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Review
. 2015 Sep 28;3(3):195-204.
doi: 10.14218/JCTH.2015.00015. Epub 2015 Sep 15.

Acute Kidney Injury in Patients with Cirrhosis

Kirk B Russ  1 , Todd M Stevens  2 , Ashwani K Singal  3
Affiliations
Review

Acute Kidney Injury in Patients with Cirrhosis

Kirk B Russ et al. J Clin Transl Hepatol. .

Abstract

Acute kidney injury (AKI) occurs commonly in patients with advanced cirrhosis and negatively impacts pre- and post-transplant outcomes. Physiologic changes that occur in patients with decompensated cirrhosis with ascites, place these patients at high risk of AKI. The most common causes of AKI in cirrhosis include prerenal injury, acute tubular necrosis (ATN), and the hepatorenal syndrome (HRS), accounting for more than 80% of AKI in this population. Distinguishing between these causes is particularly important for prognostication and treatment. Treatment of Type 1 HRS with vasoconstrictors and albumin improves short term survival and renal function in some patients while awaiting liver transplantation. Patients with HRS who fail to respond to medical therapy or those with severe renal failure of other etiology may require renal replacement therapy. Simultaneous liver kidney transplant (SLK) is needed in many of these patients to improve their post-transplant outcomes. However, the criteria to select patients who would benefit from SLK transplantation are based on consensus and lack strong evidence to support them. In this regard, novel serum and/or urinary biomarkers such as neutrophil gelatinase-associated lipocalin, interleukins-6 and 18, kidney injury molecule-1, fatty acid binding protein, and endothelin-1 are emerging with a potential for accurately differentiating common causes of AKI. Prospective studies are needed on the use of these biomarkers to predict accurately renal function recovery after liver transplantation alone in order to optimize personalized use of SLK.

Keywords: Acute kidney injury; Cirrhosis; Liver transplantation; SLK.

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Conflict of interest statement

Conflict of interest: None

Figures

Fig. 1.
Fig. 1.. The pathophysiology of renal dysfunction in decompensated cirrhosis.
See text for further discussion. SNS, sympathetic nervous system; RAAS, Renin-Angiotensin-Aldosterone System; ADH, antidiuretic hormone.
Fig. 2.
Fig. 2.. Management approach and algorithm for acute kidney injury in patients with cirrhosis.
ESLD, end-stage liver disease; AKI, acute kidney injury; USG, ultrasonogram; LVP, large volume paracentesis; HRS, hepatorenal syndrome; TIPS, transjugular intrahepatic portosystemic shunt; RRT, renal replacement therapy; LTA, liver transplant alone; SLK, simultaneous liver kidney.
Fig. 3.
Fig. 3.. Renal biopsy findings in hepatorenal syndrome.
Renal biopsy findings in hepatorenal syndrome often reveal acute tubular injury with no glomerular abnormalities, as shown here. Here we see findings of acute tubular injury consisting of thinning of proximal tubular epithelial cells with widening of tubular lumens (circled area). Note the two normal glomeruli (hematoxylin and eosin stain, 200×).
Fig. 4.
Fig. 4.. Renal biopsy findings in acute tubular necrosis.
In contrast, the histologic findings in acute tubular necrosis show necrotic and sloughed off tubule epithelial cells filling tubular lumens (arrow) (hematoxylin and eosin stain, 400×).
See this image and copyright information in PMC

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