Urinary neutrophil gelatinase-associated lipocalin as biomarker in the differential diagnosis of impairment of kidney function in cirrhosis

Fagundes, Cláudia; Pépin, Marie–Noëlle; Guevara, Mónica; Barreto, Rogelio; Casals, Gregori; Solà, Elsa; Pereira, Gustavo; Rodríguez, Ezequiel; García, Elisabet; Prado, Verónica; Poch, Esteban; Jiménez, Wladimiro; Fernández, Javier; Arroyo, Vicente; Ginès, Pere

doi:10.1016/j.jhep.2012.03.015

Cited by 192 publications

(183 citation statements)

References 42 publications

(62 reference statements)

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“…Furthermore, like HRS, the renal function does not respond to volume expansion in ATN. In this context, the usefulness of the new biomarkers of renal injury is not clearly established and further studies are needed, even if one study found that it could help to distinguish between ATN and other causes of AKI [27] . About the pathophysiology of ATN, ischemic ATN is secondary to extended and critical renal hypoperfusion, whether it is due to a brutal (acute bleeding, for example) or to a gradual further decrease of previously low RBF.…”

Section: Acute Tubular Necrosismentioning

confidence: 99%

Acute kidney injury in patients with chronic liver disease

Rognant¹

2015

WJH

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Acute kidney injury (AKI) is a frequent clinical event in patients with liver disease, compounding their prognosis. Furthermore, it is likely that the occurrence of AKI has a detrimental impact on the subsequent renal function and the long-term survival of these patients. Recently, some authors advocated the use of new diagnostic criteria for detecting acute kidney injury in patients with cirrhosis. These criteria are based on the rapidity and extent of the creatinine increase comparing to the basal creatinine and also on the kinetics of diuresis decrease. Although their validity in this population requires further studies to be clearly established, these new criteria could have two advantages: (1) to allow earlier diagnosis of AKI and, thus, hepatorenal syndrome for which earlier intervention could improve patients' survival; and (2) to promote more intensive monitoring of renal function in these patients with high risk of AKI. Finally, recent practice guidelines about the prevention and treatment of general AKI have been published which should be useful in optimising the management of AKI in cirrhotic patients.

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Section: Acute Tubular Necrosismentioning

confidence: 99%

Acute kidney injury in patients with chronic liver disease

Rognant¹

2015

WJH

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“…After initial promising reports of the superiority of NGAL to other acute kidney injury biomarkers including creatinine [51] more recent reports have failed to substantiate the earlier studies, especially when studies include patients with preexisting chronic kidney disease. NGAL has been evaluated in patients with cirrhosis [52] . Patients with kidney dysfunction irrespective of aetiology had greater serum NGAL levels compared to those without kidney dysfunction irrespective of the presence of ascites.…”

Section: Neutrophil Gelatinase Associated Lipocalinmentioning

confidence: 99%

Difficulties in diagnosing acute kidney injury post liver transplantation using serum creatinine based diagnostic criteria

Agarwal

Davenport

2014

WJH

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Renal function in patients with advanced cirrhosis is an important prognostic factor for survival both prior to and following liver transplantation. The importance of renal function is reflected by the introduction of the model for end stage liver disease (MELD) score, which includes serum creatinine. The MELD score has been shown to predict the short term risk of death for transplant wait listed patients and is currently used by many countries to allocate liver transplants on the basis of severity of underlying illness. Changes in serum creatinine are also used to stage acute kidney injury. However prior to liver transplantation the serum creatinine typically over estimates underlying renal function, particularly when a colorimetric Jaffe based assay is used, and paradoxically then under estimates renal function post liver transplantation, particularly when immunophyllins are started early as part of transplant immunosuppression. As acute kidney injury is defined by changes in serum creatinine, this potentially leads to over estimation of the incidence and severity of acute kidney injury in the immediate post-operative period. Key words: Serum creatinine; Acute kidney injury; Liver transplantationCore tip: Acute kidney injury is defined and severity graded based on changes in serum creatinine. Increasing concentrations of bilirubin interefere with laboratory determination of creatinine and reduce creatinine estimations. Post transplantation serum creatinine increases due to a combination of fall bilirubin and the loading doses of calcineurin inhibitor immunosupressants. This combination leads to an over estimation of the lesser grades of acute kidney injury post liver transplantation.Agarwal B, Davenport A. Difficulties in diagnosing acute kidney injury post liver transplantation using serum creatinine based diagnostic criteria. World J Hepatol 2014; 6(10): 696-703 Available from:

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“…Additionally, patients with prolonged Type I HRS may eventually develop acute tubular necrosis due to intense renal arteriole vasoconstrition. As a result of these limitations, several renal biomarkers are being studied to help decipher HRS from other causes of AKI in patients with cirrhosis; but further studies are required before they can be applied in clinical practice [10][11][12].…”

Section: Diagnosis Of Hrsmentioning

confidence: 99%

Hepatorenal Syndrome

Kiser¹

2014

IJCM

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Hepatorenal syndrome (HRS) is the most serious hepatorenal disorder and one of the most difficult to treat. To date, the best treatment options are those that reverse the mechanisms underlying HRS: portal hypertension, splanchnic vasodilation, and/or renal vasoconstriction. Therefore, liver transplantation is the preferred definitive treatment option. The role of other therapies is predominantly to prolong survival sufficiently to allow patients to undergo transplantation. Terlipressin with the addition of adjunctive albumin volume expansion is the preferred pharmacologic therapy for the treatment of patients with HRS. Norepinephrine and vasopressin are acceptable alternatives in countries where terlipressin is not yet available. For patients with Type II HRS, midodrine plus octreotide appears to be an effective pharmacologic regimen that can be administered outside of an intensive care unit setting. Regardless of chosen vasoconstrictor therapy, careful monitoring is needed to ensure tissue ischemia and severe adverse effects do not occur. Artificial hepatic support devices, renal replacement therapy, and transjugular intrahepatic portosystemic shunt (TIPS) are non-pharmacologic options for patients with HRS. However, hepatic support devices and renal replacement therapies have not yet demonstrated improved outcomes and TIPS is difficult to be employed in patients with Type I HRS due to contraindications in the majority of patients. Despite advances in our understanding of hepatorenal syndrome, the disease is still associated with significant morbidity, mortality, and costs. More evidence is urgently needed to help improve patient outcomes in this difficult-to-treat population.

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Urinary neutrophil gelatinase-associated lipocalin as biomarker in the differential diagnosis of impairment of kidney function in cirrhosis

Cited by 192 publications

References 42 publications

Acute kidney injury in patients with chronic liver disease

Acute kidney injury in patients with chronic liver disease

Difficulties in diagnosing acute kidney injury post liver transplantation using serum creatinine based diagnostic criteria

Hepatorenal Syndrome

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