Renal Failure In Cirrhosis Research Articles

Impact of alcohol abstinence on survival after hepatic resection for hepatocellular carcinoma in patients with alcohol-related liver disease

BackgroundThis study aimed to evaluate the prognostic impact of alcohol abstinence on survival after hepatic resection for hepatocellular carcinoma (HCC) in patients with alcohol-related liver disease (ALD). Patients and methodsIn total, 92 patients with ALD-HCC who underwent initial and curative hepatic resection were identified, including 56 and 36 patients with and without alcohol abstinence, respectively. ResultsThe 3-, 5-, and 7-year recurrence-free survival (RFS) were 46%, 43%, and 37% in the abstinence group, and 61%, 36%, and 36% in the non-abstinence group, respectively (p = 0.71). The 3-, 5-, and 7-year overall survival (OS) were 91%, 76%, and 66% in the abstinence group, and 87%, 57%, and 44% in the non-abstinence group, respectively (p = 0.023). Multivariate analysis revealed that non-abstinence was an independent prognostic factor for OS (P = 0.026). The incidence rate of liver-related death including HCC-specific death, liver failure, and renal failure in cirrhosis (hepatorenal syndrome) between the non-abstinence and abstinence groups were 41.7% vs. 19.6% (p = 0.032). Worsening of the Child–Pugh grade at intrahepatic recurrence was more frequently observed in the non-abstinence (33.3%) than that in the abstinence group (6.5%) (p = 0.039). ConclusionsAlcohol abstinence might improve the long-term survival of patients with ALD-HCC undergoing hepatic resection.

Renal failure in cirrhosis: Emerging concepts.

Acute renal failure, now termed acute kidney injury (AKI), is frequently found in patients with cirrhosis. The occurrence of AKI, irrespective of the underlying cause, is associated with reduced in-hospital, 3-mo and 1-year survival. Hepatorenal syndrome is associated with the worst outcome among AKI patients with cirrhosis. Several definitions for AKI that have been proposed are outlined and evaluated in this paper. Among these, the International Club for Ascites-AKI criteria substantially strengthen the quality of early diagnosis and intervention according to underlying cause of AKI.

Evaluating Acute Renal Failure in Cirrhosis Based on a Point-of-Care Echocardiography Approach

Evaluating Acute Renal Failure in Cirrhosis Based on a Point-of-Care Echocardiography Approach

Insuffisance rénale aigüe chez le patient cirrhotique : particularités diagnostiques et thérapeutiques

BackgroundPatients with cirrhosis are candidates to develop acute renal injury because of their progressive vasodilatory state. It is a common complication, however, exact incidence is unknown. Acute renal injury consistently portends worse survival. Therefore, identifying and treating the cause of renal dysfunction in cirrhosis is essential.AimTo review new advances in the knowledge of diagnosis and treatment of acute renal failure in cirrhosis. Possible causes and prevalence are also studied.MethodsSystematic review of the literature using medical data bases (Medline) with the following key words: acute renal injury, cirrhosis, hepatorenal syndrome, diagnosis, treatment.ResultsWe identified a specific definition of acute renal injury in cirrhosis, estimated its prevalence and main causes. We propose a diagnostic and therapeutic approach to the patient with cirrhosis and acute renal failure.ConclusionAcute renal injury occurs in approximately 20% of patients with cirrhosis. It is mainly due to prerenal failure and acute tubular necrosis. Except for type 1 hepatorenal syndrome, little attention has been paid to diagnosis and treatment of acute renal injury in cirrhosis. Prevention and early specific therapy depending on the most likely mechanism can improve prognosis.

Pathophysiology, Diagnosis and Clinical Management of Hepatorenal Syndrome: From Classic to New Drugs

Advanced cirrhosis is frequently associated with renal dysfunction. Hepatorenal syndrome (HRS) is characterized by the occurrence of kidney injury in cirrhotic patients in the absence of other identifiable causes. HRS is classified in 2 different types. Type 1 is characterized by acute renal failure and rapid functional deterioration of other organs, usually related to a precipitating event. Type 2 is characterized by slowly progressive renal failure and refractory ascites. Advanced liver disease induces the progression of hemodynamic alterations such as arterial vasodilation of splanchnic circulation and impairment of cardiac function. The resulting ineffective circulating blood volume promotes the activation of both the renin-angiotensin-aldosterone and sympathetic nervous system, by an increase of antidiuretic hormone activity, in an attempt to restore volemia. Despite fluid retention, ascites and dilutional hyponatremia, renal function is often initially preserved by renal production of vasodilators. However, further insults can lead to an imbalance between systemic vasoconstriction and local renal vasodilation, resulting in progressive renal failure. Over the last decade, clinical strategies to prevent HRS have been improved by a better understanding of the natural history of renal failure in cirrhosis, resulting in a reduction of HRS prevalence in cirrhotic patients. Vasoconstrictor drugs may improve renal function, but the effect on mortality has not yet been established. Vaptans, nonpeptide vasopressin receptor antagonists, may also reduce hyponatraemia and ascites, even if the clinical effects in HRS remain unknown. This review updates the pathophysiology, diagnosis and management of HRS.

