Advances in the pathogenesis and treatment of type-1 and type-2 hepatorenal syndrome

Arroyo, Vicente; Terra, Carlos; Ginès, Pere

doi:10.1016/j.jhep.2007.02.001

Cited by 138 publications

(124 citation statements)

References 89 publications

(142 reference statements)

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“…The kidney, in response to the relative hypovolemia, retains sodium and water. Rather than a decrease in intravascular volume, the relative hypovolemia is the result of an increase of the vascular compartment caused by vasodilatation, leading to a reduction in central blood volume, and activation of vasoconstrictive and volume retaining neuro-humoral mechanisms that perpetuate the sodium-and water-retention [4,37].…”

Section: Hepato-renal Syndromementioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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The hyperdynamic syndrome is a late consequence of portal hypertension in cirrhosis. The principal hemodynamic manifestations of the hyperdynamic syndrome are high cardiac output, and increased heart rate and total blood volume, accompanied by reduced total systemic vascular resistance. Pathophysiology involves a complex of humoral and neural mechanisms that can determine hemodynamic changes, and lead to hyperdynamic circulation. In this review we focus our attention on the manifestations of the hyperdynamic syndrome. Some of these are well described and directly related to portal hypertension (varices, ascites, hepatic encephalopathy, and hepatorenal syndrome), while others, such as hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy, are less known as clinical manifestations related to cirrhosis and, therefore, merit further investigation.

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Section: Hepato-renal Syndromementioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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“…Second, as cirrhosis progresses, there is a reduction in cardiac performance resulting in maladaptive neuro-hormonal activation (i.e., renin-angiotensin, sympathetic nervous system, nonosmotic release of arginine vasopressin) characterized by progressive renal vasoconstriction. 79 This is manifest as avid urinary sodium retention and oliguria that may be refractory to diuretic therapy. Renal histology classically fails to show any significant glomerular or tubular abnormalities that are consistent with functional AKI.…”

Section: Secondary Cardio-renal Syndromes (Type 5 Crs)mentioning

confidence: 99%

Review article: Acute kidney injury in critical illness

Bagshaw

Bellomo

Devarajan

et al. 2010

Can J Anesth/J Can Anesth

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Purpose This review provides a focused and comprehensive update on emerging evidence related to acute kidney injury (AKI).Principal findings Acute kidney injury is a significant clinical problem that increasingly complicates the course of hospitalization and portends worse clinical outcome for sick hospitalized patients. The recent introduction of consensus criteria for the diagnosis of AKI (i.e., RIFLE/AKIN classification) have greatly improved our capacity not only to standardize the diagnosis and classification of severity of AKI, but also to facilitate conducting comparative epidemiologic studies in an effort to better understand the burden of adult and pediatric AKI and its syndromes (i.e., septic, cardio-renal, hepato-renal). The characterization of several novel AKI-specific biomarkers (i.e., neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, and interleukin-18) is extending our understanding of the pathophysiology of AKI. Moreover, these biomarkers appear to have clinical relevance for early detection and they provide prognostic value. These innovations are aiding in the design of epidemiologic surveys and randomized trials of therapeutic interventions. Strategies for prevention Editor's Note: This article is the first of two linked special review articles published in this issue of the Journal. The concept of these articles emerged from the scientific content of the 2010 Acute Kidney Injury (AKI) and Renal Support in Critical Illness Symposium, hosted in Edmonton, Alberta. This review (Part 1) provides a focused and comprehensive update on emerging evidence in the diagnosis and classification of AKI, on specific AKI syndromes, and on the prevention and conservative management of hospitalized patients with AKI. Abstracts presented at this meeting were selected on the basis of peer review by the Scientific Committee and were accepted for presentation at the AKI 2010 Symposium, and appear as Electronic Supplementary Material at

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“…The local and circulating RAS can interact with each other and with other regulatory systems [7] . Liver cirrhosis has 2 major circulatory dysfunctions: portal hypertension and a hyperdynamic circulation characterized by elevated cardiac output and low systemic vascular resistance [8] . It is well established that Ang Ⅱ plays a role in the pathogenesis of portal hypertension by increasing intrahepatic vascular resistance and also by contributing to liver fibrosis [5] .…”

Section: Introductionmentioning

confidence: 99%

“…Early in the course of the disease, the decrease in systemic vascular resistance is compensated by the development of a hyperdynamic circulation [10] . Despite a reduction in systemic vascular resistance, the effective arterial blood volume remains normal, as does the circulating RAS components and antidiuretic hormone [8] . However, as the disease progresses and arterial vasodilation increases, the hyperdynamic circulation is insufficient to correct the effective arterial hypovolemia [8] .…”

Section: Introductionmentioning

confidence: 99%

Relationship between angiotensin-(1-7) and angiotensin II correlates with hemodynamic changes in human liver cirrhosis

Vilas-Boas¹,

Ribeiro‐Oliveira²,

Pereira³

et al. 2009

WJG

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AIM: To measure circulating angiotensins at different stages of human cirrhosis and to further evaluate a possible relationship between renin angiotensin system (RAS) components and hemodynamic changes. METHODS:Patients were allocated into 4 groups: mild-to-moderate liver disease (MLD), advanced liver disease (ALD), patients undergoing liver transplantation, and healthy controls. Blood was collected to determine plasma renin activity (PRA), angiotensin (Ang) Ⅰ, Ang Ⅱ, and Ang-(1-7) levels using radioimmunoassays. During liver transplantation, hemodynamic parameters were determined and blood was simultaneously obtained from the portal vein and radial artery in order to measure RAS components. RESULTS:PRA and angiotensins were elevated in ALD when compared to MLD and controls (P < 0.05). In contrast, Ang Ⅱ was significantly reduced in MLD. Ang-(1-7)/Ang Ⅱ ratios were increased in MLD when compared to controls and ALD. During transplantation, Ang Ⅱ levels were lower and Ang-(1-7)/Ang Ⅱ ratios were higher in the splanchnic circulation than in the peripheral circulation (0.52 ± 0.08 vs 0.38 ± 0.04, P < 0.02), whereas the peripheral circulating Ang Ⅱ/Ang Ⅰ ratio was elevated in comparison to splanchnic levels (0.18 ± 0.02 vs 0.13 ± 0.02, P < 0.04). Ang-(1-7)/ Ang Ⅱ ratios positively correlated with cardiac output (r = 0.66) and negatively correlated with systemic vascular resistance (r = -0.70). CONCLUSION:Our findings suggest that the relationship between Ang-(1-7) and Ang Ⅱ may play a role in the hemodynamic changes of human cirrhosis.

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Advances in the pathogenesis and treatment of type-1 and type-2 hepatorenal syndrome

Cited by 138 publications

References 89 publications

Clinical implications of the hyperdynamic syndrome in cirrhosis

Clinical implications of the hyperdynamic syndrome in cirrhosis

Review article: Acute kidney injury in critical illness

Relationship between angiotensin-(1-7) and angiotensin II correlates with hemodynamic changes in human liver cirrhosis

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