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Urinary Biomarkers of Acute Kidney Injury in Patients with Liver Cirrhosis

DOI: 10.1155/2014/376795

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Abstract:

Acute kidney injury (AKI) is a common complication in cirrhotic patients. Serum creatinine is a poor biomarker for detection of renal impairment in cirrhotic patients. This study aimed to evaluate urinary neutrophil gelatinase-associated lipocalin (NGAL) and urinary interleukin-18 (IL-18) as early biomarkers of acute kidney injury in cirrhotic patients. 160 patients with cirrhosis admitted to the Liver Units at Zagazig University Hospitals were classified into three groups: (I) nonascitic patients, (II) ascitic patients without renal impairment, and (III) ascitic patients with renal impairment. Patients with renal impairment were further divided into four subgroups: [A] prerenal azotemia, [B] chronic kidney disease (CKD), [C] hepatorenal syndrome (HRS), and [D] acute tubular necrosis (ATN). Significant elevation of both urinary NGAL and urinary IL-18 in cirrhotic patients with renal impairment especially in patients with ATN was observed. Urinary NGAL and urinary IL-18 have the ability to differentiate between AKI types in patients with cirrhosis. This could improve risk stratification for patients admitted to the hospital with cirrhosis, perhaps leading to early ICU admission, transplant evaluation, and prompt initiation of HRS therapy and early management of AKI. 1. Introduction Egypt was blessed with the River Nile and ancient culture but was deemed with liver diseases. Liver cirrhosis is a common disease in Egypt as Egypt has the highest incidence rate of HCV infection worldwide [1]. Acute kidney injury (AKI) in patients with cirrhosis is common. Up to 20% of hospitalized patients with cirrhosis develop AKI [2] and once AKI occurs, there is a reported fourfold increased risk of mortality [3]. Typically, patients with decompensated liver cirrhosis have significant circulatory dysfunction, which is characterized by a vasodilatory state, lower total peripheral resistance, activated renin-angiotensin-aldosterone system (RAAS), and finally renal arterial vasoconstriction [4]. In cirrhosis, AKI types include prerenal azotemia, hepatorenal syndrome (HRS), and acute tubular necrosis (ATN) with prevalence rates of 68%, 25%, and 33%, respectively, but their effect on mortality risk varies [2]. Unfortunately, these forms of AKI are difficult to distinguish clinically as serum creatinine (sCr), the clinical standard to define kidney function, poorly discriminates AKI type in cirrhosis [5]. Furthermore, various factors can affect serum creatinine in cirrhotic patients such as age, gender, nutritional status, muscle mass, and drug and volume distribution; in

