Procalcitonin levels predict acute kidney injury and prognosis in acute pancreatitis: a prospective study.

BACKGROUND: Acute kidney injury (AKI) has been proposed as a leading cause of mortality for acute pancreatitis (AP) patients admitted to the intensive care unit (ICU). This study investigated the predictive value of procalcitonin (PCT) for AKI development and relevant prognosis in patients with AP, and compared PCT's predictive power with that of other inflammation-related variables. METHODS: Between January 2011 and March 2013, we enrolled 305 cases with acute pancreatitis admitted to ICU. Serum levels of PCT, serum amyloid A (SAA), interleukin-6 (IL-6), and C reactive protein (CRP) were determined on admission. Serum PCT was tested in patients who developed AKI on the day of AKI occurrence and on either day 28 after occurrence (for survivors) or on the day of death (for those who died within 28 days). RESULTS: Serum PCT levels were 100-fold higher in the AKI group than in the non-AKI group on the day of ICU admission (p<0.05). The area under the receiver-operating characteristic (ROC) curve of PCT for predicting AKI was 0.986, which was superior to SAA, CRP, and IL-6 (p<0.05). ROC analysis revealed all variables tested had lower predictive performance for AKI prognosis. The average serum PCT level on day 28 (2.67 (0.89, 7.99) ng/ml) was significantly (p<0.0001) lower than on the day of AKI occurrence (43.71 (19.24,65.69) ng/ml) in survivors, but the serum PCT level on death (63.73 (34.22,94.30) ng/ml) was higher than on the day of AKI occurrence (37.55 (18.70,74.12) ng/ml) in non-survivors, although there was no significant difference between the two days in the latter group (p = 0.1365). CONCLUSION: Serum PCT is superior to CRP, IL-6, and SAA for predicting the development of AKI in patients with AP, and also can be used for dynamic evaluation of AKI prognosis.

Serum procalcitonin predicts development of acute kidney injury in patients with suspected infection.

BACKGROUND: Procalcitonin (PCT) is an early, sensitive, and accurate marker for diagnosing infection and sepsis. As sepsis and septic shock are dominant causes of acute kidney injury (AKI), we investigated whether PCT is an early predictor of AKI in patients with symptoms of infection. METHODS: Between January 2011 and October 2011, 1361 inpatients in West China Hospital who displayed infection symptoms were enrolled in our study. Levels of PCT, serum amyloid A (SAA), C-reactive protein (CRP), interleukin-6 (IL-6), and white blood cell count (WBC) were determined and participants' renal function was monitored for 3 consecutive days. RESULTS: The rate of AKI occurrence 3 days after enrollment was 14.6%. Higher PCT levels were correlated with higher AKI occurrence rates and higher levels of serum urea, creatinine, and cystatin C (p<0.05). The area under the receiver-operating characteristic (ROC) curve (AUC) for PCT was 0.823, making it more predictive (p<0.0001) than SAA, CRP, IL-6, or WBC. The cut-off value of 1.575 ng/mL for PCT had the highest validity for predicting AKI in patients with infection symptoms. The sensitivity, specificity, negative-predictive value (NPV), positive-predictive value (PPV), negative-likelihood ratio (LR-), and positive-likelihood ratio (LR+) for this cut-off value were 61.7%, 84.6%, 93.6%, 37.5%, 0.415, and 4.98, respectively. CONCLUSIONS: PCT can be used as a predictive marker for sepsis-induced acute kidney injury in patients with symptoms of infection.

Partial pressure of NH3 in cirrhotic patients with and without hepatic encephalopathy.

BACKGROUND AND AIMS: Although the exact pathogenetic factor in hepatic encephalopathy is still unknown, ammonia is considered to be the major cause of neurotoxicity. However, previous studies on the relationship between ammonia and the severity of hepatic encephalopathy have yielded variable results. Since unionized ammonia is the only form of ammonia that is able to freely spread through the blood-brain barrier and cause cerebral dysfunction, we tested the hypothesis that concentration of unionized ammonia is correlated with the severity of hepatic encephalopathy. METHODS: 156 patients with cirrhosis (74 with hepatic encephalopathy and 82 without) were enrolled, and underwent clinical examination and blood testing. Ammonia, pNH3 and pH determinations were repeated after two days of treatment. The differences in venous ammonia, pNH3, and pH among patients with and without encephalopathy were analyzed. RESULTS: Among cirrhotic patients with hepatic encephalopathy, pH, pNH3 and ammonia levels were all higher than those among patients without hepatic encephalopathy, and alkalosis was more common in patients with hepatic encephalopathy. Both venous ammonia and pNH3 were significantly correlated to the clinical grade of hepatic encephalopathy; however, the r was similar for venous ammonia (r=0.63) and pNH3 (r=0.68). The follow-up of 20 patients showed that the median levels of pH, pNH3 and venous ammonia decreased; venous ammonia levels were unchanged or higher in some patients after resolution of hepatic encephalopathy. CONCLUSION: This study supports that pH-dependant pNH3 and pH could be useful diagnostic and prognostic tools in cirrhotic patients with hepatic encephalopathy.

