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Figure 1 Hepatorenal syndrome: Pathogenesis. In cirrhotic patients portal hypertension can lead to markedly dilated splanchnic arterial vessels. The bacterial translocation of intestinal germs, the gradual decrease in systemic vascular resistances, the hepatic vascular neoformation are potential risk factors. The fall in mean arterial pressure is compensated by increase in cardiac output and by activation of renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS) to improve systemic vascular resistence. The response mechanisms to the decreased effective circulating volume caused by Enhanced vascular capacitance (so-called “arterial underfilling”) include the non-osmotic release of vasopressin accounting for renal tubular sodium resorption and water retention leading to the onset of ascites, edema and hypervolemic hyponatremia. These compensatory mechanisms ultimately have repercussions on kidney function causing reduced glomerular filtration rate (GFR) and further water retention thereby worsening the water overload.

Footnotes

Conflict-of-interest statement: The authors do not have any disclosures to report.

Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

Peer-review started: April 15, 2015

First decision: May 13, 2015

Article in press: September 18, 2015

P- Reviewer: Kelesidis T, Nechifor G, Trimarchi H, Trumper L, Yorioka N S- Editor: Tian YL L- Editor: A E- Editor: Wu HL


Table 1 Diagnostic criteria for hepatorenal syndrome

Cirrhosis with ascites

Serum Creatinine > 1.5 mg/dL

Absence of shock

No improvement of serum creatinine (decrease to a level of 1.5 mg/dL or less) after at least 2 d of diuretic withdraw and volume expansion with albumin (The recommended dose of albumin is 1 g/kg of body weight per day up to a maximum of 100 g/d)

No current o recent exposure to nephrotoxic drugs

Absence of parenchymal disease as indicated by proteinuria > 500 mg/d, microscopic hematuria (50 red blood cells per high power field) and abnormal renal ultrasonography

HRS: Hepatorenal syndrome.



Table 2 Characteristics of type I and type II hepatorenal syndrome

HRS I	Doubling of serum creatinine in < 2 wk	A precipitating event is present in the most of case	No history of diuretic resistant ascites	10% survival in 90 d without treatment
HRS II	Renal impairment gradually progressive	No precipitating events	Always ascites diuretic resistance	Median survival 6 mo

HRS: Hepatorenal syndrome.



Table 3 Risk factors for the onset of hepatorenal syndrome

Spontaneous bacterial peritonitis

Large volume paracentesis (> 5 L) with inadequate albumin substitution

NSAID and other nephrotoxic drugs, iv contrast

Bleeding from esophageal varices

Post TIPS syndrome

Diuretic treatment

Spontaneous bacterial peritonitis are leading trigger of HRS. One-third of patients with SBP develop HRS in the absence of septic shock. Diuretic treatment has been suggested as a potential trigger of HRS, but there are no clear supportive data for this. HRS: Hepatorenal syndrome; NSAID: Non-steroidal anti-inflammatory drug; TIPS: Transjugular intrahepatic portosystemic shunt.




Table 4 Differential diagnosis of renal failure in cirrhosis

Pre-renal	History of fluid loss, gastrointestinal bleeding, treatment with diuretics or non-steroidal anti-inflammatory drugs
Organic	Medical history, laboratory tests (cryoglobulinemia, complementemia, etc.)
Obstructive	Ultrasound imaging
Chronic kidney disease	Anemia, proteinuria, secondary hyperparathyroidism, ultrasound evidence of renal cortical thinning

Table 5 Prevention of hepatorenal syndrome and general patient management strategies

Avoid drugs that reduce renal perfusion or nephrotoxic substances

Minimize exposure to organ-iodated contrast agents

Intravenous albumin is recommended for volemic filling after large volume paracentesis (8 g of albumin for each liter of ascites removed)

Diuretic therapy should be suspended

Pentoxifylline as drug’s anti-TNFa activity

Antibiotic prophylaxis to prevent infections reducing intestinal bacterial translocation (norfloxacin 400 mg/d)

Intravenous albumin administered in association with ceftriaxone in SPB

Adrenal insufficiency should be identified and treated

Drug dosages must be adjusted according to renal function