Giuseppe Cullaro1, Grace Kim1, Marcus R Pereira2, Robert S Brown3, Elizabeth C Verna4. 1. Center for Liver Disease and Transplantation, Columbia University Medical Center, 622 West 168th St., PH 14-105K, New York, NY, 10032, USA. 2. Division of Infectious Diseases, Department of Medicine, Columbia University Medical Center, New York, NY, USA. 3. Center for Liver Disease and Transplantation, Weill Cornell Medicine, New York, NY, USA. 4. Center for Liver Disease and Transplantation, Columbia University Medical Center, 622 West 168th St., PH 14-105K, New York, NY, 10032, USA. ev77@columbia.edu.
Abstract
BACKGROUND: Neutrophil gelatinase-associated lipocalin (NGAL) is a marker of both tissue injury and infection. Urine NGAL levels strongly predict acute kidney injury and mortality in patients with cirrhosis, but ascites NGAL is not well characterized. We hypothesized that ascites NGAL level is a marker of spontaneous bacterial peritonitis (SBP) and mortality risk in patients with cirrhosis. METHODS: Hospitalized patients with cirrhosis and ascites undergoing diagnostic paracentesis were prospectively enrolled and followed until death or discharge. Patients with secondary peritonitis, prior transplantation, or active colitis were excluded. NGAL was measured in the ascites and serum. Ascites NGAL level was evaluated as a marker of SBP (defined as ascites absolute neutrophil count > 250 cells/mm3) and predictor of in-patient mortality. RESULTS: A total of 146 patients were enrolled, and of these, 29 patients (20%) had SBP. Baseline characteristics were similar between subjects with and without SBP. Median (IQR) ascites NGAL was significantly higher in patients with SBP compared to those without SBP (221.3 [145.9-392.9] vs. 139.2 [73.9-237.2], p < 0.01). Sixteen (11%) patients died in the hospital. In the final multivariable model, ascites NGAL (OR 1.02 per 10 units, p < 0.01) remained predictive of in-hospital mortality, controlling for SBP (OR 9.76, p < 0.01) and MELD (OR 1.11, p = 0.01). In ROC analysis, ascites NGAL had an AUC of 0.79 for inhospital mortality, and the final model including ascites NGAL, MELD, and SBP had an AUC of 0.94. CONCLUSIONS: Ascites NGAL level may be a biomarker of peritonitis in hospitalized patient with cirrhosis and an independent predictor of short-term in-hospital mortality, even controlling for SBP and MELD.
BACKGROUND:Neutrophil gelatinase-associated lipocalin (NGAL) is a marker of both tissue injury and infection. Urine NGAL levels strongly predict acute kidney injury and mortality in patients with cirrhosis, but ascitesNGAL is not well characterized. We hypothesized that ascitesNGAL level is a marker of spontaneous bacterial peritonitis (SBP) and mortality risk in patients with cirrhosis. METHODS: Hospitalized patients with cirrhosis and ascites undergoing diagnostic paracentesis were prospectively enrolled and followed until death or discharge. Patients with secondary peritonitis, prior transplantation, or active colitis were excluded. NGAL was measured in the ascites and serum. AscitesNGAL level was evaluated as a marker of SBP (defined as ascites absolute neutrophil count > 250 cells/mm3) and predictor of in-patient mortality. RESULTS: A total of 146 patients were enrolled, and of these, 29 patients (20%) had SBP. Baseline characteristics were similar between subjects with and without SBP. Median (IQR) ascitesNGAL was significantly higher in patients with SBP compared to those without SBP (221.3 [145.9-392.9] vs. 139.2 [73.9-237.2], p < 0.01). Sixteen (11%) patients died in the hospital. In the final multivariable model, ascitesNGAL (OR 1.02 per 10 units, p < 0.01) remained predictive of in-hospital mortality, controlling for SBP (OR 9.76, p < 0.01) and MELD (OR 1.11, p = 0.01). In ROC analysis, ascitesNGAL had an AUC of 0.79 for inhospital mortality, and the final model including ascitesNGAL, MELD, and SBP had an AUC of 0.94. CONCLUSIONS:AscitesNGAL level may be a biomarker of peritonitis in hospitalized patient with cirrhosis and an independent predictor of short-term in-hospital mortality, even controlling for SBP and MELD.
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Authors: Erawan Borkham-Kamphorst; Eddy van de Leur; Henning W Zimmermann; Karlin Raja Karlmark; Lidia Tihaa; Ute Haas; Frank Tacke; Thorsten Berger; Tak W Mak; Ralf Weiskirchen Journal: Biochim Biophys Acta Date: 2013-01-31