Examination of bilirubin, INR and creatinine

values were

Examination of bilirubin, INR and creatinine

values were used in the MELD calculation (Model for End-stage Liver Disease).16 The Na/Ku ratio is calculated on the values of sodium and potassium in “spot” urine sample. Urine was collected within less than or equal to 48 h from admission. Collection of 24-h urine sample for calculation of sodium was done in sterile plastic containers by recording the volume in 24 h; starting at 8:00 a.m. Instructions were given to assure completeness of collection. All samples GSK1120212 were processed on the day of collection. In order to obtain the whole 24-h urinary sodium, sodium concentration was multiplied by the volume in litters. Random urine samples were obtained before or after completion of 24-h collection for measurement of ‘spot’ Na/K ratio. Any kidney disease was excluded by medical history, urinalysis, serum creatinine and ultrasound

examination of the kidneys. Numerical variables were expressed as mean and standard deviation, whereas categorical variables were described Nivolumab mouse in absolute numbers and proportions. Continuous variables were compared using either Student’s t test or Mann–Whitney when appropriate, categorical variables were analysed using either Chi-squared test or Fisher’s exact test. A P-value < 0.050 was considered statistically significant. The correlation between the Nau24h and Na/Ku ratio was evaluated by the Spearman's correlation coefficient. Diagnostic accuracy of the Na/Ku ratio was analysed by estimating the area under the receiver operating characteristics curve (AUROC) and by calculating sensitivity, specificity, positive and negative predictive value. All tests were performed by the statistics software SPSS, version 17.0 (SPSS, Chicago, IL, USA). Between August 2010 and January 2012, 42 patients admitted in the gastroenterology ward were evaluated for inclusion as they present liver Phenylethanolamine N-methyltransferase cirrhosis decompensated in ascites. Twenty-two patients without urinary sodium dosage were excluded. Twenty patients with decompensated liver cirrhosis and ascites were included. Among them, 60% presented poor urinary sodium excretion (Nau24h dosage lower than 78 mequiv.).

Among the 20 included individuals, the mean age, standard deviation and median were 56.1 ± 11.8 (54.5) years, 70.0% were men, 66.7% were Caucasian. Regard to the aetiology of cirrhosis: 33.3% had alcohol abuse and hepatitis C virus, 27.8% had alcohol only (Table 1). Three patients had hepatocellular carcinoma. When individuals with poor urinary sodium excretion were compared to those with Nau24h ≥ 78 mequiv. (Table 1 and Table 2), they exhibited a higher proportion of male sex (91.7% vs. 37.5%; P = 0.018); higher mean MELD scores (16.3 ± 9.3 vs. 5.0 ± 3.5; P = 0.002), higher mean creatinine (1.1 ± 0.4 mg/dL vs. 0.8 ± 0.2 mg/dL; P = 0.029), higher AST means (3.1 ± 1.7 vs. xULN 1.6 ± 0.7; P = 0.027), higher median bilirubin (1.1 g/dL vs. 0.3 g/dL; P = 0.013) and lower median spot urine sodium (21.5 mequiv.

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