Relationship between circulatory function and severity of renal failure in patients with cirrhosis and hepatorenal syndrome

2003 ◽  
Vol 38 ◽  
pp. 60
Author(s):  
M. Guevara ◽  
O. Ozdogan ◽  
P. Gines ◽  
C. Alessandria ◽  
T. Restuccia ◽  
...  
1997 ◽  
Vol 92 (5) ◽  
pp. 433-443 ◽  
Author(s):  
Kevin Moore

1. The hepatorenal syndrome is the development of renal failure in patients with severe liver disease in the absence of any identifiable renal pathology. 2. Decreased glomerular filtration is caused by a reduction in both renal blood flow and the renal filtration fraction. These changes arise as a consequence of a fall in mean arterial pressure due to systemic vasodilatation, activation of the sympathetic nervous system causing renal vasoconstriction, and increased synthesis of several vasoactive mediators, which together modulate both renal blood flow and the glomerular capillary ultrafiltration coefficient, and thence filtration fraction. 3. Patients with liver disease developing renal failure should have hypovolaemia excluded by volume challenge, and all nephrotoxic drugs including diuretics should be stopped. Broad-spectrum antibiotics should be given for subclinical infection, which may be a treatable precipitant of renal failure in cirrhosis. Renal perfusion should be optimized by ensuring that the blood pressure and systemic haemodynamics are adequate, and that if renal venous pressure is elevated, due to tense ascites, it is alleviated. 4. The prognosis of hepatorenal syndrome is poor with a >90% mortality. However, patients can and do recover from the hepatorenal syndrome, but only if there is a significant improvement of their liver function, or if they undergo liver transplantation.


Author(s):  
Vicente Arroyo ◽  
Mónica Guevara ◽  
Javier Fernández

A major event in liver cirrhosis is the development of a progressive deterioration of circulatory function due to splanchnic arterial vasodilation and impairment in cardiac function. This feature determines a homeostatic activation of the renin–angiotensin–aldosterone system, sympathetic nervous system, and antidiuretic hormone. The splanchnic microcirculation is resistant to the vasoconstrictor effect of these systems. Therefore, the homeostasis of arterial pressure in cirrhosis occurs in the extrasplanchnic, mainly renal circulation. The activation of these systems produces renal fluid retention, which accumulates as ascites, and water retention and dilutional hyponatraemia. In the latest phase of cirrhosis, when circulatory dysfunction is severe, renal vasoconstriction is intense and patients develop type 2 hepatorenal syndrome (HRS) and refractory ascites.Type 1 HRS is an acute and rapidly progressive renal failure that occurs in the setting of a precipitating event, commonly an infection. Patients with type 1 HRS also present with rapid deterioration of liver function (encephalopathy, jaundice) and relative adrenal insufficiency. The mechanism of this multiorgan failure is an acute deterioration in circulatory function due to both an accentuation of arterial vasodilation and of cardiac dysfunction.There is no specific test for the diagnosis of HRS. The most accepted diagnostic criteria are those proposed by the International Ascites Club which are based on the exclusion of other types of renal failure. The course of renal failure following treatment of the precipitating event of HRS is another important diagnostic feature.The treatment of choice of tense ascites in cirrhosis is paracentesis associated with intravenous albumin infusion. Moderate sodium restriction and diuretics (spironolactone alone or associated with furosemide) are subsequently given to prevent re-accumulation of ascites. Diuretics are the treatment of choice in patients with moderate ascites. Patients with type 2 HRS and refractory ascites (not responding to diuretics) could be treated by frequent paracentesis or by the insertion of a transjugular intrahepatic portosystemic shunt (TIPS).Terlipressin plus albumin is the treatment of choice in type 1 HRS


2012 ◽  
Vol 57 (4) ◽  
pp. 1110-1111
Author(s):  
Marco A. Olivera-Martínez ◽  
Marius C. Florescu

2016 ◽  
Vol 54 (3) ◽  
pp. 143-150 ◽  
Author(s):  
Aurelia Enescu ◽  
F. Petrescu ◽  
P. Mitruţ ◽  
Ileana Octavia Petrescu ◽  
V. Pădureanu ◽  
...  

Abstract Hepatorenal syndrome (HRS) is defined as renal failure that occurs in the presence of severe acute or chronic liver disease in the absence of underlying renal pathology. Due to the functional nature of the disease and the absence of specific diagnostic markers, HRS diagnosis is determined based on positive criteria associated with excluding other causes of renal failure in patients with liver cirrhosis and ascites. Differentiation from other types of acute or chronic renal disease is extremely difficult and therapeutic options are limited, prophylactic behavior is most appropriate in patients with severe hepatic disease and risk factors for the installation of hepatorenal syndrome. Highlighting all precipitating factors of acute renal insufficiency and therapeutic modalities in order to minimize adverse events is an important step in improving the follow-up of the patients with liver cirrhosis. The prognosis is reserved especially for type 1 HRS. Liver transplantation is the best option for patients without contraindications. The therapies introduced in recent years, such as vasoconstrictor drugs or transjugular intrahepatic portosystemic shunt are effective methods in the renal function improvement.


Author(s):  
Andrés Cárdenas ◽  
Pere Ginès

Hepatorenal syndrome (HRS) is a dreaded and common complication of patients with end-stage liver disease. The syndrome is characterized by functional renal failure due to renal vasoconstriction in the absence of underlying kidney pathology. The pathogenesis of HRS is the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodilation located in the splanchnic circulation. This phenomenon triggers a compensatory response with activation of vasoconstrictor systems leading to intense renal vasoconstriction.Besides HRS, there are several other causes of renal failure in patients with cirrhosis including those secondary to bacterial infections, hypovolaemia, nephrotoxicity, and intrinsic renal disease. Thus, the diagnosis of HRS is based on established diagnostic criteria aimed at excluding non-functional causes of renal failure.The prognosis of patients with HRS is poor, especially in those who have a rapidly progressive course. Liver transplantation is the best option in suitable candidates, but it is not always applicable due to the short survival expectancy of listed candidates.Pharmacological therapies based on the use of vasoconstrictor drugs to reverse splanchnic vasodilation are the standard first line of therapy. The vasopressin analogue terlipressin is the best proven. Transjugular intrahepatic portosystemic shunts may be helpful in limited circumstances. Prevention of HRS can be attained with the use of albumin infusion in patients with spontaneous bacterial peritonitis, with norfloxacin in patients very advanced liver disease and with N-acetylcysteine in those with severe acute alcoholic hepatitis.


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