Kinetic changes in serum procalcitonin predict persistent acute kidney injury in critical patients.

PURPOSE: Persistent acute kidney injury (AKI) has been shown to be closely associated with poor prognosis in critical patients. Recent studies have shown that procalcitonin (PCT) is valuable for the early prediction of AKI in critically patients. Our aim was to determine whether PCT and its kinetic changes could predict the occurrence of persistent AKI in critical patients. METHODS: This is a prospective observational study. The definition of AKI was based on the Kidney Disease: Improving Global Outcomes criteria. Persistent AKI was defined as renal function that does not return to baseline serum creatinine levels within 48 h. Blood samples were obtained at the onset of AKI and two subsequent days of hospital stay. 24-h PCT change (ΔPCT-24 h) was defined as 24 h PCT minus baseline PCT (day 0). RESULTS: A total of 91 critical patients with AKI were included in this study. The persistent AKI group had a stepwise increase in PCT concentration. ΔPCT-24 h was higher in the persistent AKI group (p < .01). Logistic regression analysis showed that ΔPCT-24 h (p = .04) was independent predictors of persistent AKI. The receiver operating characteristic curves showed that area under the curve of ΔPCT-24 h was 0.84 (p < .01), and the cut-off value for PCT to predict persistent AKI was 0.56 ng/ml. CONCLUSION: Our study showed that the observation of kinetic changes in PCT is more significant for the early prediction of persistent AKI than the index of PCT at a single time point. ΔPCT-24 h is a good predictor of persistent AKI in critical patients.

Combination of hepcidin with neutrophil gelatinase-associated lipocalin for prediction of the development of sepsis-induced acute kidney injury.

BACKGROUND AND AIMS: The early prediction of the development of acute kidney injury (AKI) in critically ill patients with sepsis would facilitate early effective intervention. Recently, interest has focused on the biomarkers for AKI-linked iron metabolism. This study aimed to assess the early predictive values of hepcidin, neutrophil gelatinase-associated lipocalin (NGAL), and their combination for secondary AKI in patients with sepsis. MATERIALS AND METHODS: A prospective cohort study was performed in septic patients. Serum and urine hepcidin, and urine NGAL were analyzed at admission. The primary outcome measure was occurrence of sepsis-induced AKI based on 2011 Kidney Disease: Improving Global Outcomes (KDIGO) criteria during the first week of ICU stay. RESULTS: Of the 90 patients analyzed finally in the study, 44 (48.9%) patients developed AKI. Patients with AKI occurrence were more likely than those without AKI to have higher serum hepcidin and urine NGAL levels at admission (P < 0.01). Higher concentrations of these biomarkers were each independent predictor of the development of AKI in critically septic patients within the first week of their ICU stay. Serum hepcidin and urine NGAL (AUROC 0.787, 95% CI 0.688 to 0.8660 and AUROC 0.729, 95% CI 0.625 to 0.818, respectively) were comparable predictive indicators of AKI occurrence (P = 0.43 for DeLong's test). Combining both biomarkers increased the AUROC to 0.828(95% CI 0.733 to 0.899), and this performance was statistically significantly better than urine NGAL alone (P = 0.03 for DeLong's test). CONCLUSION: Serum hepcidin measured at admission predicts the development of AKI similarly to urine NGAL. However, serum hepcidin adds significant accuracy to this prediction in combination with urine NGAL alone and has a good predictive value in patients with sepsis. Larger studies are needed to validate and explain these findings.

Visfatin levels in patients with severe pneumonia.

