Transplantation of cadaveric kidneys from patients with hepatorenal syndrome. Evidence for the functional nature of renal failure in advanced liver disease

Koppel, M H; Jw, Coburn; Mims, Matt M.; Goldstein, H. H.; Boyle, J D; Rubini, Milton E.

doi:10.1097/00007890-197001000-00011

Cited by 49 publications

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“…This pathophysiologic correlation was first described by Hecker and Sherlock in 1958 [1]. The functional nature of HRS was confirmed further by the ability to transplant kidneys from patients with HRS and the normalization of renal function after liver transplantation [2,3]. The pathophysiologic hallmark of HRS is splanchnic vasodilation and renal vasoconstriction which has been established in multiple studies [4][5][6][7][8].…”

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confidence: 82%

Hepatorenal Syndrome-Current Concepts in Pathophysiology

Mathur¹,

Agarwal²

2017

GHOA

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Hepatorenal syndrome (HRS) is a functional renal impairment that occurs in advanced liver cirrhosis or fulminant hepatic failure due to diminished renal blood flow in histological normal kidneys. The pathophysiologic hallmark of HRS is splanchnic vasodilation and renal vasoconstriction leading to renal hypoperfusion and decline in glomerular filtration rate. Two subtypes of HRS i.e. Type 1 and type 2 have been identified with type 1 carrying poor prognosis.Keywords: Hepatorenal syndrome; Splanchnic vasodilation; Renal vasoconstriction; Glomerular filtration rate kidneys. This pathophysiologic correlation was first described by Hecker and Sherlock in 1958 [1]. The functional nature of HRS was confirmed further by the ability to transplant kidneys from patients with HRS and the normalization of renal function after liver transplantation [2,3]. The pathophysiologic hallmark of HRS is splanchnic vasodilation and renal vasoconstriction which has been established in multiple studies [4][5][6][7][8]. Here we present brief overview of current concepts in pathophysiology of HRS. DefinitionThe hepatorenal syndrome is defined as potentially reversible functional impairment of renal function in a patient who has established or clinically evident acute or chronic liver disease. It is characterized clinically by progressive rise in serum creatinine with or without oliguria and urine sediment is often bland. Two subtypes of HRS have been identified: Type 1 HRS: It is defined as at least a twofold increase in serum creatinine to a level greater than 2.5 mg/dL or by 50% reduction in creatinine clearance to a level <20 ml/min during a period of less than two weeks. It is usually precipitated by infection and has a worse prognosis with median survival of less than 10% at 3 months [9-11]. Type 2 HRS:It is defined as renal impairment that is less severe than that observed with type 1 disease and is characterized by refractory ascites. Pathophysiology-Current ConceptsThe pathophysiologic process of HRS begins early and progresses with worsening liver function and involves multiple interrelated pathways ultimately leading to splanchnic vasodilation and renal vasoconstriction which are the hallmark of HRS. In liver disease, portal hypertension leads to splanchnic vasodilation, which progressively increases with advancing disease causing altered cardiovascular function and hyperdynamic circulation leading to decrease in effective arterial volume with activation of endogenous vasoactive systems. These hemodynamic changes ultimately lead to renal hypoperfusion and decline in glomerular filtration rate (GFR). Figure 1 shows pathophysiology of HRS.

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confidence: 82%

Hepatorenal Syndrome-Current Concepts in Pathophysiology

Mathur¹,

Agarwal²

2017

GHOA

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“…Die volle Reversibilität dieser Niereninsuffizienz bei Normalisierung der Leberfunktion konnte bereits im Jahr 1969 gezeigt werden, indem die Nieren von Patienten mit Zirrhose, die im Nierenversagen verstorben waren, erfolgreich transplantiert wurden und beim Empfänger eine normale Nierenfunktion zeigten [19]. Die Arbeitsgruppe von Murray Epstein beschrieb im Jahr 1970 eine massive renale Vasokonstriktion als Ursache des Nierenversagen bei Patienten mit Leberzirrhose, wobei diese Vasokonstriktion der Nierengefäße postmortem bei Zirrhosepatienten, die im Nierenversagen verstarben, nicht mehr nachweisbar war [7].…”

Section: » Bei Normalisierung Der Leberfunktion Ist Die Niereninsuffiunclassified

Hepatorenales Syndrom bei dekompensierter Leberzirrhose

Lenz

Buder

Lohr

et al. 2016

Med Klin Intensivmed Notfmed

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“…The absence of protein and the presence of low levels of sodium excretion in the urine of patients with HRS were reported by Hecker and Sherlock in 1956. 7 The functional nature of this renal insuffi ciency was emphasized by Koppel et al, 8 who proved in the 1960s that kidneys obtained from dead patients with HRS could be transplanted into patients with renal insufficiency of different etiology, since these kidneys could recover their functional capacity after the transplantation. In the 1970s, Iwatsuki et al 9 showed that HRS patients recovered renal function after orthotopic liver transplantation, thus further highlighting the functional Hepatorenal syndrome (HRS) is the development of renal failure in patients with chronic previous liver disease, without clinical or laboratory evidence of previous kidney disease.…”

Section: Introductionmentioning

confidence: 99%

Hepatorenal syndrome: an update

Genzini

Torricelli

2007

Sao Paulo Med. J.

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RESUMO Síndrome hepatorrenal: estado atualA síndrome hepatorrenal (SHR) é o desenvolvimento do quadro de insufi ciência renal em pacientes com doença hepática crônica prévia sem evidências clínica ou laboratorial de nefropatia prévia. Atinge até 18% dos pacientes cirróticos com ascite em um ano, chegando a 39% em cinco anos, com uma sobrevida média em torno de duas semanas após estabelecido o quadro. O diagnóstico da SHR baseia-se em critérios clínicos e laboratoriais. Seu aparecimento está relacionado ao mecanismo de formação de ascite, que envolve vasoconstrição e hipofl uxo renal, retenção de água e sódio, aumento do volume plasmático, e conseqüentemente hiperfl uxo no território esplâncnico. Mediadores vasoativos renais e humorais, como a endotelina 1, tromboxano A2 e leucotrienos, estão ainda envolvidos na gênese desta síndrome que culmina com insufi ciência renal funcional. O tratamento preconizado da SHR pode ser farmacológico ou cirúrgico, sendo o transplante de fígado o único efetivo e permanente, com sobrevida de até 60% em quatro anos. Após melhora da função hepática, geralmente há a reversão da insufi ciência renal. O diagnóstico precoce e a rápida terapêutica podem ampliar a expectativa de vida destes hepatopatas enquanto se aguarda o transplante hepático para seu tratamento defi nitivo. PALAVRAS-CHAVE:

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Transplantation of cadaveric kidneys from patients with hepatorenal syndrome. Evidence for the functional nature of renal failure in advanced liver disease

Cited by 49 publications

References 0 publications

Hepatorenal Syndrome-Current Concepts in Pathophysiology

Hepatorenal Syndrome-Current Concepts in Pathophysiology

Hepatorenales Syndrom bei dekompensierter Leberzirrhose

Hepatorenal syndrome: an update

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