References

[1]  M. M. El Gaafary, C. Rekacewicz, A. G. Abdel-Rahman et al., “Surveillance of acute hepatitis C in Cairo, Egypt,” Journal of Medical Virology, vol. 76, no. 4, pp. 520–525, 2005.
[2]  G. Garcia-Tsao, C. R. Parikh, and A. Viola, “Acute kidney injury in cirrhosis,” Hepatology, vol. 48, no. 6, pp. 2064–2077, 2008.
[3]  D. du Cheyron, B. Bouchet, J. Parienti, M. Ramakers, and P. Charbonneau, “The attributable mortality of acute renal failure in critically ill patients with liver cirrhosis,” Intensive Care Medicine, vol. 31, no. 12, pp. 1693–1699, 2005.
[4]  Y. Iwakiri and R. J. Groszmann, “The hyperdynamic circulation of chronic liver diseases: from the patient to the molecule,” Hepatology, vol. 43, pp. S121–S131, 2006.
[5]  E. Cholongitas, V. Shusang, L. Marelli et al., “Review article: renal function assessment in cirrhosis—difficulties and alternative measurements,” Alimentary Pharmacology and Therapeutics, vol. 26, no. 7, pp. 969–978, 2007.
[6]  F. Wong, M. K. Nadim, J. A. Kellum et al., “Working Party proposal for a revised classification system of renal dysfunction in patients with cirrhosis,” Gut, vol. 60, no. 5, pp. 702–709, 2011.
[7]  F. Salerno, A. Gerbes, P. Ginès, F. Wong, and V. Arroyo, “Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis,” Gut, vol. 56, no. 9, pp. 1310–1318, 2007.
[8]  R. Bellomo, C. Ronco, J. A. Kellum, R. L. Mehta, and P. Palevsky, “Acute renal failure—definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group,” Critical Care, vol. 8, no. 4, pp. R204–R212, 2004.
[9]  R. L. Mehta and J. Bouchard, “Controversies in acute kidney injury: effects of fluid overload on outcome,” Contributions to Nephrology, vol. 174, pp. 200–211, 2011.
[10]  P. Ginès, P. Angeli, K. Lenz et al., “EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis,” Journal of Hepatology, vol. 53, no. 3, pp. 397–417, 2010.
[11]  H. Bachorzewska-Gajewska, J. Malyszko, E. Sitniewska, J. S. Malyszko, and S. Dobrzycki, “Neutrophil-gelatinase-associated lipocalin and renal function after percutaneous coronary interventions,” American Journal of Nephrology, vol. 26, no. 3, pp. 287–292, 2006.
[12]  K. Makris, N. Markou, E. Evodia et al., “Urinary neutrophil gelatinase-associated lipocalin (NGAL) as an early marker of acute kidney injury in critically ill multiple trauma patients,” Clinical Chemistry and Laboratory Medicine, vol. 47, no. 1, pp. 79–82, 2009.
[13]  T. L. Nickolas, M. J. O'Rourke, J. Yang et al., “Sensitivity and specificity of a single emergency department measurement of urinary neutrophil gelatinase-associated lipocalin for diagnosing acute kidney injury,” Annals of Internal Medicine, vol. 148, no. 11, pp. 810–819, 2008.
[14]  T. Jeong, S. Kim, W. Lee et al., “Neutrophil gelatinase-associated lipocalin as an early biomarker of acute kidney injury in liver transplantation,” Clinical Transplantation, vol. 26, pp. 775–781, 2012.
[15]  C. R. Parikh, A. Jani, V. Y. Melnikov, S. Faubel, and C. L. Edelstein, “Urinary interleukin-18 is a marker of human acute tubular necrosis,” American Journal of Kidney Diseases, vol. 43, no. 3, pp. 405–414, 2004.
[16]  C. R. Parikh and P. Devarajan, “New biomarkers of acute kidney injury,” Critical Care Medicine, vol. 36, pp. S159–S165, 2008.
[17]  R. N. Pugh, I. M. Murray-Lyon, J. L. Dawson, et al., “Transection of the esophagus in the bleeding esophageal varices,” British Journal of Surgery, vol. 60, pp. 648–652, 1973.
[18]  R. Moreau and D. Lebrec, “Acute renal failure in patients with cirrhosis: perspectives in the age of MELD,” Hepatology, vol. 37, no. 2, pp. 233–243, 2003.
[19]  A. S. Levey, J. P. Bosch, J. B. Lewis, T. Greene, N. Rogers, and D. Roth, “A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation,” Annals of Internal Medicine, vol. 130, no. 6, pp. 461–470, 1999.
[20]  V. Arroyo, C. Terra, and P. Ginès, “Advances in the pathogenesis and treatment of type-1 and type-2 hepatorenal syndrome,” Journal of Hepatology, vol. 46, no. 5, pp. 935–946, 2007.
