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Titolo:
Acute cholestatic liver disease protects against glycerol-induced acute renal failure in the rat
Autore:
Leung, N; Croatt, AJ; Haggard, JJ; Grande, JP; Nath, KA;
Indirizzi:
Mayo Clin & Mayo Fdn, Dept Nephrol & Pathol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 thol, Rochester, MN 55905 USA
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 3, volume: 60, anno: 2001,
pagine: 1047 - 1057
SICI:
0085-2538(200109)60:3<1047:ACLDPA>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEME OXYGENASE INDUCTION; ALBUMIN-BOUND BILIRUBIN; OXIDATIVE STRESS; OBSTRUCTIVE-JAUNDICE; EMERGING PERSPECTIVES; HEPATORENAL-SYNDROME; ACQUIRED-RESISTANCE; REPERFUSION INJURY; LIPID-PEROXIDATION; PROXIMAL TUBULES;
Keywords:
bile duct ligation; hepatorenal syndrome; bilirubin; renal injury; cytoprotection; heme protein-induced nephrotoxicity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Nath, KA Mayo Clin, 200 1st St SW,Guggenheim 542, Rochester, MN 55905 USA Mayo Clin 200 1st St SW,Guggenheim 542 Rochester MN USA 55905 USA
Citazione:
N. Leung et al., "Acute cholestatic liver disease protects against glycerol-induced acute renal failure in the rat", KIDNEY INT, 60(3), 2001, pp. 1047-1057

Abstract

Background. It is widely held that liver disease predisposes toward acute tubular necrosis. The present study examines the effect of acute cholestatic liver disease on the susceptibility to glycerol-induced acute tubular necrosis in the rat. Methods. Acute cholestatic liver disease was induced by ligation of the common bile duct, while the intramuscular injection of hypertonic glycerol was used to induce acute tubular necrosis. Renal injury was assessed by plasma creatinine concentration and renal histology. An in vitro model of heme protein-induced renal injury (hemoglobin in conjunction with glutathione depletion) was employed to assess the cytoprotective effects of bilirubin. Results. Ligation of the common bile duct markedly reduced acute renal injury that occurs in the glycerol model (7.5 mL/kg body weight), as evidencedby a lower plasma creatinine concentration and less severe renal histologic injury. At a higher dose of glycerol (10 mL/kg body weight), ligation of the common bile duct again reduced renal injury and cumulative mortality that occurs five days after the induction of this model of acute renal failure. These protective effects of ligation of the common bile duct could not be ascribed to less severe muscle injury or red cell damage. Ligation of thecommon bile duct induced heme oxygenase-1 in the kidney and markedly so inthe liver. Inhibition of heme oxygenase significantly attenuated, but did not prevent, the protective effects conferred by ligation of the common bile duct. Bilirubin, in low micromolar concentrations, was cytoprotective against heme protein-induced cell injury in vitro. Conclusions. Ligation of the common bile duct confers resistance to glycerol-induced acute tubular necrosis in the rat, actions that arise, in part, from the induction of heme oxygenase-1 in the kidney and liver. Bilirubin, in micromolar concentrations, protects against heme protein-induced renal injury. Our studies uncover a novel form of acquired resistance to renal injury, occurring, unexpectedly, in the setting of acute cholestatic liver disease. We speculate that such potentially cytoprotective alterations may safeguard the kidney against irreversible functional and structural injury in the hepatorenal syndrome.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 11:43:56