hospital AKI occurring after hospital admission. Logistic regression analysis was performed to obtain the odds ratio (OR) of AKI of various admission SUA levels using the most common SUA level range (5.8–7.6 mg/dL) as the reference group.

Of 1435 patients enrolled, AKI occurred in 263 patients (18%). The incidence of AKI and need for dialysis was increased in patients with higher admission SUA levels. After adjusting for potential confounders, SUA >9.4 mg/dL was associated with an increased risk of developing AKI, with ORs of 1.79 [95% confidence interval (CI) 1.13–2.82]. Conversely, admission SUA <3.4 and 3.4–4.5 mg/dL were associated with a decreased risk of developing AKI, with ORs of 0.38 (95% CI 0.17–0.75) and 0.50 (95% CI 0.28–0.87), respectively.

Elevated admission SUA was associated with an increased risk for in-hospital AKI.

• acute kidney injury
• hyperuricemia
• length of hospital stay
• mortality
• uric acid

AIM: To assess the value of plasma melatonin in predicting acute pancreatitis when combined with the acute physiology and chronic health evaluation II (APACHEII) and bedside index for severity in acute pancreatitis (BISAP) scoring systems.

METHODS: APACHEII and BISAP scores were calculated for 55 patients with acute physiology (AP) in the first 24 h of admission to the hospital. Additionally, morning (6:00 AM) serum melatonin concentrations were measured on the first day after admission. According to the diagnosis and treatment guidelines for acute pancreatitis in China, 42 patients suffered mild AP (MAP). The other 13 patients developed severe AP (SAP). A total of 45 healthy volunteers were used in this study as controls. The ability of melatonin and the APACHEII and BISAP scoring systems to predict SAP was evaluated using a receiver operating characteristic (ROC) curve. The optimal melatonin cutoff concentration for SAP patients, based on the ROC curve, was used to classify the patients into either a high concentration group (34 cases) or a low concentration group (21 cases). Differences in the incidence of high scores, according to the APACHEII and BISAP scoring systems, were compared between the two groups.

RESULTS: The MAP patients had increased melatonin levels compared to the SAP (38.34 ng/L vs 26.77 ng/L) (P = 0.021) and control patients (38.34 ng/L vs 30.73 ng/L) (P = 0.003). There was no significant difference inmelatoninconcentrations between the SAP group and the control group. The accuracy of determining SAP based on the melatonin level, the APACHEII score and the BISAP score was 0.758, 0.872, and 0.906, respectively, according to the ROC curve. A melatonin concentration ≤ 28.74 ng/L was associated with an increased risk of developing SAP. The incidence of high scores (≥ 3) using the BISAP system was significantly higher in patients with low melatonin concentration (≤ 28.74 ng/L) compared to patients with high melatonin concentration (> 28.74 ng/L) (42.9% vs 14.7%, P = 0.02). The incidence of high APACHEII scores (≥ 10) between the two groups was not significantly different.

CONCLUSION: The melatonin concentration is closely related to the severity of AP and the BISAP score. Therefore, we can evaluate the severity of disease by measuring the levels of serum melatonin.

• Pancreatitis
• Melatonin concentrations
• Predict
• Cutoff
• Bedside index for severity in acute pancreatitis
• Acute physiology and chronic health evaluation II

• APACHE
• Acute Disease
• Adolescent
• Adult
• Aged
• Aged, 80 and over
• Biomarkers/blood
• Case-Control Studies
• Female
• Humans
• Male
• Melatonin/blood
• Middle Aged
• Pancreatitis/blood
• Pancreatitis/diagnosis
• Predictive Value of Tests
• Sensitivity and Specificity
• Severity of Illness Index
• Young Adult

Melatonin, a product of the pineal gland, is released from the gut mucosa in response to food ingestion. Specific receptors for melatonin have been detected in many gastrointestinal tissues including the pancreas. Melatonin as well as its precursor, L-tryptophan, attenuates the severity of acute pancreatitis and protects the pancreatic tissue from the damage caused by acute inflammation. The beneficial effect of melatonin on acute pancreatitis, which has been reported in many experimental studies and supported by clinical observations, is related to: (1) enhancement of antioxidant defense of the pancreatic tissue, through direct scavenging of toxic radical oxygen (ROS) and nitrogen (RNS) species, (2) preservation of the activity of antioxidant enzymes; such as superoxide dismutase (SOD), catalase (CAT), or glutathione peroxidase (GPx), (3) the decline of pro-inflammatory cytokine tumor necrosis α (TNFα) production, accompanied by stimulation of an anti-inflammatory IL-10, (4) improvement of pancreatic blood flow and decrease of neutrophil infiltration, (5) reduction of apoptosis and necrosis in the inflamed pancreatic tissue, (6) increased production of chaperon protein (HSP60), and (7) promotion of regenerative process in the pancreas. Conclusion. Endogenous melatonin produced from L-tryptophan could be one of the native mechanisms protecting the pancreas from acute damage and accelerating regeneration of this gland. The beneficial effects of melatonin shown in experimental studies suggest that melatonin ought to be employed in the clinical trials as a supportive therapy in acute pancreatitis and could be used in people at high risk for acute pancreatitis to prevent the development of pancreatic inflammation.