2021
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Abstract: Renal dysfunction occurs frequently in hospitalized patients with advanced chronic liver disease (ACLD)/cirrhosis and has profound prognostic implications. In ACLD patients with ascites, hepatorenal syndrome (HRS) may result from circulatory dysfunction that leads to reduced kidney perfusion and glomerular filtration rate (in the absence of structural kidney damage). The traditional subclassification of HRS has recently been replaced by acute kidney injury (AKI) type of HRS (HRS-AKI) and non-AKI type of HRS (H… Show more

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Cited by 3 publications
(4 citation statements)
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References 133 publications
(180 reference statements)
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“…A wealth of evidence indicates that circulatory dysfunction plays a key role in the pathophysiology of hepatorenal syndrome [ 34 ]. However, recently, evidence has emerged to support the impact of systemic inflammation on disease progression and development in extrahepatic organs, particularly renal dysfunction [ 35 ]. After liver I/R injury, circulating pro-inflammatory cytokines such as interleukin-6 (IL-6), IL-8, TNF-alpha, vascular cell adhesion protein 1 (VCAM-1), fractalkine, and macrophage inflammatory protein-1 alpha (MIP-1 alpha) have been found significantly increased [ 36 ].…”
Section: Discussionmentioning
confidence: 99%
“…A wealth of evidence indicates that circulatory dysfunction plays a key role in the pathophysiology of hepatorenal syndrome [ 34 ]. However, recently, evidence has emerged to support the impact of systemic inflammation on disease progression and development in extrahepatic organs, particularly renal dysfunction [ 35 ]. After liver I/R injury, circulating pro-inflammatory cytokines such as interleukin-6 (IL-6), IL-8, TNF-alpha, vascular cell adhesion protein 1 (VCAM-1), fractalkine, and macrophage inflammatory protein-1 alpha (MIP-1 alpha) have been found significantly increased [ 36 ].…”
Section: Discussionmentioning
confidence: 99%
“…It is of a functional origin and caused by systemic circulatory dysfunction, which leads to renal vasoconstriction secondary to the effect of increased vasoactive substances intended to compensate for initial splanchnic vasodilation [1]. HRS always develops in the context of circulatory dysfunction, mainly in the splanchnic arterial territory, and is generally associated with ascites and hyponatremia due to the activation of neurohormonal systems [2].…”
Section: Dear Editormentioning
confidence: 99%
“…(1) Previous diagnosis of chronic liver disease and ascites; (2) AKI diagnosis; (3) No response after 2 consecutive days of diuretic withdrawal and plasma volume expansion with albumin (1 g/kg body weight); (4) Absence of shock; (5) Current or recent use of nephrotoxic drugs (nonsteroidal anti-inflammatory drugs, aminoglycosides, iodinated contrast media, etc. ); and (6) No macroscopic evidence of structural kidney injury, defined as no proteinuria (>500 mg/day), no microhaematuria (>50 red blood cells per high-power field), and normal renal ultrasound findings [2][3].…”
Section: Dear Editormentioning
confidence: 99%
“…Finally, the AASLD Guidance (1) adopted the continuous administration of terlipressin, which is better tolerated, as compared to bolus administration (16). This recommendation seems particularly far-seeing in the light of more recently emerging concerns about increased rates of respiratory failure in terlipressin-treated patients (17,18).…”
mentioning
confidence: 99%