BACKGROUND: As a cytokine highly expressed in internal organs, visfatin could be used as a biomarker of systemic inflammation response for chronic obstructive pulmonary diseases, but few studies have reported the use of visfatin in severe pneumonia. The present study was undertaken to determine the plasma levels of visfatin in patients with severe pneumonia. METHODS: A total of 70 patients, including 40 patients with severe pneumonia (group A) and 30 patients with non severe pneumonia (group B) who had been admitted to the ICU from June 2009 to June 2010, were enrolled in this prospective study. And another 30 healthy physical examinees served as healthy controls (group C). Patients were excluded if they suffered from severe diseases of the heart, brain and kidney, cancers, autoimmune diseases, or received special treatment in the latest month. The plasma levels of visfatin, IL-6, IL-8 and TNF-α were measured by ELISA, while the level of CRP was determined by immuneturbidimetry, and the routine blood test was performed. Blood gas analysis and Acute Physiology and Chronic Health Evaluation II (APACHE II) were performed in patients with pneumonia. Comparisons between the groups were conducted by Student's t test, ANOVA or nonparametric test. Correlation analysis was carried out by Pearson's correlation test or Spearman's rank-order correlation test. RESULTS: The plasma level of visfatin in group A was significantly higher than that in groups B and C (P<0.001), and the level of visfatin in group B was significantly higher than that in group C (P<0.001). The plasma level of visfatin was positively correlated with CRP, TNF-α, APACHE II and PMN% in patients with severe pneumonia (rho =0.653, r=0.554, r=0.558, r=0.484, respectively, P<0.05 for all), while it was negatively correlated with PaO2 and PaO2/FiO2 (rho =-0.422, r=-0.543, respectively, P<0.05 for all). CONCLUSION: Visfatin may be involved in the systematic inflammation response in patients with severe pneumonia as a pro-inflammatory cytokine, and it is valuable in assessing the severity of pneumonia..

A new inflammation marker of chronic obstructive pulmonary disease-adiponectin.

BACKGROUND: This study was undertaken to measure the concentration of adiponectin (APN) in serum and induced sputum in patients with chronic obstructive pulmonary disease (COPD during acute exacerbation (AECOPD) and at stable stage and to determine the role of APN as a marker of inflammation in the pathogenesis of COPD. METHODS: All the patients in this prospective study were enrolled from October 2008 to October 2009, including 30 male AECOPD patients from the emergency department, 30 male stable COPD patients from the department of respiratory diseases, and 30 healthy non-smoking male controls from the department of medical examination. The serum and induced sputum were collected from each patient. All of the patients had normal weight (BMI range 18.5-24.9 kg/m(2)). Patients with severe bronchial asthma, bronchiectasis or autoimmune disease were excluded. Cell count and classification was performed for the induced sputum. The concentrations of APN, IL-8, IL-6 and TNF-α were measured by ELISA. Pulmonary function was tested among the three groups. Comparisons between the groups were conducted by Student's t test, ANOVA analysis or nonparametric test. Correlation analysis was carried out by Pearson's product-moment correlation coefficient test or Spearman's rank-order correlation coefficient test. RESULTS: The concentrations of APN in the serum or induced sputum in AECOPD patients were significantly higher than those in stable COPD patients or healthy non-smoking controls (P<0.01). The concentration of APN in stable COPD patients was significantly higher than that in healthy non-smoking controls (P<0.01). For the AECOPD patients, APN was positively correlated with IL-8 and TNF-α in the serum and induced sputum (r=0.739, 0.734, 0.852, 0.857 respectively, P<0.05). For the stable COPD patients, APN was also positively correlated with IL-8 and TNF-α in the serum and induced sputum (r=0.751, 0.659, 0.707, 0.867 respectively, P<0.05). In addition, for the AECOPD patients, APN was positively correlated with the percentage of neutrophils in the induced sputum (r=0.439, P<0.05). CONCLUSIONS: APN is involved in the process of systematic and airway inflammation of COPD. This process is related to neutrophils in the airway, IL-8 and TNF-α. APN could be used as a new marker for inflammation of COPD.

[The value of serum procalcitonin in treatment of community acquired pneumonia in outpatient].

OBJECTIVE: To evaluate the value of serum procalcitonin (PCT) on antibiotic use in treatment of community acquired pneumonia (CAP) in outpatient. METHODS: From November 2006 to February 2008, a total of 127 patients with CAP in outpatient were randomly assigned into two groups: PCT group (n = 63) and control group (n = 64). PCT levels of all patients were measured after study admission. On the base of similarly normal treatment, the control group received antibiotics according to the attending physicians and the PCT group were treated with antibiotics according to serum PCT levels: antibiotic treatment was applied with PCT level > or = 0.25 microg/L and was discouraged with PCT level < 0.25 microg/L. Clinical efficacy, rate of antibiotics use, duration courses and costs of antibiotics were observed. RESULTS: Clinical efficacy of the PCT group was similar with the control group (92.1% vs 87.5%, P > 0.05); rate and costs of antibiotics use was lower, antibiotic duration of the PCT group was shorter than that of the control group (P < 0.05, P < 0.001, P < 0.001). CONCLUSION: PCT could be used in treatment of CAP for antibiotic use in outpatient, which may reduce antibiotic use, shorten antibiotic duration and lower costs of antibiotic.