Progress in Pathogenesis of Pancreatitis with Acute Kidney Injury
Journal: Journal of Clinical Medicine Research DOI: 10.32629/jcmr.v5i1.1795
Abstract
Acute pancreatitis (AP) is a common gastrointestinal disease. About 20% of patients with acute pancreatitis develop severe acute pancreatitis, often with multiple organ dysfunction and poor prognosis. In the process, about 10% of patients develop acute renal injury (AKI). Acute renal injury (AKI) is a major complication of severe pancreatitis with a case fatality rate of up to 75%. AP associated AKI (AP-AKI) has both common and significant differences from other AKIs associated with intensive care. Although its pathogenesis is not clear, systemic and regional inflammatory responses play a key role. Early detection, early and effective support and pathogen treatment can significantly improve the results.
Keywords
acute kidney injury, acute severe pancreatitis, pathogenesis
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[1] Kes, P., et al., Acute renal failure complicating severe acute pancreatitis. Ren Fail, 1996. 18(4): p. 621-8.
[2] Lankisch, P.G., M. Apte, and P.A. Banks, Acute pancreatitis. Lancet, 2015. 386(9988): p. 85-96.
[3] Lin, H.Y., et al., Acute renal failure in severe pancreatitis: A population-based study. Ups J Med Sci, 2011. 116(2): p. 155-9.
[4] Scurt, F.G., et al., [Acute kidney injury following acute pancreatitis (AP-AKI): Definition, Pathophysiology, Diagnosis and Therapy]. Z Gastroenterol, 2020. 58(12): p. 1241-1266.
[5] Halonen, K.I., et al., Severe acute pancreatitis: prognostic factors in 270 consecutive patients. Pancreas, 2000. 21(3): p. 266-71.
[6] Compañy, L., et al., Factors predicting mortality in severe acute pancreatitis. Pancreatology, 2003. 3(2): p. 144-8.
[7] Devani, K., et al., Acute pancreatitis: Trends in outcomes and the role of acute kidney injury in mortality- A propensity-matched analysis. Pancreatology, 2018. 18(8): p. 870-877.
[8] Schepers, N.J., et al., Early management of acute pancreatitis. Best Pract Res Clin Gastroenterol, 2013. 27(5): p. 727-43.
[9] Dumnicka, P., et al., The Interplay between Inflammation, Coagulation and Endothelial Injury in the Early Phase of Acute Pancreatitis: Clinical Implications. Int J Mol Sci, 2017. 18(2).
[10] Cuthbertson, C.M. and C. Christophi, Disturbances of the microcirculation in acute pancreatitis. Br J Surg, 2006. 93(5): p. 518-30.
[11] Zhang, X.P., L. Wang, and Y.F. Zhou, The pathogenic mechanism of severe acute pancreatitis complicated with renal injury: a review of current knowledge. Dig Dis Sci, 2008. 53(2): p. 297-306.
[12] Sharma, B., et al., Role of probiotics on gut permeability and endotoxemia in patients with acute pancreatitis: a double-blind randomized controlled trial. J Clin Gastroenterol, 2011. 45(5): p. 442-8.
[13] Salvo Romero, E., et al., The intestinal barrier function and its involvement in digestive disease. Rev Esp Enferm Dig, 2015. 107(11): p. 686-96.
[14] Clark, E.C., et al., Glutamine deprivation facilitates tumour necrosis factor induced bacterial translocation in Caco-2 cells by depletion of enterocyte fuel substrate. Gut, 2003. 52(2): p. 224-30.
[15] Raina, R., et al., The Role of Endothelin and Endothelin Antagonists in Chronic Kidney Disease. Kidney Dis (Basel), 2020. 6(1): p. 22-34.
[16] Levy, M., R. Geller, and S. Hymovitch, Renal failure in dogs with experimental acute pancreatitis: role of hypovolemia. Am J Physiol, 1986. 251(6 Pt 2): p. F969-77.
[17] Satake, K., et al., Renal function in experimentally induced acute pancreatitis in dogs: how it is affected by the nephrotoxic substance in pancreatic exudate from ascitic fluid. Jpn J Surg, 1991. 21(1): p. 88-95.
[18] Baker, K.S., et al., Diabetes, hypertension, and cardiovascular events in survivors of hematopoietic cell transplantation: a report from the bone marrow transplantation survivor study. Blood, 2007. 109(4): p. 1765-72.
