Rifaximin Decreases the Incidence and Severity of Acute Kidney Injury and Hepatorenal Syndrome in Cirrhosis

Dong, Tien S.; Aronsohn, Andrew; Reddy, K. Gautham; Te, Helen S.

doi:10.1007/s10620-016-4313-0

Cited by 58 publications

(42 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…62 Long term use of Rifaximin (>3 months) was also shown to reduce the incidence of AKI including HRS-AKI. 63,64 Rifaximin exerts its clinical effects by modulation of the metabolic function of the gut microbiota.…”

Section: Specific Mechanisms Involved In Non-hrs-akimentioning

confidence: 99%

Acute kidney injury in acute-on-chronic liver failure: where does hepatorenal syndrome fit?

Davenport

Sheikh

Lamb

et al. 2017

Kidney International

100

View full text Add to dashboard Cite

Renal dysfunction occurs in 25% to 50% of patients with cirrhosis admitted to the hospital with an acute episode of hepatic decompensation and may be due to underlying chronic kidney disease, an acute deterioration, or both. An acute deterioration in renal function in cirrhotic patients is now collectively referred to as acute kidney injury (AKI), which has been subclassified into different grades of severity that identify prognostic groups. Acute-on-chronic liver failure is characterized by acute hepatic and/or extrahepatic organ failure driven by a dysregulated immune response and systemic inflammatory response. AKI is also one of the defining features of ACLF and a major component in grading the severity of acute-on-chronic liver failure. As such, the pattern of AKI now observed in patients admitted to the hospital with acutely decompensated liver disease is likely to be one of inflammatory kidney injury including acute tubular injury (referred in this review as non-hepatorenal syndrome [HRS]-AKI) rather than HRS. As the management and supportive treatment of non-HRS-AKI potentially differ from those of HRS, then from the nephrology perspective, it is important to distinguish between non-HRS-AKI and HRS-AKI when reviewing patients with acute-on-chronic liver failure and AKI, so that appropriate and early management can be instituted.

show abstract

Section: Specific Mechanisms Involved In Non-hrs-akimentioning

confidence: 99%

Acute kidney injury in acute-on-chronic liver failure: where does hepatorenal syndrome fit?

Davenport

Sheikh

Lamb

et al. 2017

Kidney International

100

View full text Add to dashboard Cite

show abstract

“… 3 , 74 It may increase portal vascular resistance through the cytokine-induced release of endothelin, NO and cyclooxygenase products in the liver. 77 – 79 In turn, portal hypertension can promote BT and endotoxemia in patients with liver cirrhosis. 74 Portal endotoxin level was decreased by the transjugular intrahepatic portosystemic shunt, suggesting that microbial translocation may be alleviated by the portal venous decompression.…”

Section: Gut Impact On Various Cirrhotic Complicationsmentioning

confidence: 99%

Gut Microbiome-based Therapeutics in Liver Cirrhosis: Basic Consideration for the Next Step

Fukui

2017

JCTH

View full text Add to dashboard Cite

Infections account for significant morbidity and mortality in liver cirrhosis and most are related to the gut microbiome. Fecal dysbiosis, characterized by an overgrowth of potentially pathogenic bacteria and a decrease in autochthonous non-pathogenic bacteria, becomes prominent with the progression of liver cirrhosis. In cirrhotic patients, disruption of the intestinal barrier causes intestinal hyperpermeability (i.e. leaky gut), which is closely related to gut dysmotility, dysbiosis and small intestinal bacterial overgrowth and may induce pathological bacterial translocation. Although the involved microbial taxa are somewhat different between the cirrhotic patients from the East and the West, the common manifestation of a shortage of bacteria that contribute to the production of short-chain fatty acids and secondary bile acids may facilitate intestinal inflammation, leaky gut and gut dysbiosis. Translocated endotoxin and bacterial DNA are capable of provoking potent inflammation and affecting the metabolic and hemodynamic systems, which may ultimately enhance the progression of liver cirrhosis and its various complications, such as hepatic encephalopathy (HE), variceal bleeding, infection and renal disturbances. Among studies on the microbiome-based therapeutics, findings of probiotic effects on HE have been contradictory in spite of several supportive results. However, the effects of synbiotics and prebiotics are substantially documented. The background of their effectiveness should be evaluated again in relation to the cirrhosis-related changes in gut microbiome and their metabolic effects. Strict indications for the antibiotic rifaximin remain unestablished, although its effect is promising, improving HE and other complications with little influence on microbial populations. The final goal of microbiome-based therapeutics is to adjust the gut-liver axis to the maximal benefit of cirrhotic patients, with the aid of evolving metagenomic and metabolomic analyses.

show abstract

“…51 Rifaximin also has been reported to reduce the incidence of AKI, including HRS AKI. 52 In a retrospective analysis of data from 4 cohorts of patients treated for HRS AKI, the ACLF grade was the major determinant of response to terlipressin and albumin, with reduced response with higher grades. In addition, patient survival was lower with increasing ACLF grade independently of the response to treatment.…”

Section: Pathophysiology Of Non-hrs Akimentioning

confidence: 99%

Epidemiology, Pathophysiology, and Management of Hepatorenal Syndrome

Amin

Alabsawy

Jalan

et al. 2019

Seminars in Nephrology

View full text Add to dashboard Cite

Acute kidney injury (AKI) is a common presentation in patients with advanced cirrhosis hospitalized with acute decompensation. A new revised classification now divides AKI in cirrhotic patients into two broad subgroups: hepatorenal syndrome AKI (HRS AKI) and non−hepatorenal syndrome AKI (non-HRS AKI). HRS AKI represents the end-stage complication of decompensated cirrhosis with severe portal hypertension and is characterized by worsening of renal function in the absence of prerenal azotemia, nephrotoxicity, and intrinsic renal disease. Non-HRS AKI may be caused by prerenal hypoperfusion, bile acid nephropathy, nephrotoxicity, or acute parenchymal insult. There have been several mechanisms proposed to explain the pathophysiology of HRS AKI and non-HRS AKI, and a number of biomarkers have been suggested to aid in differentiation between these types of AKI and to act as prognostic indicators. The standard of care clinical management for patients with HRS AKI is to exclude other etiologies of AKI, followed by volume expansion with human albumin solution and then the introduction of vasopressors. However, some 40% of patients treated for HRS AKI fail to respond. In this review, we discuss the current and recent data about classification, pathophysiology, and management of AKI in general, with specific insight about the treatment of HRS AKI.

show abstract

Rifaximin Decreases the Incidence and Severity of Acute Kidney Injury and Hepatorenal Syndrome in Cirrhosis

Abstract: Long-term use of rifaximin is associated with a decrease incidence of AKI and HRS and a decrease risk of requiring RRT in a general population of cirrhotic patients.

Cited by 58 publications

References 26 publications

Acute kidney injury in acute-on-chronic liver failure: where does hepatorenal syndrome fit?

Acute kidney injury in acute-on-chronic liver failure: where does hepatorenal syndrome fit?

Gut Microbiome-based Therapeutics in Liver Cirrhosis: Basic Consideration for the Next Step

Epidemiology, Pathophysiology, and Management of Hepatorenal Syndrome

Contact Info

Product

Resources

About