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Miquel Navasa

Researcher at University of Barcelona

Publications -  185
Citations -  16466

Miquel Navasa is an academic researcher from University of Barcelona. The author has contributed to research in topics: Liver transplantation & Transplantation. The author has an hindex of 60, co-authored 181 publications receiving 15473 citations. Previous affiliations of Miquel Navasa include University of Bern & Carlos III Health Institute.

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Effect of Intravenous Albumin on Renal Impairment and Mortality in Patients with Cirrhosis and Spontaneous Bacterial Peritonitis

TL;DR: In patients with cirrhosis and spontaneous bacterial peritonitis, treatment with intravenous albumin in addition to an antibiotic reduces the incidence of renal impairment and death in comparison with treatment with an antibiotic alone.
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Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: a consensus document

TL;DR: This article represents the final consensus document and is divided into three separate sections concerning the diagnosis, treatment and prophylaxis of SBI?
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Incidence, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites

TL;DR: The hepatorenal syndrome is a relatively frequent complication in cirrhotic patients with ascites that is associated with an extremely short survival and Liver size, plasma renin activity, and serum sodium concentration are predictors of hepatorenAL syndrome occurrence in these patients.
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Primary Prophylaxis of Spontaneous Bacterial Peritonitis Delays Hepatorenal Syndrome and Improves Survival in Cirrhosis

TL;DR: In this paper, the authors showed that primary prophylaxis with norfloxacin has a great impact in the clinical course of patients with advanced cirrhosis, reducing the incidence of spontaneous bacterial peritonitis, delaying the development of hepatorenal syndrome, and improving survival.
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Hepatitis C virus kinetics during and immediately after liver transplantation.

TL;DR: A sharp decrease in HCV viral load occurs during the anhepatic phase and immediately after graft reperfusion, most likely owing to a lack of virion production and hepatic viral clearance.