Diagnostic approach to renal failure in cirrhosis.

Renal failure in patients with cirrhosis was initially described as renal dysfunction characterized by progressive azotemia associated with marked abnormalities of the systemic arterial circulation and normal renal histology; this condition later came to be known as hepatorenal syndrome (HRS). 1–3 We now know that such patients with cirrhosis can develop renal failure for a variety of reasons besides HRS, including bacterial infections, shock, the use of nonsteroidal anti-inflammatory drugs (NSAIDs), and intrinsic renal diseases. The initial management of patients with a rising serum creatinine level (SCr) depends on the cause. Therefore, the most important step in treating renal failure in a patient with cirrhosis is to identify its etiology. The aim of this article is to summarize the current approach to renal failure in patients with cirrhosis.

Results of pretransplant treatment of hepatorenal syndrome with terlipressin

Hepatorenal syndrome (HRS) is a dreaded complication of end-stage liver disease. The best treatment option for HRS is liver transplantation (LT) in suitable candidates. Pretransplant care of HRS is of utmost importance in order to secure a good posttransplant outcome. We review the advances during the last year in the diagnosis and management of HRS in candidates who are awaiting liver transplantation. New attempts at defining renal failure in cirrhosis using the Acute Kidney Injury (AKI) definition have been proposed, as this definition has the potential advantage of detecting earlier phases of kidney dysfunction. Patients who undergo liver transplantation with acute tubular necrosis recover renal function more slowly than those with HRS and have a higher incidence of chronic kidney disease at all time points after liver transplantation. Vasoconstrictor drugs, particularly terlipressin, are effective for the management of HRS; however, noradrenaline is a good choice if terlipressin is not available. Long-term treatment of HRS with vasoconstrictors until liver transplantation in those patients with HRS recurrence after the first treatment is beneficial as a bridge to liver transplantation. Data from the cohorts of patients treated with vasoconstrictors (terlipressin and midodrine) indicate that liver transplantation offers a clear survival benefit to patients with HRS regardless of prior therapy with these drugs. Ongoing advances in the management of patients with HRS before liver transplantation indicate that vasoconstrictors plus albumin should be offered to all suitable candidates. Liver transplantation remains the best treatment option for HRS.

Renal failure in cirrhosis: prerenal azotemia, hepatorenal syndrome and acute tubular necrosis

Renal failure in cirrhosis: prerenal azotemia, hepatorenal syndrome and acute tubular necrosis

A new look at renal dysfunction in the cirrhotic patient

Hepatorenal syndrome (HRS) is a pre-renal azotemia-like acute renal failure occurring in patients with end-stage cirrhosis. HRS results from arteriolar vasodilatation, arteriolar underfilling, and intense renal vasoconstriction. By definition, it is not responsive to volume expansion, and the prognosis is especially poor even with the use of terlipressin or albumin dialysis or both. It may be difficult, on the basis of the current criteria, to clearly differentiate HRS from other causes of acute renal failure in cirrhosis. In addition, patients with HRS frequently have underlying chronic kidney changes that may not be reversible after transplantation. In the previous issue of Critical Care, a group of experts proposed a new classification of acute, acute-on-chronic, or chronic renal impairment in cirrhosis on the basis of the RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria. The group proposed the term 'hepatorenal disorder' to define patients with advanced cirrhosis and kidney dysfunction at an earlier stage, regardless of the mechanisms. As stated by the authors, more data are needed to clearly identify, by non-invasive means, those with a potential for improvement with liver transplantation and those who can undergo a combined liver and kidney transplantation.