[19] Hotchkiss, R.S. and I.E. Karl, The pathophysiology and treatment of sepsis. N Engl J Med, 2003. 348(2): p. 138-50.
[20] Pohlman, T.H., et al., An endothelial cell surface factor(s) induced in vitro by lipopolysaccharide, interleukin 1, and tumor necrosis factor-alpha increases neutrophil adherence by a CDw18-dependent mechanism. J Immunol, 1986. 136(12): p. 4548-53.
[21] McDonald, B. and P. Kubes, Innate Immune Cell Trafficking and Function During Sterile Inflammation of the Liver. Gastroenterology, 2016. 151(6): p. 1087-1095.
[22] Habtezion, A., A.S. Gukovskaya, and S.J. Pandol, Acute Pancreatitis: A Multifaceted Set of Organelle and Cellular Interactions. Gastroenterology, 2019. 156(7): p. 1941-1950.
[23] Hoque, R., et al., Sterile inflammatory response in acute pancreatitis. Pancreas, 2012. 41(3): p. 353-7.
[24] Tran, D.D., et al., Acute renal failure in patients with acute pancreatitis: prevalence, risk factors, and outcome. Nephrol Dial Transplant, 1993. 8(10): p. 1079-84.
[25] Ye, B., et al., Aggressive Resuscitation Is Associated with the Development of Acute Kidney Injury in Acute Pancreatitis. Dig Dis Sci, 2019. 64(2): p. 544-552.
[26] Kopitkó, C., L. Medve, and T. Gondos, The value of combined hemodynamic, respiratory and intra-abdominal pressure monitoring in predicting acute kidney injury after major intraabdominal surgeries. Ren Fail, 2019. 41(1): p. 150-158.
[27] De Waele, J.J., Intra-abdominal hypertension and abdominal compartment syndrome. Curr Opin Crit Care, 2022. 28(6): p. 695-701.
[28] Thabet, F.C. and J.C. Ejike, Intra-abdominal hypertension and abdominal compartment syndrome in pediatrics. A review. J Crit Care, 2017. 41: p. 275-282.
[29] Cheatham, M.L., Abdominal compartment syndrome: pathophysiology and definitions. Scand J Trauma Resusc Emerg Med, 2009. 17: p. 10.
[30] Zerem, E., Treatment of severe acute pancreatitis and its complications. World J Gastroenterol, 2014. 20(38): p. 13879-92.
[31] Sandoval, D., et al., The role of neutrophils and platelet-activating factor in mediating experimental pancreatitis. Gastroenterology, 1996. 111(4): p. 1081-91.
[32] Correa-Costa, M., et al., Activation of platelet-activating factor receptor exacerbates renal inflammation and promotes fibrosis. Lab Invest, 2014. 94(4): p. 455-66.
[2] Lankisch, P.G., M. Apte, and P.A. Banks, Acute pancreatitis. Lancet, 2015. 386(9988): p. 85-96.
[3] Lin, H.Y., et al., Acute renal failure in severe pancreatitis: A population-based study. Ups J Med Sci, 2011. 116(2): p. 155-9.
[4] Scurt, F.G., et al., [Acute kidney injury following acute pancreatitis (AP-AKI): Definition, Pathophysiology, Diagnosis and Therapy]. Z Gastroenterol, 2020. 58(12): p. 1241-1266.
[5] Halonen, K.I., et al., Severe acute pancreatitis: prognostic factors in 270 consecutive patients. Pancreas, 2000. 21(3): p. 266-71.
[6] Compañy, L., et al., Factors predicting mortality in severe acute pancreatitis. Pancreatology, 2003. 3(2): p. 144-8.
[7] Devani, K., et al., Acute pancreatitis: Trends in outcomes and the role of acute kidney injury in mortality- A propensity-matched analysis. Pancreatology, 2018. 18(8): p. 870-877.
[8] Schepers, N.J., et al., Early management of acute pancreatitis. Best Pract Res Clin Gastroenterol, 2013. 27(5): p. 727-43.
[9] Dumnicka, P., et al., The Interplay between Inflammation, Coagulation and Endothelial Injury in the Early Phase of Acute Pancreatitis: Clinical Implications. Int J Mol Sci, 2017. 18(2).
[10] Cuthbertson, C.M. and C. Christophi, Disturbances of the microcirculation in acute pancreatitis. Br J Surg, 2006. 93(5): p. 518-30.