[21]  A. S. Levey, J. Coresh, E. Balk, et al., “National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification, and stratification,” Annals of Internal Medicine, vol. 139, pp. 137–147, 2003.
[22]  R. W. Schrier, “Diagnostic value of urinary sodium, chloride, urea, and flow,” Journal of the American Society of Nephrology, vol. 22, no. 9, pp. 1610–1613, 2011.
[23]  A. K. Mandal, M. Lansing, and A. Fahmy, “Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study,” American Journal of Kidney Diseases, vol. 2, no. 3, pp. 363–374, 1982.
[24]  W. G. Rector Jr., G. C. Kanel, J. Rakela, and T. B. Reynolds, “Tubular dysfunction in the deeply jaundiced patient with hepatorenal syndrome,” Hepatology, vol. 5, no. 2, pp. 321–326, 1985.
[25]  P. Angeli, R. Volpin, G. Gerunda et al., “Reversal of type 1 hepatorenal syndrome with the administration of midodrine and octreotide,” Hepatology, vol. 29, no. 6, pp. 1690–1697, 1999.
[26]  M. L. Esson and R. W. Schrier, “Diagnosis and treatment of acute tubular necrosis,” Annals of Internal Medicine, vol. 137, no. 9, pp. 744–752, 2002.
[27]  A. Ochs, M. Rossle, K. Haag et al., “The transjugular intrahepatic portosystemic stent-shunt procedure for refractory ascites,” The New England Journal of Medicine, vol. 332, no. 18, pp. 1192–1197, 1995.
[28]  S. Iwatsuki, M. M. Popovtzer, and J. L. Corman, “Recovery from “hepatorenal syndrome” after orthotopic liver transplantation,” The New England Journal of Medicine, vol. 289, no. 22, pp. 1155–1159, 1973.
[29]  C. Cassinello, E. Moreno, A. Gozalo, B. Ortu?o, B. Cuenca, and J. A. Solís-Herruzo, “Effects of Orthotopic liver transplantation on vasoactive systems and renal function in patients with advanced liver cirrhosis,” Digestive Diseases and Sciences, vol. 48, no. 1, pp. 179–186, 2003.
[30]  F. D. McDonald, L. A. Brennan, and J. G. Turcotte, “Severe hypertension and elevated plasma renin activity following transplantation of “hepatorenal donor” kidneys into anephric recipients,” The American Journal of Medicine, vol. 54, no. 1, pp. 39–43, 1973.
[31]  M. H. Koppel, J. W. Coburn, M. M. Mims, H. Goldstein, J. D. Boyle, and M. E. Rubini, “Transplantation of cadaveric kidneys from patients with hepatorenal syndrome. Evidence for the functionalnature of renal failure in advanced liver disease,” The New England Journal of Medicine, vol. 280, no. 25, pp. 1367–1371, 1969.
[32]  G. C. Kanel and R. L. Peter, “Glomerular tubular reflex. A morphologic renal lesion associated with the hepatorenal syndrome,” Hepatology, vol. 4, no. 2, pp. 242–246, 1984.
[33]  N. K. Hollenberg, “Aldosterone in the development and progression of renal injury,” Kidney International, vol. 66, no. 1, pp. 1–9, 2004.
[34]  E. D. Siew, T. A. Ikizler, T. Gebretsadik et al., “Elevated urinary IL-18 levels at the time of ICU admission predict adverse clinical outcomes,” Clinical Journal of the American Society of Nephrology, vol. 5, no. 8, pp. 1497–1505, 2010.
[35]  P. Devarajan, “Biomarkers for the early detection of acute kidney injury,” Current Opinion in Pediatrics, vol. 23, no. 2, pp. 194–200, 2011.
[36]  E. C. Verna, R. S. Brown, E. Farrand et al., “Urinary neutrophil gelatinase-associated lipocalin predicts mortality and identifies acute kidney injury in cirrhosis,” Digestive Diseases and Sciences, vol. 57, pp. 2362–2370, 2012.
[37]  M. A. Papadakis and A. I. Arieff, “Unpredictability of clinical evaluation of renal function in cirrhosis. Prospective study,” The American Journal of Medicine, vol. 82, no. 5, pp. 945–952, 1987.
[38]  A. S. Levey, J. Coresh, T. Greene et al., “Expressing the modification of diet in renal disease study equation for estimating glomerular filtration rate with standardized serum creatinine values,” Clinical Chemistry, vol. 53, no. 4, pp. 766–772, 2007.
[39]  N. Gill, J. V. Natty Jr., and R. A. Fatica, “Renal failure secondary to acute tubular necrosis: epidemiology, diagnosis, and management,” Chest, vol. 128, no. 4, pp. 2847–2863, 2005.

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