Therapy of hyponatremia in cirrhosis with a vasopressin receptor antagonist: A randomized double-blind multicenter trial

Gerbes, Alexander L.; Gülberg, Veit; Ginès, Pere; Decaux, Guy; Groß, Peter; Gandjini, Hassan; Djian, Jacques

doi:10.1053/gast.2003.50143

Cited by 278 publications

(238 citation statements)

References 18 publications

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“…This conclusion is derived from studies in cirrhotic patients receiving an AVP V 2 R antagonist that demonstrate urinary dilution and increased serum [Na ϩ ]. 60 Nephrotic syndrome, acute and chronic renal failure. Hyponatremia occurs commonly in both acute and chronic renal failure, because the kidneys cannot maximally excrete excess ingested or infused water.…”

Section: S8mentioning

confidence: 99%

Hyponatremia Treatment Guidelines 2007: Expert Panel Recommendations

Verbalis

Goldsmith

Greenberg

et al. 2007

The American Journal of Medicine

511

498

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Although hyponatremia is a common, usually mild, and relatively asymptomatic disorder of electrolytes, acute severe hyponatremia can cause substantial morbidity and mortality, particularly in patients with concomitant disease. In addition, overly rapid correction of chronic hyponatremia can cause severe neurologic deficits and death, and optimal treatment strategies for such cases are not established. Hyponatremia is the most common disorder of electrolytes encountered in clinical practice, occurring in up to 15% to 30% of both acutely and chronically hospitalized patients. 1 Although most cases are mild and relatively asymptomatic, hyponatremia is important clinically because: (1) acute severe hyponatremia can cause substantial morbidity and mortality; (2) mortality is higher in patients with hyponatremia who have a wide range of underlying diseases; and (3) overly rapid correction of chronic hyponatremia can cause severe neurologic deficits and death.Despite knowledge of hyponatremia since the mid-20th century, this common disorder remains incompletely understood in many basic areas because of its association with a plethora of underlying disease states, and its multiple etiologies with differing pathophysiologic mechanisms. 2 Optimal treatment strategies have not been well defined, both for these reasons and because of marked differences in symptomatology and clinical outcomes based on the acuteness or chronicity of the hyponatremia. 3 Vasopressin receptor antagonists have long been anticipated as a more effective method to treat hyponatremia by virtue of their unique aquaretic effect to selectively increase solute-free water excretion by the kidneys. 4 The recent approval of the first such agent, conivaptan, for clinical use by the US Food and Drug Administration (FDA) heralds the beginning of a new era in the management of hyponatremic disorders. However, effective therapy with these agents will require intelligent guidelines for their use. To this end, a panel of experts in hyponatremia convened to review current therapies for hyponatremia and to evaluate the situations in which aquaretic agents should be considered as alternatives or supplements to accepted current therapies. This review is a summary of the conclusions of this panel.

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Section: S8mentioning

confidence: 99%

Hyponatremia Treatment Guidelines 2007: Expert Panel Recommendations

Verbalis

Goldsmith

Greenberg

et al. 2007

The American Journal of Medicine

511

498

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“…Since the nonosmotic secretion of antidiuretic hormone due to a decreased effective arterial blood volume is a prime mover in the development of dilutional hyponatremia, many experts in the field use volume expansion with colloids (which are usually saline based) to try to improve renal function. There are data emerging that support the use of specific vasopressin-2 receptor antagonists in the treatment of dilutional hyponatremia, 61,62 but whether this improves overall morbidity and mortality is not yet known.…”