[11] Zhang, X.P., L. Wang, and Y.F. Zhou, The pathogenic mechanism of severe acute pancreatitis complicated with renal injury: a review of current knowledge. Dig Dis Sci, 2008. 53(2): p. 297-306.
[12] Sharma, B., et al., Role of probiotics on gut permeability and endotoxemia in patients with acute pancreatitis: a double-blind randomized controlled trial. J Clin Gastroenterol, 2011. 45(5): p. 442-8.
[13] Salvo Romero, E., et al., The intestinal barrier function and its involvement in digestive disease. Rev Esp Enferm Dig, 2015. 107(11): p. 686-96.
[14] Clark, E.C., et al., Glutamine deprivation facilitates tumour necrosis factor induced bacterial translocation in Caco-2 cells by depletion of enterocyte fuel substrate. Gut, 2003. 52(2): p. 224-30.
[15] Raina, R., et al., The Role of Endothelin and Endothelin Antagonists in Chronic Kidney Disease. Kidney Dis (Basel), 2020. 6(1): p. 22-34.
[16] Levy, M., R. Geller, and S. Hymovitch, Renal failure in dogs with experimental acute pancreatitis: role of hypovolemia. Am J Physiol, 1986. 251(6 Pt 2): p. F969-77.
[17] Satake, K., et al., Renal function in experimentally induced acute pancreatitis in dogs: how it is affected by the nephrotoxic substance in pancreatic exudate from ascitic fluid. Jpn J Surg, 1991. 21(1): p. 88-95.
[18] Baker, K.S., et al., Diabetes, hypertension, and cardiovascular events in survivors of hematopoietic cell transplantation: a report from the bone marrow transplantation survivor study. Blood, 2007. 109(4): p. 1765-72.
[19] Hotchkiss, R.S. and I.E. Karl, The pathophysiology and treatment of sepsis. N Engl J Med, 2003. 348(2): p. 138-50.
[20] Pohlman, T.H., et al., An endothelial cell surface factor(s) induced in vitro by lipopolysaccharide, interleukin 1, and tumor necrosis factor-alpha increases neutrophil adherence by a CDw18-dependent mechanism. J Immunol, 1986. 136(12): p. 4548-53.
[21] McDonald, B. and P. Kubes, Innate Immune Cell Trafficking and Function During Sterile Inflammation of the Liver. Gastroenterology, 2016. 151(6): p. 1087-1095.
[22] Habtezion, A., A.S. Gukovskaya, and S.J. Pandol, Acute Pancreatitis: A Multifaceted Set of Organelle and Cellular Interactions. Gastroenterology, 2019. 156(7): p. 1941-1950.
[23] Hoque, R., et al., Sterile inflammatory response in acute pancreatitis. Pancreas, 2012. 41(3): p. 353-7.
[24] Tran, D.D., et al., Acute renal failure in patients with acute pancreatitis: prevalence, risk factors, and outcome. Nephrol Dial Transplant, 1993. 8(10): p. 1079-84.
[25] Ye, B., et al., Aggressive Resuscitation Is Associated with the Development of Acute Kidney Injury in Acute Pancreatitis. Dig Dis Sci, 2019. 64(2): p. 544-552.
[26] Kopitkó, C., L. Medve, and T. Gondos, The value of combined hemodynamic, respiratory and intra-abdominal pressure monitoring in predicting acute kidney injury after major intraabdominal surgeries. Ren Fail, 2019. 41(1): p. 150-158.
[27] De Waele, J.J., Intra-abdominal hypertension and abdominal compartment syndrome. Curr Opin Crit Care, 2022. 28(6): p. 695-701.
[28] Thabet, F.C. and J.C. Ejike, Intra-abdominal hypertension and abdominal compartment syndrome in pediatrics. A review. J Crit Care, 2017. 41: p. 275-282.
[29] Cheatham, M.L., Abdominal compartment syndrome: pathophysiology and definitions. Scand J Trauma Resusc Emerg Med, 2009. 17: p. 10.
[30] Zerem, E., Treatment of severe acute pancreatitis and its complications. World J Gastroenterol, 2014. 20(38): p. 13879-92.
[31] Sandoval, D., et al., The role of neutrophils and platelet-activating factor in mediating experimental pancreatitis. Gastroenterology, 1996. 111(4): p. 1081-91.
[32] Correa-Costa, M., et al., Activation of platelet-activating factor receptor exacerbates renal inflammation and promotes fibrosis. Lab Invest, 2014. 94(4): p. 455-66.
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