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Acute Kidney Injury in Patients with Cirrhosis.

Russ KB, Stevens TM, Singal AK - J Clin Transl Hepatol (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, UAB, Birmingham, AL, USA.

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.

No MeSH data available.


Related in: MedlinePlus

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×).
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f03: 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×).

Mentions: The first step after AKI is diagnosed is volume expansion (with crystalloids or intravenous albumin) and discontinuation of precipitating medications (such as diuretics, lactulose, and NSAIDs). If renal function does not normalize or improve with this intervention, HRS is an important differential diagnosis to consider as the cause for AKI.3,26 HRS is a functional form of renal failure without any major structural or histological changes in the kidneys that is characterized by intense renal vasoconstriction (Fig. 3 and Fig. 4).31 Since HRS has been recognized, there remains an unmet need for an accurate biomarker for diagnosis of HRS. It is important to differentiate HRS from intrarenal causes such as ATN, because management and prognosis differ. In the absence of renal biopsy, the diagnosis of HRS remains difficult and is essentially a diagnosis of exclusion (Table 2).14,31 Due to concurrent coagulopathy and thrombocytopenia in advanced cirrhosis, renal biopsy carries a high risk of internal bleeding and is rarely performed. In one study on 55 patients with cirrhosis undergoing transjugular renal biopsy, eight patients developed internal bleeding, and four had perinephric hematoma.32 In another study on 44 patients undergoing percutaneous renal biopsy, bleeding complications occurred in about one-third of the patients.33 In another study of 20 patients (five transjugular and 15 percutaneous biopsies), bleeding complication occurred in two patients.34 In our prospective study on 278 patients with cirrhosis listed for liver transplantation, none of the 109 patients who developed AKI underwent renal biopsy for evaluation of AKI.15


Acute Kidney Injury in Patients with Cirrhosis.

Russ KB, Stevens TM, Singal AK - J Clin Transl Hepatol (2015)

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×).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4663201&req=5

f03: 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×).
Mentions: The first step after AKI is diagnosed is volume expansion (with crystalloids or intravenous albumin) and discontinuation of precipitating medications (such as diuretics, lactulose, and NSAIDs). If renal function does not normalize or improve with this intervention, HRS is an important differential diagnosis to consider as the cause for AKI.3,26 HRS is a functional form of renal failure without any major structural or histological changes in the kidneys that is characterized by intense renal vasoconstriction (Fig. 3 and Fig. 4).31 Since HRS has been recognized, there remains an unmet need for an accurate biomarker for diagnosis of HRS. It is important to differentiate HRS from intrarenal causes such as ATN, because management and prognosis differ. In the absence of renal biopsy, the diagnosis of HRS remains difficult and is essentially a diagnosis of exclusion (Table 2).14,31 Due to concurrent coagulopathy and thrombocytopenia in advanced cirrhosis, renal biopsy carries a high risk of internal bleeding and is rarely performed. In one study on 55 patients with cirrhosis undergoing transjugular renal biopsy, eight patients developed internal bleeding, and four had perinephric hematoma.32 In another study on 44 patients undergoing percutaneous renal biopsy, bleeding complications occurred in about one-third of the patients.33 In another study of 20 patients (five transjugular and 15 percutaneous biopsies), bleeding complication occurred in two patients.34 In our prospective study on 278 patients with cirrhosis listed for liver transplantation, none of the 109 patients who developed AKI underwent renal biopsy for evaluation of AKI.15

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, UAB, Birmingham, AL, USA.

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.

No MeSH data available.


Related in: MedlinePlus