Section: Treatment Of Dilutional Hyponatremiamentioning

confidence: 99%

The management of ascites in cirrhosis: Report on the consensus conference of the International Ascites Club

et al. 2003

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Ascites is a common complication of cirrhosis, and heralds a new phase of hepatic decompensation in the progression of the cirrhotic process. The development of ascites carries a significant worsening of the prognosis. It is important to diagnose noncirrhotic causes of ascites such as malignancy, tuberculosis, and pancreatic ascites since these occur with increased frequency in patients with liver disease. The International Ascites Club, representing the spectrum of clinical practice from North America to Europe, have developed guidelines by consensus in the management of cirrhotic ascites from the early ascitic stage to the stage of refractory ascites. Mild to moderate ascites should be managed by modest salt restriction and diuretic therapy with spironolactone or an equivalent in the first instance. Diuretics should be added in a stepwise fashion while maintaining sodium restriction. Gross ascites should be treated with therapeutic paracentesis followed by colloid volume expansion, and diuretic therapy. Refractory ascites is managed by repeated large volume paracentesis or insertion of a transjugular intrahepatic portosystemic stent shunt (TIPS). Successful placement of TIPS results in improved renal function, sodium excretion, and general well-being of the patient but without proven survival benefits. Clinicians caring for these patients should be aware of the potential complications of each treatment modality and be prepared to discontinue diuretics or not proceed with TIPS placement should complications or contraindications develop. Liver transplantation should be considered for all ascitic patients, and this should preferably be performed prior to the development of renal dysfunction to prevent further compromise of their prognosis. (HEPATOLOGY 2003;38:258-266.)

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“…1), 18 trials met the eligibility criteria or reported data for an eligible subgroup. Two trials assessed conivaptan, 13,14 four assessed lixivaptan, [15][16][17][18] three assessed satavaptan [19][20][21] and nine assessed tolvaptan. [22][23][24][25][26][27][28][29] There were no RCTs published assessing other known interventions such as urea, sodium tablets or mannitol.…”

Section: Resultsmentioning

confidence: 99%

“…Some trials reported data for a specific population and others included patients with various underlying causes. Three trials assessed hyponatraemia in patients with SIADH, 15,21,22 four assessed hyponatraemia in patients with congestive heart failure, [24][25][26][27] two assessed hyponatraemia in patients with cirrhosis, 17,20 and one assessed hyponatraemia in patients with cancer. 28 The other eight trials assessed hyponatraemia in patients with a range of underlying conditions.…”

Section: Resultsmentioning

confidence: 99%

Untitled

2017

Clinical Endocrinology

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International and national guidelines on the treatment of chronic nonhypovolaemic hypotonic hyponatraemia differ; therefore, we have undertaken this systematic review and metaanalysis to investigate the efficacy and safety of interventions for the treatment of chronic nonhypovolaemic hypotonic hyponatraemia. Following registration of the review protocol with PROSPERO, systematic literature searches were conducted to identify randomized and quasi-randomized controlled trials assessing any degree of fluid restriction or any drug treatment with the aim of increasing serum sodium concentration in patients with chronic nonhypovolaemic hypotonic hyponatraemia. Where appropriate, outcome data were synthesized in a meta-analysis. A total of 45 716 bibliographic records were identified from the searches and 18 trials (assessing conivaptan, lixivaptan, tolvaptan and satavaptan) met the eligibility criteria. Results suggest that all four vasopressin receptor agonists ("vaptans") significantly improve serum sodium concentration. Lixivaptan, satavaptan and tolvaptan were associated with greater rates of response versus placebo. There was no evidence of a difference between each of the vaptans compared with placebo for mortality, discontinuation and rates of hypernatraemia. No RCT evidence of treatments other than the vaptans for hyponatraemia such as oral urea, salt tablets, mannitol, loop diuretics demeclocycline or lithium was identified. Vaptans demonstrated superiority over placebo for outcomes relating to serum sodium correction. Few trials documented the potential benefit of vaptans on change in health-related quality of life as a result of treatment. There was also a lack of high-quality RCT evidence on the comparative efficacy of the vaptans and other treatment strategies for the treatment of chronic nonhypovolaemic hypotonic hyponatraemia.

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Therapy of hyponatremia in cirrhosis with a vasopressin receptor antagonist: A randomized double-blind multicenter trial

Cited by 278 publications

References 18 publications

Hyponatremia Treatment Guidelines 2007: Expert Panel Recommendations

Hyponatremia Treatment Guidelines 2007: Expert Panel Recommendations

The management of ascites in cirrhosis: Report on the consensus conference of the International Ascites Club

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