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Renal insufficiency in patients with hepatic insufficiency
Renal dysfunction is a common complication of cirrhosis, occurring in approximately 20 % of all hospitalized patients with cirrhosis and associated with increased mortality. In about two thirds of the patients, renal dysfunction is caused by prerenal disorders (e.g. gastrointestinal bleeding, diuret...
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Published in: | Medizinische Klinik, Intensivmedizin und Notfallmedizin Intensivmedizin und Notfallmedizin, 2014-05, Vol.109 (4), p.240-245 |
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container_title | Medizinische Klinik, Intensivmedizin und Notfallmedizin |
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creator | Lenz, K Binder, M Buder, R Gruber, A Gutschreiter, B Voglmayr, M |
description | Renal dysfunction is a common complication of cirrhosis, occurring in approximately 20 % of all hospitalized patients with cirrhosis and associated with increased mortality. In about two thirds of the patients, renal dysfunction is caused by prerenal disorders (e.g. gastrointestinal bleeding, diuretics, bacterial infection); one third is caused by intrarenal diseases (e.g. hepatitis associated glomerulonephritis). In most patients, prerenal failure can be successfully handled by volume therapy. In one third, volume replacement is not effective any more to improve kidney function. This kind of prerenal failure is called hepatorenal syndrome (HRS).
The pathophysiology is based on an increased splanchic vasodilation, which cannot be compensated any more by an increased cardiac output. Therefore, patients with cardiac insufficiency are more at risk of developing HRS. The decompensation leads to a stimulation of the baroreceptors with consecutive activation of the sympathetic nerve system, the renin-angiotensin-aldosteron system (RAAS), and nonosmotic release of vasopressin. This results in renal vasoconstriction, which is strengthened by the activation of hepatorenal reflex secondary to an increase in intrahepatic pressure and/or decrease in sinusoidal blood flow.
Several studies have shown that the vasopressin analogue terlipressin combined with albumin can reverse HRS in up to 50 % of patients. Long-term survival can only be achieved by liver transplantation. Improving kidney function before transplantation improves outcome after transplantation. |
doi_str_mv | 10.1007/s00063-013-0322-3 |
format | article |
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The pathophysiology is based on an increased splanchic vasodilation, which cannot be compensated any more by an increased cardiac output. Therefore, patients with cardiac insufficiency are more at risk of developing HRS. The decompensation leads to a stimulation of the baroreceptors with consecutive activation of the sympathetic nerve system, the renin-angiotensin-aldosteron system (RAAS), and nonosmotic release of vasopressin. This results in renal vasoconstriction, which is strengthened by the activation of hepatorenal reflex secondary to an increase in intrahepatic pressure and/or decrease in sinusoidal blood flow.
Several studies have shown that the vasopressin analogue terlipressin combined with albumin can reverse HRS in up to 50 % of patients. Long-term survival can only be achieved by liver transplantation. Improving kidney function before transplantation improves outcome after transplantation.</description><identifier>EISSN: 2193-6226</identifier><identifier>DOI: 10.1007/s00063-013-0322-3</identifier><identifier>PMID: 24763526</identifier><language>ger</language><publisher>Germany</publisher><subject>Critical Care - methods ; Hemodynamics - physiology ; Hepatorenal Syndrome - diagnosis ; Hepatorenal Syndrome - physiopathology ; Hepatorenal Syndrome - therapy ; Humans ; Kidney - physiopathology ; Liver - physiopathology ; Liver Cirrhosis - complications ; Liver Cirrhosis - physiopathology ; Liver Cirrhosis - therapy ; Multiple Organ Failure - diagnosis ; Multiple Organ Failure - physiopathology ; Multiple Organ Failure - therapy ; Renin-Angiotensin System - physiology</subject><ispartof>Medizinische Klinik, Intensivmedizin und Notfallmedizin, 2014-05, Vol.109 (4), p.240-245</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24763526$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lenz, K</creatorcontrib><creatorcontrib>Binder, M</creatorcontrib><creatorcontrib>Buder, R</creatorcontrib><creatorcontrib>Gruber, A</creatorcontrib><creatorcontrib>Gutschreiter, B</creatorcontrib><creatorcontrib>Voglmayr, M</creatorcontrib><title>Renal insufficiency in patients with hepatic insufficiency</title><title>Medizinische Klinik, Intensivmedizin und Notfallmedizin</title><addtitle>Med Klin Intensivmed Notfmed</addtitle><description>Renal dysfunction is a common complication of cirrhosis, occurring in approximately 20 % of all hospitalized patients with cirrhosis and associated with increased mortality. In about two thirds of the patients, renal dysfunction is caused by prerenal disorders (e.g. gastrointestinal bleeding, diuretics, bacterial infection); one third is caused by intrarenal diseases (e.g. hepatitis associated glomerulonephritis). In most patients, prerenal failure can be successfully handled by volume therapy. In one third, volume replacement is not effective any more to improve kidney function. This kind of prerenal failure is called hepatorenal syndrome (HRS).