Prevention of acute kidney injury in a rodent model of cirrhosis following selective gut decontamination is associated with reduced renal TLR4 expression

Superimposed infection and/or inflammation precipitate renal failure in cirrhosis. This study aimed at testing the hypothesis that increased gut bacterial translocation in cirrhosis primes the kidney to the effect of superimposed inflammation by upregulating expression of Toll-like receptor 4 (TLR4), NFκB, and cytokines. A well-characterized bile-duct ligated (BDL) model of cirrhosis, which develops renal failure following superimposed inflammatory insult with lipopolysaccharide (LPS), was used and selective gut decontamination was performed using norfloxacin. Sprague-Dawley rats were studied: Sham, Sham+LPS; BDL, BDL+LPS; an additional BDL and BDL+LPS groups were selectively decontaminated with norfloxacin. Plasma biochemistry, plasma renin activity (PRA) and cytokines and, protein expression of TLR4, NFκB, and cytokines were measured in the kidney homogenate. The kidneys were stained for TLR4, TLR2, and caspase-3. Endotoxemia was measured using neutrophil burst and Limulus amoebocyte lysate (LAL) assays. The groups treated with norfloxacin showed significant attenuation of the increase in plasma creatinine, plasma and renal TNF-α and renal tubular injury on histology. The increased renal protein expression of TLR4, NFκB, and caspase-3 in the untreated animals was significantly attenuated in the norfloxacin treated animals. PRA was reduced in the treated animals and severity of endotoxemia was also reduced. The results show for the first time that kidneys in cirrhosis show an increased expression of TLR4, NFκB, and the pro-inflammatory cytokine TNF-α, which makes them susceptible to a further inflammatory insult. This increased susceptibility to LPS can be prevented with selective decontamination, providing novel insights into the pathophysiology of renal failure in cirrhosis.

Renal failure in chronic liver disease and the hepatorenal syndrome

Hepatorenal syndrome is a distinctive complication of cirrhosis. Advances in understanding its pathogenesis have lead to new treatments with improved outcomes. This article focuses on evidence-based management of renal failure in cirrhosis including hepatorenal syndrome, in the context of pathophysiological changes that occur.

Hepatorenal syndrome

Introduction: Renal failure in cirrhosis is a common complication that is associated with poor survival. A rapid diagnosis of the cause of renal failure is mandatory because it is associated with prognosis.Areas covered: This review covers the differential diagnosis between hepatorenal syndrome (HRS) and other causes of renal failure, as well as the difficulty in making a correct diagnosis, caused by the differentiation between hepatorenal syndrome and acute tubular necrosis. This review also discusses the multifactorial mechanisms involved in the pathogenesis of HRS. The paper provides diagnostic algorithms to use in clinical practice, emphasized by the fact that some patients may have HRS superimposed on pre-existent renal failure.Expert opinion: The correct diagnosis of renal failure is essential to initiate the correct treatment of this complication. In patients with HRS type 1, treatment with vasopressin and albumin is the treatment of choice; however, 50% of patients do not respond to this treatment.

Acute-on-chronic liver failure: the kidneys

Acute-on-chronic liver failure (ACLF) is defined as an abrupt deterioration of liver function in patients with established liver disease. Kidney function is almost universally altered in patients with ACLF due to underlying circulatory abnormalities. We review current advances during the past year in the diagnosis and management of renal failure in ACLF. The adequate measurement of renal function by means of clearance methods remains the gold standard for estimation of the glomerular filtration rate in patients with cirrhosis. The new definition of acute kidney injury needs to be specifically studied in patients with cirrhosis. Alternative kidney biomarkers of renal function in cirrhosis are promising and need further investigation. The most common cause of renal failure in cirrhosis is that associated with infections followed by hypovolemia-induced renal failure, intrinsic renal diseases, hepatorenal syndrome, and drug-induced renal failure. Adrenal insufficiency commonly occurs in patients with cirrhosis and hemodynamic instability. The proper diagnosis relies on corticotropin stimulation testing and the role of hydrocortisone therapy in these patients merits further investigation. Hyponatremia in cirrhosis is a major risk factor for the development of hepatic encephalopathy and is associated with a poor outcome in patients with ACLF and also after deceased donor and living-related liver transplantation. Vasoconstrictor drugs, particularly terlipressin, are effective for the management of hepatorenal syndrome. Predictive factors of response to terlipressin include serum bilirubin levels and the presence of an early increase in mean arterial pressure. The ongoing advances in the diagnosis and management of patients with ACLF and renal failure will improve the diagnosis, therapy and outcome of these patients.

