Hepatorenal syndrome: an update

Genzini, Tércio; Torricelli, Fábio César Miranda

doi:10.1590/s1516-31802007000100010

Cited by 13 publications

(11 citation statements)

References 54 publications

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“…AKI associated with liver failure is a grave clinical problem with high mortality rate. In fact, the diagnosis of AKI in patients with liver failure implies a significant increase in mortality and morbidity (4,25–27). Supportive therapies for AKI associated with liver failure are limited to hydration, blood pressure support and short-term hemodialysis until renal function recovers.…”

Section: Discussionmentioning

confidence: 99%

Acute kidney injury after hepatic ischemia and reperfusion injury in mice

Lee

Park

Kim

et al. 2009

Laboratory Investigation

105

128

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Hepatic ischemia reperfusion (IR) is the leading cause of acute liver failure (ALF) during the perioperative period and patients with ALF frequently develop acute kidney injury (AKI). There is no effective therapy for AKI associated with ALF because pathomechanisms are incompletely characterized, in part due to the lack of an animal model. In this study, we characterize a novel murine model of AKI following hepatic IR. Mice subjected to ~70% liver IR not only developed acute liver dysfunction, but also developed severe AKI 24 hr after liver injury. Mice subjected to liver IR developed histological changes of acute tubular injury including focal proximal tubular cell necrosis involving the S3 segment, cortical tubular ectasia, focal tubular simplification and granular bile/heme cast formation. In addition, there was focal interstitial edema and hyperplasia of the juxtaglomerular apparatus. Inflammatory changes in the kidney after hepatic IR included neutrophil infiltration of the interstitium and upregulation of several pro-inflammatory mRNAs (tumor necrosis factor-α, keratinocyte derived cytokine, monocyte chemotactic protein-1, macrophage inflammatory protein-2, intercellular adhesion molecule-1). In addition, marked renal endothelial cell apoptosis was detected involving peritubular interstitial capillaries, accompanied by increased renal vascular permeability. Finally, there was severe disruption of renal proximal tubule epithelial filamentous-actin. Our results show that AKI rapidly and reproducibly develops in mice after hepatic IR and is characterized by renal tubular necrosis, inflammatory changes and interstitial capillary endothelial apoptosis. Our murine model of AKI after liver injury closely mimics human AKI associated with ALF and may be useful in delineating the mechanisms and potential therapies for this common clinical condition.

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Section: Discussionmentioning

confidence: 99%

Acute kidney injury after hepatic ischemia and reperfusion injury in mice

Lee

Park

Kim

et al. 2009

Laboratory Investigation

105

128

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“…Advanced cirrhosis with ascites refractory to a diuretic therapy was complicated in 20% of HRS cases, one year mortality being approximately 50% [18]. The diagnosis of "refractory ascites" indicates possible future complications like HRS; International Ascites Club, thus defining this therapeutic situation [19].…”

Section: Treatment Prevention and Initial Treatment Of Hrsmentioning

confidence: 99%

Hepatorenal Syndrome: Diagnosis and Treatment – newsreel –

Petrescu

Mitruţ

Petrescu

et al. 2016

Romanian Journal of Internal Medicine

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Hepatorenal syndrome (HRS) is defined as renal failure that occurs in the presence of severe acute or chronic liver disease in the absence of underlying renal pathology. Due to the functional nature of the disease and the absence of specific diagnostic markers, HRS diagnosis is determined based on positive criteria associated with excluding other causes of renal failure in patients with liver cirrhosis and ascites. Differentiation from other types of acute or chronic renal disease is extremely difficult and therapeutic options are limited, prophylactic behavior is most appropriate in patients with severe hepatic disease and risk factors for the installation of hepatorenal syndrome.Highlighting all precipitating factors of acute renal insufficiency and therapeutic modalities in order to minimize adverse events is an important step in improving the follow-up of the patients with liver cirrhosis. The prognosis is reserved especially for type 1 HRS. Liver transplantation is the best option for patients without contraindications. The therapies introduced in recent years, such as vasoconstrictor drugs or transjugular intrahepatic portosystemic shunt are effective methods in the renal function improvement.

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“…The pathogenesis of HRS is not completely understood but various hypotheses linking the alterations of renal haemodynamics and ascites formation have been made [13,14]. The most popular hypothesis is the ‘arteral vasodilation hypothesis', proposed by Schrier et al in 1988 [15], the development of HRS is associated with the circulatory changes seen in cirrhosis with portal hypertension, including splanchnic arterial vasodilation.…”

Section: Pathogenesis Of Hrsmentioning

confidence: 99%

Hepatorenal Syndrome and Novel Advances in its Management

Fabrizi¹,

Aghemo

Messa³

2013

Kidney Blood Press Res

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Hepatorenal syndrome is a complication of end stage liver disease. It is a unique form of functional renal failure related to kidney vasoconstriction in the absence of underlying kidney pathology. Hepatorenal syndrome is classified into 2 types: type-1 HRS shows a rapid and progressive decline in renal function with a very poor prognosis (median survival of about 2 weeks); type-2 HRS has a more stable kidney failure, with a median survival of 6 months; its main clinical manifestation is refractory ascites. The most appropriate therapy for HRS is liver transplantation but only a minority of HRS patients undergo the procedure due to the high mortality; survival among liver transplant recipients is lower in HRS than among their counterparts without HRS. A large body of evidence, based on observational studies and randomized controlled trials, has been accumulated in the last decade showing that terlipressin represents a milestone in the management of HRS. According to our meta-analysis of randomized trials comparing terlipressin vs. placebo (five trials, n=243 patients), the pooled rate of patients who reversed HRS by terlipressin was 8.09 (95% CI, 3.52; 18.59) (P<0.001). Among vasoconstrictors, terlipressin (a V1 vasopressin agonist) is the most widely used; however, noradrenaline is another good choice. Vasoconstrictor drugs alone or with albumin reduce mortality compared with no intervention or albumin (RR of mortality, 0.82; 95% Confidence Intervals, 0.70; 0.96) (P<0.01). Two series of patients with HRS recurrence after the first treatment have recently shown that long-term therapy with terlipressin and albumin is beneficial as a bridge to liver transplant. Nevertheless, recovery of renal function can be achieved in less than 50% of patients with HRS after terlipressin use and the recovery of renal function may also be partial in patients who are defined full responders. Renal replacement therapy should not be considered a first-line therapy for HRS Clinical trials are under way in order to assess efficacy and safety of novel therapeutic agents for the treatment of type-1 and type-2 HRS.

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Hepatorenal syndrome: an update

Cited by 13 publications

References 54 publications

Acute kidney injury after hepatic ischemia and reperfusion injury in mice

Acute kidney injury after hepatic ischemia and reperfusion injury in mice

Hepatorenal Syndrome: Diagnosis and Treatment – newsreel –

Hepatorenal Syndrome and Novel Advances in its Management

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