The Hepatorenal Syndrome

1997 ◽  
Vol 92 (5) ◽  
pp. 433-443 ◽  
Author(s):  
Kevin Moore
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Liver Disease ◽  
Renal Blood Flow ◽  
Hepatorenal Syndrome ◽  
Venous Pressure ◽  
Renal Perfusion ◽  
Filtration Fraction ◽  
Renal Vasoconstriction ◽  
Vasoactive Mediators

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.

The patient with hepatorenal syndrome

2018 ◽  
Author(s):  
Andrés Cárdenas ◽  
Pere Ginès
Keyword(s):  
Renal Failure ◽  
Liver Disease ◽  
Bacterial Infections ◽  
Hepatorenal Syndrome ◽  
Compensatory Response ◽  
Renal Vasoconstriction ◽  
Bacterial Peritonitis ◽  
Portosystemic Shunts ◽  
Line Of Therapy ◽  
End Stage

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.

scholarly journals Hepatorenal syndrome: an update

2007 ◽  
Vol 125 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Tércio Genzini ◽  
Fábio César Miranda Torricelli
Keyword(s):  
Liver Transplantation ◽  
Renal Failure ◽  
Hepatorenal Syndrome ◽  
Laboratory Data ◽  
Renal Perfusion ◽  
Definitive Treatment ◽  
First Year ◽  
Vasoactive Mediators ◽  
Function Recovery ◽  
Cirrhotic Patients

Hepatorenal syndrome (HRS) is the development of renal failure in patients with chronic previous liver disease, without clinical or laboratory evidence of previous kidney disease. It affects up to 18% of cirrhotic patients with ascites during the first year of follow-up, reaching 39% in five years and presenting a survival of about two weeks after its establishment. HRS diagnosis is based on clinical and laboratory data. The occurrence of this syndrome is related to the mechanism for ascites development, involving vasoconstriction, low renal perfusion, water and sodium retention, increased plasma volume, and consequent overflow at the splanchnic level. Renal vasoactive mediators like endothelin 1, thromboxane A2, and leukotrienes are also involved in the genesis of this syndrome, which culminates in functional renal insufficiency. The treatment of choice can be pharmacological or surgical, although liver transplantation is the only permanent and effective treatment, with a four-year survival rate of up to 60%. Liver function recovery is usually followed by renal failure reversion. Early diagnosis and timely therapeutics can increase life expectancy for these patients while they are waiting for liver transplantation as a definitive treatment.

Sympathetic nervous system in the loss of autoregulation in acute renal failure

1984 ◽  
Vol 246 (4) ◽  
pp. F379-F386 ◽  
Author(s):  
S. P. Kelleher ◽  
J. B. Robinette ◽  
J. D. Conger
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Nervous System ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Renal Denervation ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Renal Blood Flow Autoregulation

The responsiveness of the renal vascular system was investigated in uninephrectomized Sprague-Dawley rats in which acute renal failure had been induced by norepinephrine. The animals were studied at 1' and 3 wk after norepinephrine infusion. Uninephrectomized littermates served as controls. Compared with controls, there was an absence of renal blood flow autoregulation in 1-wk acute renal failure that returned in part by 3 wk. In 1-wk rats there was a marked increase, rather than decrease, in renovascular resistance as renal perfusion pressure was decreased. The renal vasculature was significantly less responsive in 1-wk rats than in control or 3-wk animals when acetylcholine, angiotensin II, or norepinephrine was infused into the renal artery at minimal vasoactive doses (all P less than 0.01). Paradoxically, renal vasoconstriction in response to renal nerve stimulation was greater in 1-wk than in 3-wk and control rats (P less than 0.01) and was not inhibited by renal artery infusion of phenoxybenzamine. Renal denervation significantly improved renal blood flow autoregulation in 1-wk animals (P less than 0.001) and completely abolished the increase in renovascular resistance as renal perfusion pressure was lowered. No effects of renal denervation on renal blood flow autoregulation were seen in control and 3-wk rats. It is concluded that renovascular responses to neurohumoral stimuli are aberrant in acute renal failure. The loss of renal blood flow autoregulation is related to an increased renovascular resistance that is due to increased activity of non-alpha-adrenergic mechanisms of the autonomic nervous system.

scholarly journals Dissociation of glomerular filtration and renal blood flow in HgCl2-induced acute renal failure

1982 ◽  
Vol 22 (2) ◽  
pp. 162-170 ◽  
Author(s):  
Raymond C. Vanholder ◽  
Marleen M. Praet ◽  
Piet A. Pattyn ◽  
Isidoor R. Leusen ◽  
Norbert H. Lameire
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Glomerular Filtration ◽  
Renal Blood Flow

scholarly journals Hepatorenal Syndrome: Physiology, Diagnosis and Management

2018 ◽  
Vol 35 (03) ◽  
pp. 194-197 ◽  
Author(s):  
Joseph Chmielewski ◽  
Robert Lewandowski ◽  
Haripriya Maddur
Keyword(s):  
Liver Disease ◽  
Hepatorenal Syndrome ◽  
Hepatic Dysfunction ◽  
Underlying Liver Disease ◽  
Free Survival ◽  
Renal Vasoconstriction ◽  
End Stage Liver Disease ◽  
Widespread Implementation ◽  
Intrahepatic Portosystemic Shunt ◽  
End Stage

AbstractIndividuals with end-stage liver disease are susceptible to a myriad of highly morbid complications, including hepatorenal syndrome (HRS). This specific type of renal dysfunction in patients with underlying liver disease occurs in pathophysiologically normal kidneys and is a result of renal vasoconstriction secondary to diminished renal blood flow in the setting of worsening hepatic dysfunction. Liver transplantation is curative; shortage of available organs limits access to this beneficial therapy. Medical management of HRS has demonstrated increasing promise. Transjugular intrahepatic portosystemic shunt creation has also been shown to be efficacious in enhancing transplant-free survival, although further study is advisable before widespread implementation of this strategy.

