Arteriolar vasodilation and the pathogenesis of the hyperdynamic circulation and renal sodium and water retention in cirrhosis

Arroyo, Vicente; Ginès, Pere

doi:10.1016/0016-5085(92)90203-b

Cited by 41 publications

(22 citation statements)

References 16 publications

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“…Refractory ascites: Ascites that cannot be mobilized or early recurrence of which (i.e., after therapeutic paracentesis) that cannot be satisfactorily prevented by medical therapy [3].…”

Section: Definitionsmentioning

confidence: 99%

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Alfapump® system vs. large volume paracentesis for refractory ascites: A multicenter randomized controlled study

Bureau

Adebayo

Rieu

et al. 2017

Journal of Hepatology

107

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“…Refractory ascites: Ascites that cannot be mobilized or early recurrence of which (i.e., after therapeutic paracentesis) that cannot be satisfactorily prevented by medical therapy [3].…”

Section: Definitionsmentioning

confidence: 99%

“…Treatment of ascites includes restriction of dietary sodium and diuretics [2]. However, some patients develop diuretic-resistant or intractable ascites, because of diuretic-induced complications such as renal dysfunction, hyponatremia or hepatic encephalopathy (HE) [3,4].…”

mentioning

confidence: 99%

Alfapump® system vs. large volume paracentesis for refractory ascites: A multicenter randomized controlled study

Bureau

Adebayo

Rieu

et al. 2017

Journal of Hepatology

107

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“…All pain this situation [1,2]. Recently some investigators have tients had evidence of portal hypertension as indicated by esophageal hypothesized that an increase in the synthesis and release varices and characteristic features of liver cirrhosis by ultrasound.…”

Section: Stances Both Atrial Natriuretic Peptic and Prostaglandinsmentioning

confidence: 99%

Renal Function in Compensated Hepatic Cirrhosis: Effects of an Amino Acid Infusion and Relationship with Nitric Acid

Rodriquez¹,

Martín²,

Oterino³

et al. 1999

Dig Dis

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Aims: In order to assess the possible participation of nitric oxide (NO) in renal function during compensated hepatic cirrhosis, we studied renal function, the plasma and urinary levels of cGMP and the concentration of nitrates and nitrites, as markers of NO synthesis in blood and urine, in 10 patients with Child A hepatic cirrhosis as compared with 10 control subjects, both under basal conditions and during stimulation (amino acid-induced glomerular hyperfiltration). Methods: To study renal function, the glomerular filtration rate (GFR), effective renal plasma flow (ERPF), renal functional reserve (RFR), renal venous resistance (RVR) and the filtration fraction (FF) were measured. Renin and aldosterone levels were determined to assess the possible involvement of these compounds in the renin-angiotensin-aldosterone axis. Results: GFR and ERPF were significantly lower in the patients with cirrhosis than in the controls (mean GFR: 82±12.3 vs. 105±15 ml/min, p = 0.01; ERPF 452±86 vs. 543±56 ml/min, p = 0.002). The RFR value was similar in both groups. In the basal situation cGMP levels were higher in plasma and urine in patients with cirrhosis than in the controls (plasma cGMP in cirrhosis 8.4±2.4 vs. 4.2±3.5 pmol/ml; urine cGMP in cirrhosis 1.2±2.1 vs. 0.68±0.1 pmol/ml). The NO levels were also higher in plasma and urine in patients with cirrhosis vs. controls (plasma NO in cirrhosis 45.5±9.2 vs. 30.3±1.2 μmol/l; urinary NO in cirrhosis 6.2±1.3 vs. 3.1±2.3 μmol/ml). In both groups the amino acid perfusion increased GFR, ERPF, cGMP and NO levels in plasma and urine. In the patients with cirrhosis the RVR decreased significantly during perfusion and no noteworthy changes in FF were observed. The GFR values observed during amino acid perfusion were similar in patients with cirrhosis and portal hypertension to those observed in the controls (27.2±12 vs. 25.3±16%). However, the changes induced the ERPF were more marked in patients with cirrhosis (cirrhosis 35.3±15 vs. 22.2±13%, p = 0.02). Conclusions: The present findings point to certain alterations in renal function in patients with hepatic cirrhosis and portal hypertension without ascitis, a clear difference being visible between the ERPF and GFR following amino acid-induced stimulation. The significant elevation in cGMP and NO levels in plasma and urine implies a maintained vasodilatory action that may at least partly compensate the vasoconstrictor effects of angiotensin II.

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“…creased microvascular hydrostatic pressure and, therefore, in the passage of fluid from the intravascular comFurosemide is highly bound to plasma proteins and reaches the tubular lumen by active secretion in the partment to the interstitial space during portal hypertension. 66 proximal tubule. Once in the luminal compartment, furosemide reaches the luminal membrane of the cells…”

Section: M4533$0033mentioning

confidence: 99%

Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis

Arroyo¹

1996

Hepatology

420

717

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During the last decade great advances have been made of water retention and dilutional hyponatremia in human cirrhosis. Finally, the field of spontaneous infection of concerning the pathogenesis and treatment of ascites. A new hypothesis on the mechanism of renal dysfunction ascitic fluid (spontaneous bacterial peritonitis) is also experiencing major changes. The demonstration of intestiand ascites formation in cirrhosis has been proposed 1 and this has greatly stimulated research in this area. The nal bacterial translocation in experimental models of cirrhosis, 12 the potential role of cytokines in some discovery of the important role played by the vascular endothelium in the homeostasis of systemic hemodynam-complications associated with this infection, 13 the identification of subgroups of cirrhotic patients predisposed to ics and renal function 2,3 has also opened an important field of research into pathophysiology, and evidence has develop spontaneous bacterial peritonitis, 14 and the effectiveness of selective intestinal decontamination in the been presented implicating endothelial factors in the pathogenesis of systemic circulatory dysfunction in cir-primary and secondary prophylaxis of spontaneous bacterial peritonitis 15,16 are the most relevant developments. rhosis 4,5 and hepatorenal syndrome (HRS). 6 The reintroduction of therapeutic paracentesis has greatly modifiedIn clear contrast to these advances, little attention has been paid to the standardization of the nomenclathe treatment of cirrhotic patients with tense or refractory ascites. 7 The transjugular intrahepatic portosys-ture and diagnostic criteria of different syndromes associated with ascites in cirrhosis. The existence of a temic shunt is another therapeutic tool of potential interest in the management of refractory ascites. 8 The uniform language, however, is essential in modern medicine. It facilitates communication among clinisynthesis of orally-active specific antagonists of the tubular effect of antidiuretic hormone and inhibitors of antidi-cians and researchers and ensures unambiguous diagnoses and more confident prognoses. Moreover, it uretic hormone release will probably add new drugs to the pharmacological armamentarium for patients with improves pathophysiological and therapeutic investigations, simplifies the analysis of therapeutic trials, cirrhosis and ascites. These ''aquaretic drugs,'' which normalize renal water metabolism in experimental cirrhosis and stimulates multicenter studies. and ascites, 9-11 are of potential interest for the treatment PREVIOUS CONSENSUS DEFINITIONS OF HEPATORENAL SYNDROME AND

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Arteriolar vasodilation and the pathogenesis of the hyperdynamic circulation and renal sodium and water retention in cirrhosis

Cited by 41 publications

References 16 publications

Alfapump® system vs. large volume paracentesis for refractory ascites: A multicenter randomized controlled study

Alfapump® system vs. large volume paracentesis for refractory ascites: A multicenter randomized controlled study

Renal Function in Compensated Hepatic Cirrhosis: Effects of an Amino Acid Infusion and Relationship with Nitric Acid

Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis

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