The pathophysiology is based on an increased splanchic vasodilation, which cannot be compensated any more by an increased cardiac output. Therefore, patients with cardiac insufficiency are more at risk of developing HRS. The decompensation leads to a stimulation of the baroreceptors with consecutive activation of the sympathetic nerve system, the renin-angiotensin-aldosteron system (RAAS), and nonosmotic release of vasopressin. This results in renal vasoconstriction, which is strengthened by the activation of hepatorenal reflex secondary to an increase in intrahepatic pressure and/or decrease in sinusoidal blood flow.
Several studies have shown that the vasopressin analogue terlipressin combined with albumin can reverse HRS in up to 50 % of patients. Long-term survival can only be achieved by liver transplantation. Improving kidney function before transplantation improves outcome after transplantation.</description><subject>Critical Care - methods</subject><subject>Hemodynamics - physiology</subject><subject>Hepatorenal Syndrome - diagnosis</subject><subject>Hepatorenal Syndrome - physiopathology</subject><subject>Hepatorenal Syndrome - therapy</subject><subject>Humans</subject><subject>Kidney - physiopathology</subject><subject>Liver - physiopathology</subject><subject>Liver Cirrhosis - complications</subject><subject>Liver Cirrhosis - physiopathology</subject><subject>Liver Cirrhosis - therapy</subject><subject>Multiple Organ Failure - diagnosis</subject><subject>Multiple Organ Failure - physiopathology</subject><subject>Multiple Organ Failure - therapy</subject><subject>Renin-Angiotensin System - physiology</subject><issn>2193-6226</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNpVj0FLw0AUhBdBbKn9AV4kRy_R995uNllvUrQKBUH0HDa7b2kkSWM3QfrvTbEePAwzAx8DI8QVwi0C5HcRALRMASdJolSeiTmhkakm0jOxjPETjghAlsOFmJHKtcxIz8X9G3e2SeoujiHUrubOHaaW9HaY8hCT73rYJls-dvcfuxTnwTaRlydfiI-nx_fVc7p5Xb-sHjZpjwqH1DvDjhSbDBUHiUysFYNn8hZZIxYqYGGkUVahQxNMVWibY-UJfW5BLsTN726_332NHIeyraPjprEd78ZYYkZKKlKUT-j1CR2rln3Z7-vW7g_l31_5A_azVho</recordid><startdate>201405</startdate><enddate>201405</enddate><creator>Lenz, K</creator><creator>Binder, M</creator><creator>Buder, R</creator><creator>Gruber, A</creator><creator>Gutschreiter, B</creator><creator>Voglmayr, M</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>201405</creationdate><title>Renal insufficiency in patients with hepatic insufficiency</title><author>Lenz, K ; Binder, M ; Buder, R ; Gruber, A ; Gutschreiter, B ; Voglmayr, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p141t-dc9ec24e9514ef31e2e64e0de2da1e61184f189394a41c19f9b86a71bd21d7a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>ger</language><creationdate>2014</creationdate><topic>Critical Care - methods</topic><topic>Hemodynamics - physiology</topic><topic>Hepatorenal Syndrome - diagnosis</topic><topic>Hepatorenal Syndrome - physiopathology</topic><topic>Hepatorenal Syndrome - therapy</topic><topic>Humans</topic><topic>Kidney - physiopathology</topic><topic>Liver - physiopathology</topic><topic>Liver Cirrhosis - complications</topic><topic>Liver Cirrhosis - physiopathology</topic><topic>Liver Cirrhosis - therapy</topic><topic>Multiple Organ Failure - diagnosis</topic><topic>Multiple Organ Failure - physiopathology</topic><topic>Multiple Organ Failure - therapy</topic><topic>Renin-Angiotensin System - physiology</topic><toplevel>online_resources</toplevel><creatorcontrib>Lenz, K</creatorcontrib><creatorcontrib>Binder, M</creatorcontrib><creatorcontrib>Buder, R</creatorcontrib><creatorcontrib>Gruber, A</creatorcontrib><creatorcontrib>Gutschreiter, B</creatorcontrib><creatorcontrib>Voglmayr, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Medizinische Klinik, Intensivmedizin und Notfallmedizin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lenz, K</au><au>Binder, M</au><au>Buder, R</au><au>Gruber, A</au><au>Gutschreiter, B</au><au>Voglmayr, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Renal insufficiency in patients with hepatic insufficiency</atitle><jtitle>Medizinische Klinik, Intensivmedizin und Notfallmedizin</jtitle><addtitle>Med Klin Intensivmed Notfmed</addtitle><date>2014-05</date><risdate>2014</risdate><volume>109</volume><issue>4</issue><spage>240</spage><epage>245</epage><pages>240-245</pages><eissn>2193-6226</eissn><abstract>Renal dysfunction is a common complication of cirrhosis, occurring in approximately 20 % of all hospitalized patients with cirrhosis and associated with increased mortality. In about two thirds of the patients, renal dysfunction is caused by prerenal disorders (e.g. gastrointestinal bleeding, diuretics, bacterial infection); one third is caused by intrarenal diseases (e.g. hepatitis associated glomerulonephritis). In most patients, prerenal failure can be successfully handled by volume therapy. In one third, volume replacement is not effective any more to improve kidney function. This kind of prerenal failure is called hepatorenal syndrome (HRS).
The pathophysiology is based on an increased splanchic vasodilation, which cannot be compensated any more by an increased cardiac output. Therefore, patients with cardiac insufficiency are more at risk of developing HRS. The decompensation leads to a stimulation of the baroreceptors with consecutive activation of the sympathetic nerve system, the renin-angiotensin-aldosteron system (RAAS), and nonosmotic release of vasopressin. This results in renal vasoconstriction, which is strengthened by the activation of hepatorenal reflex secondary to an increase in intrahepatic pressure and/or decrease in sinusoidal blood flow.
Several studies have shown that the vasopressin analogue terlipressin combined with albumin can reverse HRS in up to 50 % of patients. Long-term survival can only be achieved by liver transplantation. Improving kidney function before transplantation improves outcome after transplantation.</abstract><cop>Germany</cop><pmid>24763526</pmid><doi>10.1007/s00063-013-0322-3</doi><tpages>6</tpages></addata></record> |
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subjects | Critical Care - methods Hemodynamics - physiology Hepatorenal Syndrome - diagnosis Hepatorenal Syndrome - physiopathology Hepatorenal Syndrome - therapy Humans Kidney - physiopathology Liver - physiopathology Liver Cirrhosis - complications Liver Cirrhosis - physiopathology Liver Cirrhosis - therapy Multiple Organ Failure - diagnosis Multiple Organ Failure - physiopathology Multiple Organ Failure - therapy Renin-Angiotensin System - physiology |
title | Renal insufficiency in patients with hepatic insufficiency |
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