Autoregulation of renal blood flow in the puppy

1975 ◽  
Vol 229 (4) ◽  
pp. 983-988 ◽  
Author(s):  
PA Jose ◽  
LM Slotkoff ◽  
S Montgomery ◽  
PL Calcagno ◽  
G Eisner
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Electromagnetic Flowmeter ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Angiotensin System ◽  
Group Of Seven ◽  
Selective Blockade

The ability of the immature kidney to autoregulate blood flow was investigated. Renal blood flow was measured by electromagnetic flowmeter. In six puppies, selective blockade of the intrarenal effects of angiotensin II (AII) by [1-sarcosine, 8-alanine]angiotensin II (anti-AII) administered into the renal artery did not change renal blood flow. During selective renal AII blockade, intravenous AII raised perfusion pressure from 76 +/- 2 to 100 +/- 6 mmHg. Renal blood flow increased from 1.59 +/- 0.29 to 1.98 +/- 0.59 ml/g kidney per min, but returned to control levels within 40 s in spite of persistent arterial pressure elevation. In another group of seven puppies, renal blood flow remained constant despite reduction of renal perfusion pressure by aortic constriction to 60 mmHg. In two of these seven puppies intrarenal anti-AII did not abolish autoregulation. Autoregulation of renal blood flow occurs in the puppy and is not influenced by inhibition of angiotensin. The renin-angiotensin system does not appear to be involved in the normal regulation of renal blood flow in the puppy.

Mechanism of intrarenal blood flow redistribution after carotid artery occlusion

1977 ◽  
Vol 232 (2) ◽  
pp. F167-F172 ◽  
Author(s):  
E. H. Prosnitz ◽  
E. J. Zambraski ◽  
G. F. DiBona
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Outer Cortex ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Perfusion Pressure

Bilateral carotid artery occlusion results in an increase in mean arterial pressure, an increase in renal sympathetic nerve activity, and a redistribution of renal blood flow from inner to outer cortex. To elucidate the mechanism of the renal blood flow redistribution, carotid artery occlusion was performed in anesthetized dogs with the left kidney either having renal perfusion pressure maintained constant (aortic constriction) or having alpha-adrenergic receptor blockade (phenoxybenzamine); the right kidney of the same dog served to document the normal response. When renal perfusion pressure was maintained constant, renal blood flow distribution (microspheres) was unchanged by carotid artery occlusion. In the presence of renal alpha-adrenergic receptor blockade, carotid artery occlusion elicited the usual redistribution of renal blood flow from inner to outer cortex. The redistribution of renal blood flow observed after carotid artery occlusion is mediated by the increase in renal perfusion pressure rather than the increase in renal sympathetic nerve activity.

scholarly journals Renal hemodynamics and oxygenation during experimental cardiopulmonary bypass in sheep under total intravenous anesthesia

2020 ◽  
Vol 318 (2) ◽  
pp. R206-R213 ◽  
Author(s):  
Roger G. Evans ◽  
Naoya Iguchi ◽  
Andrew D. Cochrane ◽  
Bruno Marino ◽  
Sally G. Hood ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Renal Blood Flow ◽  
Kidney Injury ◽  
Conscious State ◽  
Renal Perfusion ◽  
Total Intravenous Anesthesia ◽  
Intravenous Anesthesia ◽  
Isoflurane Anesthesia ◽  
Conscious Sheep

Renal medullary hypoxia may contribute to the pathophysiology of acute kidney injury, including that associated with cardiac surgery requiring cardiopulmonary bypass (CPB). When performed under volatile (isoflurane) anesthesia in sheep, CPB causes renal medullary hypoxia. There is evidence that total intravenous anesthesia (TIVA) may preserve renal perfusion and renal oxygen delivery better than volatile anesthesia. Therefore, we assessed the effects of CPB on renal perfusion and oxygenation in sheep under propofol/fentanyl-based TIVA. Sheep ( n = 5) were chronically instrumented for measurement of whole renal blood flow and cortical and medullary perfusion and oxygenation. Five days later, these variables were monitored under TIVA using propofol and fentanyl and then on CPB at a pump flow of 80 mL·kg−1·min−1 and target mean arterial pressure of 70 mmHg. Under anesthesia, before CPB, renal blood flow was preserved under TIVA (mean difference ± SD from conscious state: −16 ± 14%). However, during CPB renal blood flow was reduced (−55 ± 13%) and renal medullary tissue became hypoxic (−20 ± 13 mmHg versus conscious sheep). We conclude that renal perfusion and medullary oxygenation are well preserved during TIVA before CPB. However, CPB under TIVA leads to renal medullary hypoxia, of a similar magnitude to that we observed previously under volatile (isoflurane) anesthesia. Thus use of propofol/fentanyl-based TIVA may not be a useful strategy to avoid renal medullary hypoxia during CPB.

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