Prognostic Importance of the Cause of Renal Failure in Patients With Cirrhosis

The prognostic value of the different causes of renal failure in cirrhosis is not well established. This study investigated the predictive value of the cause of renal failure in cirrhosis. Five hundred sixty-two consecutive patients with cirrhosis and renal failure (as defined by serum creatinine > 1.5 mg/dL on 2 successive determinations within 48 hours) hospitalized over a 6-year period in a single institution were included in a prospective study. The cause of renal failure was classified into 4 groups: renal failure associated with bacterial infections, renal failure associated with volume depletion, hepatorenal syndrome (HRS), and parenchymal nephropathy. The primary end point was survival at 3 months. Four hundred sixty-three patients (82.4%) had renal failure that could be classified in 1 of 4 groups. The most frequent was renal failure associated with infections (213 cases; 46%), followed by hypovolemia-associated renal failure (149; 32%), HRS (60; 13%), and parenchymal nephropathy (41; 9%). The remaining patients had a combination of causes or miscellaneous conditions. Prognosis was markedly different according to cause of renal failure, 3-month probability of survival being 73% for parenchymal nephropathy, 46% for hypovolemia-associated renal failure, 31% for renal failure associated with infections, and 15% for HRS (P < .0005). In a multivariate analysis adjusted for potentially confounding variables, cause of renal failure was independently associated with prognosis, together with MELD score, serum sodium, and hepatic encephalopathy at time of diagnosis of renal failure. A simple classification of patients with cirrhosis according to cause of renal failure is useful in assessment of prognosis and may help in decision making in liver transplantation.

Renal Failure in Cirrhosis

Renal failure, a challenging complication of cirrhosis, is one of the most important risk factors for liver transplantation. In recent years, substantial progress has been made toward understanding the pathogenesis and natural history of renal failure in cirrhosis. This review discusses recently identified information about renal failure in cirrhosis and clinical interventions that may assist in the prevention and management of this complication.

Study of relationship between upper gastrointestinal bleeding and hepato renal failure in cirrhosis

Study of relationship between upper gastrointestinal bleeding and hepato renal failure in cirrhosis

Renal failure in liver disease.

Progressive renal failure in cirrhosis and fulminant liver disease remains an adverse prognostic factor. Irrespective of the type of renal functional impairment which ranges form "prerenal failure" to "hepatorenal syndrome" and "acute tubular necrosis", renal hypoperfusion, as a consequence of either reduced perfusion pressure or increased renal vascular resistance, is an important pathomechanism. Awareness of the risk of renal failure and avoidance of nephrotoxic agents and of brisk reductions in effective circulating volume are important for prevention. Plasma volume expansion, on the other hand, is mandatory in trying to reverse incipient renal functional impairment. Pharmacological attempts to improve renal hemodynamics by lowering renal and increasing extrarenal vascular resistance have so far largely been disappointing. However, increasing knowledge about mediators and synthesis of specific agonists and antagonists, such as those against endothelin or antidiuretic hormone, may add promising treatment options in the near future. TIPS is another therapeutic tool of potential interest in the management of renal failure in liver disease which needs further evaluation. Renal replacement therapy, preferentially in the form of continuous procedures, may be life-saving in those patients awaiting liver transplantation or spontaneous recovery of their hepatic function.

Management of Ascites and Renal Failure in Cirrhosis

Management of Ascites and Renal Failure in Cirrhosis

Dipyridamole induces renal failure in cirrhosis with ascites

Dipyridamole induces renal failure in cirrhosis with ascites

Treatment of ascites and renal failure in cirrhosis

Ascites is a frequent complication in patients with liver cirrhosis. The accumulation of fluid in the abdominal cavity is associated with disturbances of systemic and splanchnic haemodynamics and of kidney function, which contribute to the poor prognosis of these patients. Classically, the treatment of ascites in patients with cirrhosis has been based on the combination of a sodium-restricted diet and the administration of diuretics. However, this treatment is not entirely satisfactory, since it is associated with a relatively high incidence of side-effects, and about 20% of patients hospitalized for the treatment of an episode of ascites do not respond to such therapy. In the last two decades, alternative therapies to diuretics have been introduced. PVS is an effective method of treating ascites. The high incidence of complications observed in early studies may be reduced by adequate perioperative management and careful selection of patients. The role of the PVS in the treatment of cirrhotics with ascites, however, still remains to be established. Recently, paracentesis has emerged as an alternative method of treating ascites in patients with cirrhosis. Several studies have shown that therapeutic paracentesis plus i.v. albumin infusion is more effective than conventional diuretic therapy and is associated with a lower incidence of complications. It has also been demonstrated that therapeutic paracentesis without the i.v. administration of albumin is associated with a marked increase in plasma renin activity, suggesting an impairment of effective blood volume, and with the development of hyponatraemia and/or renal failure in 20% of cases. Therefore, the i.v. administration of albumin is an essential measure in preventing the impairment of systemic haemodynamics and renal function that frequently follows the mobilization of ascites by paracentesis.