Acute kidney injury (AKI) is common in patients with cirrhosis.
It occurs in up to 50% of hospitalized patients with cirrhosis and a 58% of such patients in the ICU.
Acute kidney injury is associated with high morbidity and mortality and an increased incidence of chronic kidney disease after liver transplantation for cirrhosis.
The major causes of AKI are hypoperfusion, which, in most cases is due to hypovolemia, intrinsic structure of kidney injury, and postrenal injury due to urinary obstruction.
Cirrhosis can causes AKI by renal hypoperfusion, known as the hepatorenal syndrome, which is the result of renal vasoconstriction.
Hypoperfusion from hypovolemia accounts for approximately half of the cases of AKI in patients with cirrhosis, intrinsic causes, such as acute tubular necrosis account for approximately 30%, and hepatorenal syndrome accounts were approximately 15 to 20% with less than 1% of cases attributable to post renal obstruction.
Patients with cirrhosis, especially those with ascites, have increased susceptibility to AKI because of hemodynamic alterations from portal hypertension.
Portal hypertension increases, intrahepatic resistance due to distorted liver architecture with fibrosis and nodules, and then increases in intrahatic vascular tone.
Activation of vasodilators in the splanchnic circulation, most importantly, nitric oxide, leads to progressive splanchnic and systemic vasodilation.
Increased translocation of bacteria and bacterial products due to intestinal
dysbiosis, bacterial overgrowth, and altered proteins, also contribute to vasodilatation resulting in the reduction in effective arterial blood volume that activates neurohormonal systems: renin angiotensin-aldosterone, sympathetic and arginine vasopressin systems, leading to sodium and water retention and ascites formation.
In advanced stages of cirrhosis, progressive dilatation leads to more retention of sodium and water, resulting in refractory, ascites and dilutional hyponatremia.
With progressive vasodilatation construction systems with mainly renin and angiotensin are activated, resulting in renal vasoconstriction and decreased renal blood flow.
The reduced GFR results in prerenal kidney injury that does not respond to volume expansion.
Patients with cirrhosis who have ascites are at the highest risk for the development of AKI but also for the most severe clinical form hepatorenal syndrome (HRS-AKI).
Evaluation of kidney function, in patients with cirrhosis is challenging in that creatinine level overestimates the GFR in patients with cirrhosis due to decreased creatinine production from liver disease, protein calorie malnutrition, and muscle wasting.
Medications have a role in precipitating or worsening AKI-diuretics vasodilators, non-selective beta blockers, nonsteroidal anti-inflammatory drugs used in cirrrhosis.
Volume expansion is essential in reversing AKI due to volume depletion.
Pharmacological management of HRS-AKI is the use of vasoconstrictors combined with intravenous albumin.
Vasoconstrictors do not improve survival but their use is considered as a bridge to transplantation.
Terlipressin, a vasopressin analogue is the most common vasal constrictor used and is the first line agent for HRS-AKI.
Terlipressin is administered intravenously.
In patients with portal hypertension placement of transjugular intrahepatic portosystemic shunt (TIPS) may improve kidney function by distributing blood volume and reducing portal pressure, however, there is insufficient evidence to recommend TIPS for HRS-AKI.
Renal replacement therapy has been used as a bridge to liver transplantation, but its use for patients with HRS-AKi who are not candidates for liver transplantation is controversial because of the high mortality rate.
Liver transplantation is the treatment of choice in patient with HRS-AKI.
Simultaneous liver and kidney transplantation is a potential therapeutic option if patients have prolonged kidney dysfunction before liver transplantation.
Strategies for preventing acute kidney injury in patients with cirrhosis:include:
early diagnosis and treatment of bacterial infections, especially spontaneous bacterial peritonitis (SBP); use of albumin in addition to antibiotics for SBP; judicious use of diuretics and laxatives; albumin infusion during large-volume paracentesis; prompt management of gastrointestinal bleeding with antibiotics; avoidance of nephrotoxic drugs (such as NSAIDs, ACE inhibitors, ARBs, and radiographic contrast agents); and primary and secondary antibiotic prophylaxis against SBP in high-risk individuals, avoidance of alcohol and careful adjustment of lactulose to prevent diarrhea are also recommended.
Maintaining intravascular volume, and reducing inflammation, as both hemodynamic instability and infection are major contributors to AKI in cirrhosis.
Early recognition and prompt management of infections, gastrointestinal bleeding, and hypovolemia—are essential to reduce AKI incidence and improve outcomes.
Avoidance of nephrotoxic agents—including NSAIDs, ACE inhibitors, ARBs, and radiographic contras is critical, as these drugs can exacerbate renal hypoperfusion and injury.
Judicious use of diuretics and lactulose, with close monitoring of volume status and renal function, further reduces risk.
Large-volume paracentesis should always be accompanied by albumin infusion (4–6 g per liter of ascites removed) to prevent circulatory dysfunction and AKI.
The role of long-term albumin infusions remains controversial, with no clear benefit outside of specific indications such as spontaneous bacterial peritonitis (SBP).