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10.3748/wjg.v16.i41.5139 http://scihub22266oqcxt.onion/10.3748/wjg.v16.i41.5139 21049548!2975085!21049548     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       World+J+Gastroenterol 2010 ; 16 (41): 5139-47 Nephropedia Template TP {{tp|p=21049548|t=2010. Terlipressin and hepatorenal syndrome: what is important for nephrologists and hepatologists |pdf=|usr=}}{{21049548}} gab.com Text Terlipressin and hepatorenal syndrome: what is important for nephrologists and hepatologists JO: World J Gastroenterol http://www.kidney.de/pget.php?&tw=1&pmid=21049548 #FOAvip Hepatorenal syndrome (HRS) is a reversible form of functional renal failure that occurs with advanced hepatic cirrhosis and liver failure. Despite mounting research in HRS, its etiology and medical therapy has not been resolved. HRS encompasses 2 distinct types. Type 1 is characterized by the rapid development of renal failure that occurs within 2 wk and involves a doubling of initial serum creatinine. Type 2 has a more insidious onset and is often associated with ascites. Animal studies have shown that both forms, in particular type 1 HRS, are often precipitated by bacterial infections and circulatory changes. The prognosis for HRS remains very poor. Type 1 and 2 both have an expected survival time of 2 wk and 6 mo, respectively. Progression of liver cirrhosis and the resultant portal hypertension leads to the pooling of blood in the splanchnic vascular bed. The ensuing hyperdynamic circulation causes an ineffective circulatory volume which subsequently activates neurohormonal systems. Primarily the sympathetic nervous system and the renin angiotensin system are activated, which, in the early stages of HRS, maintain adequate circulation. Both advanced cirrhosis and prolonged activation of neurohormonal mechanisms result in fatal complications. Locally produced nitric oxide may have the potential to induce a deleterious vasodilatory effect on the splanchnic circulation. Currently medical therapy is aimed at reducing splanchnic vasodilation to resolve the ineffective circulation and maintain good renal perfusion pressure. Terlipressin, a vasopressin analogue, has shown potential benefit in the treatment of HRS. It prolongs both survival time and has the ability to reverse HRS in the majority of patients. In this review we aim to focus on the pathogenesis of HRS and its treatment with terlipressin vs other drugs. Twit Text FOAVip Terlipressin and hepatorenal syndrome: what is important for nephrologists and hepatologists ????World J Gastroenterol http://www.kidney.de/pget.php?&tw=1&pmid=21049548 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21049548 #FOAvip English Wikipedia <ref>{{Cite pmid|21049548}}</ref> Terlipressin and hepatorenal syndrome: what is important for nephrologists and hepatologists #MMPMID21049548 Magan AA; Khalil AA; Ahmed MH World J Gastroenterol 2010[Nov]; 16 (41): 5139-47 PMID21049548show ga Hepatorenal syndrome (HRS) is a reversible form of functional renal failure that occurs with advanced hepatic cirrhosis and liver failure. Despite mounting research in HRS, its etiology and medical therapy has not been resolved. HRS encompasses 2 distinct types. Type 1 is characterized by the rapid development of renal failure that occurs within 2 wk and involves a doubling of initial serum creatinine. Type 2 has a more insidious onset and is often associated with ascites. Animal studies have shown that both forms, in particular type 1 HRS, are often precipitated by bacterial infections and circulatory changes. The prognosis for HRS remains very poor. Type 1 and 2 both have an expected survival time of 2 wk and 6 mo, respectively. Progression of liver cirrhosis and the resultant portal hypertension leads to the pooling of blood in the splanchnic vascular bed. The ensuing hyperdynamic circulation causes an ineffective circulatory volume which subsequently activates neurohormonal systems. Primarily the sympathetic nervous system and the renin angiotensin system are activated, which, in the early stages of HRS, maintain adequate circulation. Both advanced cirrhosis and prolonged activation of neurohormonal mechanisms result in fatal complications. Locally produced nitric oxide may have the potential to induce a deleterious vasodilatory effect on the splanchnic circulation. Currently medical therapy is aimed at reducing splanchnic vasodilation to resolve the ineffective circulation and maintain good renal perfusion pressure. Terlipressin, a vasopressin analogue, has shown potential benefit in the treatment of HRS. It prolongs both survival time and has the ability to reverse HRS in the majority of patients. In this review we aim to focus on the pathogenesis of HRS and its treatment with terlipressin vs other drugs. |Antihypertensive Agents/*therapeutic use[MESH] |Baroreflex/physiology[MESH] |Cardiac Output[MESH] |Hemodynamics[MESH] |Hepatorenal Syndrome/*drug therapy/etiology/physiopathology[MESH] |Humans[MESH] |Lypressin/*analogs & derivatives/therapeutic use[MESH] |Meta-Analysis as Topic[MESH] |Renin-Angiotensin System/physiology[MESH] |Sympathetic Nervous System/physiology[MESH] |Terlipressin[MESH]Terlipressin and hepatorenal syndrome: what is important for nephrolog(epmc).pdf DeepDyve Pubget Overpricing