[Pathogenic effects of level of nitric oxide, hyponatremia and heart function on hepatorenal syndrome].

OBJECTIVE: To analyze the changes of liver function, renal function, electrolytes, heart function and serum nitric oxide (NO) in chronic severe hepatitis patients with hepatorenal syndrome (HRS) by plasma exchange (PE), study the relationship of NO, hyponatremia, heart function with HRS. METHODS: A total of 20 chronic severe hepatitis patients with HRS were recruited. All were treated thrice by PE. The parameters of blood pressure, heart rate, 24 h urinary volume, liver function indicators, renal function indicators, NO, cardiac troponin T (cTnT), brain natriuretic peptide (BNP), aldosterone, interleukin-6, tumor necrosis factor-α and plasma ammonia were measured before PE, during PE and after PE. Their differences were compared before, during and after PE. RESULTS: The NO level of HRS before PE was (113 ± 26) µmol/L, the level of Day 1 after PE (78 ± 24) µmol/L and the level of Day 3 after PE was (85 ± 29) µmol/L. All NO levels were lower than that before PE (all P < 0.05). Creatine level of HRS before PE was (191 ± 43) µmol/L and the level of Day 1 after PE (142 ± 42) µmol/L. All levels were lower than that before PE (all P < 0.05). The level of Day 3 after PE was 221 ± 105 µmol/L and it was higher than that before PE (P < 0.05). At pre-, during- and post-PE, the level of sodium was low than normal (normal range: 135 - 145 mmol/L), the level of aldosterone higher than normal (normal range: 10 - 27 ng/L), the level of cTnT higher than normal (normal range: < 14 ng/L) and the level of BNP higher than normal (normal range: < 366 ng/L). The levels of model for end-stage liver disease (MELD) score, bilirubin, urea, cysteine proteinase inhibitor C and ammonia decreased during PE, but increased post-PE. Systolic pressure and 24 h urinary volume decreased gradually. In this study, 8 patients died and 12 were discharged from hospital. CONCLUSION: Serum nitric oxide is not the sole occurring factor for hepatorenal syndrome. Hyponatremia and impaired heart function may be the key factors for hepatorenal syndrome.

[The relationship of CPS-I, OCT and hepatic encephalopathy].

OBJECTIVE: To study the role of carbamyl phosphate I (CPS-I)and ornithine transcarbamoylase (OCT) levels in cirrhosis patients with and without hepatic encephalopathy, and to analyze the correlations between CPS-Iand OCT with the development of hepatic encephalopathy. METHODS: CPS-I, OCT, plasma ammonia and liver function of 95 cirrhosis patients with hepatic encephalopathy and 25 cirrhosis patients without hepatic encephalopathy in our hospital from January 2008 to December 2009 were analyzed. 60 healthy controls were recruited in the control group. The differences of serum CPS-I, OCT levels among the cirrhosis patients with and without hepatic encephalopathy and the healthy controls were analyzed; the correlations of CPS-I, OCT levels with plasma ammonia and total protein in cirrhosis patients,and the correlations of CPS-I, OCT levels with Child-Pugh classification of cirrhosis symptom severity in cirrhosis were analyzed. the clinical characteristics between patients who had HE and no HE with chi-square tests were compared. Comparisons of CPS-I, OCT levels across patients based on the Child-Pugh classification were performed with One-Way ANOVA and Student-Newman-Keuls, correlation of CPS-I, OCT with other indicators were performed with Pearson correlation analysis. RESULTS: Serum CPS-I and OCT levels in cirrhosis patients with hepatic encephalopathy were (143.3+/-48.5) U/L, (297.0+/-102.6) is multiplied by 10 U/L, which were lower than that in cirrhosis patients without hepatic encephalopathy (180.3+/-51.5) U/L, (351.8+/-109.0) is multiplied by 10 U/L (t = 2.53, t = 2.78, P < 0.01). Compared with healthy controls, serum CPS-I and OCT levels in cirrhosis patients with and without hepatic encephalopathy were all lower (t = 3.21, t = 4.16, t = 2.12, t = 3.15, P < 0.05). CPS-I was correlated with OCT, (r = 0.946, P < 0.05); CPS-I and OCT were negatively correlated with ALT and AST (r = -0.284, r = -0.239, r = -0.303, r = -0.322, P < 0.05). Additionally, CPS-I and OCT levels were negatively correlated with the Child-Pugh classification in Cirrhosis (F = 10.13, F = 20.28, P < 0.01). CONCLUSION: The serum CPS-I and COT levels were important factors affecting plasma ammonia in patients with cirrhosis and played an important role in the development of hepatic encephalopathy.