Hepatorenal Syndrome: Diagnosis and Treatment – newsreel –

Petrescu, Florin; Mitruţ, Paul; Petrescu, Ileana Octavia; Pădureanu, Vlad; Enescu, A

doi:10.1515/rjim-2016-0024

Cited by 5 publications

(4 citation statements)

References 38 publications

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“…En ausencia de un marcador bioquímico o radiológico especí co, el diagnóstico del SHR se basa en criterios que excluyen otras causas de daño renal como: hipovolemia, la presencia de daño renal estructural (necrosis tubular aguda, glomerulonefritis y nefritis intersticial aguda) o daño renal obstructivo (uropatía obstructiva) [31][32][33]. Es necesario determinar si hay evidencia de infección sobre diuresis, hemorragia gastrointestinal, uso reciente de vasodilatadores o nefrotoxinas (incluidos medicamentos antiin amatorios no esteroideos) o paracentesis de gran volumen sin el uso de albúmina.…”

Section: Diagnósticounclassified

Síndrome Hepatorrenal: Revisión De La Literatura

Aguilar¹

2022

Rev. Colomb. Nefrol.

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El síndrome hepatorrenal es una disfunción renal que ocurre en pacientes con enfermedad hepática crónica como cirrosis hepática o enfermedad hepática aguda, caracterizada por la activación de mecanismos reguladores que conducen a disminución de la tasa de filtrado glomerular. Clínicamente el síndrome hepatorrenal se divide en dos tipos, el tipo 1 y el tipo 2. El tipo 1 se caracteriza por una pérdida rápida y progresiva de la función renal mientras que el tipo 2 se caracteriza por ser de progresión lenta y de mejor pronóstico. No existen hallazgos clínicos específicos, sin embargo, sus manifestaciones clínicas reflejan la enfermedad hepática avanzada subyacente, la insuficiencia renal y las anomalías circulatorias presentes. La opción terapéutica más adecuada es el trasplante hepático, pero no todos los pacientes pueden recibirlo, mientras se accede a dicho manejo una opción es el tratamiento medicamentoso con vasoconstrictores y albúmina.

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Section: Diagnósticounclassified

Síndrome Hepatorrenal: Revisión De La Literatura

Aguilar¹

2022

Rev. Colomb. Nefrol.

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“…It has been shown that acute reductions in blood flow or increased hepatic resistance cause rapid stimulation of the SNS resulting in renal vasoconstriction and reduced kidney function with stimulation of the RAAS (Figure 2). 16,17 Liver cirrhosis is associated with a substantial release of glutamine into the portal vein, and that causes hepatocyte swelling and activates chemoreceptors that lead to more activation of the SNS. 17 The reflex nature of the response to low hepatic blood flow is supported by studies which show that denervation of the liver and/or kidney decreases SNS and improves renal blood flow and Na + excretion.…”

Section: Pathophysiologymentioning

confidence: 99%

Hepatorenal Syndrome

2018

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Hepatorenal syndrome is a form of acute kidney injury that occurs in chronic liver diseaseand acute fulminant liver failure. This syndrome features a rapid progressive decline in renalfunction in the absence of other obvious causes of renal dysfunction. The pathophysiologyof this syndrome is still not completely understood, and several mechanisms have beenproposed to explain its pathogenesis. The characteristic feature of hepatorenal syndrome isintense renal vasoconstriction. The local production of vasodilator substances as a result ofportal hypertension have a central role in the pathogenesis of the hepatorenal syndrome asthey lead to splanchnic pooling and decreased effective systemic arterial plasma volume andrenal vasoconstriction. Hepatorenal syndrome is a diagnosis of exclusion and is considered achallenging medical condition in both diagnosis and treatment as it is associated with a poorprognosis. This article will review the two main hypotheses about the pathogenesis, diagnosticcriteria, and treatment approaches to the hepatorenal syndrome.

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“…It is due to splanchnic vasodilation, which results in renal vasoconstriction with consequent reduction in renal plasma flow and glomerular filtration rate. 1 In the United States, treatment is with a combination of octreotide, midodrine, and human albumin to increase the effective blood volume and subsequently improve renal function. 2 While octreotide, a long-acting somatostatin analog, is used to induce splanchnic vasoconstriction in this setting, it also affects the secretion of insulin and glucagon.…”

Section: Introductionmentioning

confidence: 99%

Octreotide-Induced Hypoglycemia in a Cirrhotic Patient

Chen¹

2018

TMF

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The patient was briefly treated with high-dose octreotide (up to 200mcg every 8 hour), hydrochlorothiazide, and diazoxide when the etiology of his hypoglycemia was thought to be a result of excess insulin secretion. The hydrochlorothiazide and diazoxide were discontinued in the setting of hyperkalemia and worsening kidney function. There was no appreciable improvement in the patient's blood glucose levels until the octreotide was discontinued and high-dose steroids was initiated. The patient was weaned off of all continuous dextrose infusion about three weeks after he last received octreotide, and was subsequently discharged home one week later on prednisone 5mg once daily. As an outpatient, the patient was tapered off of prednisone.

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Hepatorenal Syndrome: Diagnosis and Treatment – newsreel –

Cited by 5 publications

References 38 publications

Síndrome Hepatorrenal: Revisión De La Literatura

Síndrome Hepatorrenal: Revisión De La Literatura

Hepatorenal Syndrome

Octreotide-Induced Hypoglycemia in a Cirrhotic Patient

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