NOVEL BIOLOGICAL MARKERS OF ACUTE KIDNEY INJURY IN SEPSIS
Volume 2, Issue 1, Pp 19-22, 2024
DOI: 10.61784/wjbs240144
Author(s)
Estelle Patel
Affiliation(s)
University of Bordeaux, Bordeaux, France.
Corresponding Author
Estelle Patel
ABSTRACT
Sepsis is a problem faced by every ICU medical staff, and its concurrent acute kidney injury is an even more difficult challenge. So far, there are still many deficiencies in its early diagnosis. How to detect and intervene early has become an academic issue. hot issues in research circles. With the in-depth early research on acute kidney injury caused by sepsis in recent years, several markers of septic acute kidney injury have gradually come into people's field of vision. This article summarizes these new markers based on new advances in academic circles in recent years.
KEYWORDS
Sepsis; Acute kidney injury; Biological markers; Neutrophil gelatinase-associated apolipoprotein; Renal injury factor
CITE THIS PAPER
Estelle Patel. Novel biological markers of acute kidney injury in sepsis. World Journal of Biomedical Sciences. 2024, 2(1): 19-22. DOI: 10.61784/wjbs240144.
REFERENCES
[1] Singer M,Deutschman CS,Seymour CW—The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis- 3). JAMA,2016,315(8): 801-810.
[2] Chvojka J,Sykora R , Karvunidis T.New Developments in Septic Acute Kidney Injury—Physiol Res,2010,9(6): 859-869.
[3] Khwaja A. KDIGO clinical practice guidelines for acute kidney injury. Nephron Clin Pract, 2012, 120(4): c179-c184.
[4] Yang L, Xing G, Wang L. Acute kidney injury in China: a cross- sectional survey. Lancet, 2015, 386(10002): 1465-1471.
[5] Shemesh O, Golbetz H, Kriss JP. Limitations of creatinine as a filtration marker in glomerulopathic patients. Kidney Int, 1985, 28 (5): 830-838.
[6] Doi K, Yuen P, Eisner C. Reduced production of creatinine limits its use as marker of kidney injury in sepsis. J Am Soc Nephrol, 2009, 20(6): 1217.
[7] Waikar SS, Betensky RA, Emerson SC. Imperfect gold standards for kidney injury biomarker evaluation. J Am Soc Nephrol, 2012, 23 (1): 13-21.
[8] SPRINT Research Group, Wright JT Jr, Williamson JD. A Randomized Trial of Intensive versus Standard Blood-Pressure Control. N Engl J Med, 2015, 373(22): 2103-2116.
[9] Kjeldsen L, Johnsen AH, Sengelφv H. Isolation and primary structure of NGAL, a novel protein associated with human neutrophil gelatinase. J Biol Chem, 1993, 268(14): 10425-10432.
[10] Bao G, Clifton M, Hoette TM. Iron traffics in circulation bound to a siderocalin (Ngal ) -catechol complex. Nat Chem Biol, 2010, 6 (8): 602-609.
[11] Yang J, Goetz D, Li JY. An iron delivery pathway mediated by a lipocalin. Mol Cell, 2002, 10(5): 1045-1056.
[12] Singer E, Markó L. Paragas N. Neutrophil gelatinase-associated lipocalin: pathophysiology and clinical applications. Acta Physiol (Oxf), 2013, 207(4): 663-672.
[13] Xia Yanmei, Shi Haipeng, Wu Weidong. Analysis of urinary NGAL on the timing of CRRT treatment in septic acute kidney injury. Medical Journal of the People's Liberation Army, 2019, 44(7): 605-610.
[14]Wang M, Zhang Q, Zhao X. Diagnostic and prognostic value of neutrophil gelatinase-associated lipocalin, matrix metalloproteinase-9, and tissue inhibitor of matrix metalloproteinases-1 for sepsis in the Emergency Department: an observational study. Crit Care, 2014, 18 (6): 634.
[15]Rampoldi B, Tessarolo S, Giubbilini P. Neutrophil gelatinase- associated lipocalin and acute kidney injury in endovascular aneurysm repair or open aortic repair: a pilot study. Biochem Med(Zagreb) , 2018, 28(1): 010904.
[16]Shapiro NI, Trzeciak S, Hollander JE. The diagnostic accuracy of plasma neutrophil gelatinase-associated lipocalin in the prediction of acute kidney injury in emergency department patients with suspected sepsis. Ann Emerg Med, 2010, 56(1): 52-59.
[17]Paragas N, Qiu A, Hollmen M. NGAL-Siderocalin in kidney disease. Biochim Biophys Acta, 2012, 1823(9): 1451-1458.
[18]Kashani K, Al-Khafaji A, Ardiles T. Discovery and validation of cell cycle arrest biomarkers in human acute kidney injury. Crit Care, 20136, 17(1): R25.
[19]Wajapeyee N, Serra RW, Zhu X. Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. Cell, 2008, 132(3): 363-374.
[20]Godi I, De Rosa S, Martino F. Urinary[TIMP-2] ×[IGFBP7] and serum procalcitonin to predict and assess the risk for short-term outcomes in septic and non-septic critically ill patients. Ann Intensive Care, 2020, 10(1): 46.
[21]Honore PM, Nguyen HB, Gong M. Urinary Tissue Inhibitor of Metalloproteinase-2 and Insulin-Like Growth Factor-Binding Protein 7 for Risk Stratification of Acute Kidney Injury in Patients With Sepsis. Crit Care Med, 2016, 44(10): 1851-1860.
[22]Maizel J, Daubin D, Vong LV. Urinary TIMP2 and IGFBP7 Identifies High Risk Patients of Short-Term Progression from Mild and Moderate to Severe Acute Kidney Injury during Septic Shock: A Prospective Cohort Study. Dis Markers, 2019, 2019: 3471215.
[23]Wu M, Chen W, Yu X. Celastrol aggravates LPS-induced inflammation and injuries of liver and kidney in mice. Am J Transl Res, 2018, 10(7): 2078-2086.
[24]Sabbisetti VS, Waikar SS, Antoine DJ. Blood kidney injury molecule-1 is a biomarker of acute and chronic kidney injury and predicts progression to ESRD in type I diabetes. J Am Soc Nephrol, 2014, 25(10): 2177-2186.
[25]Dieterle F, Sistare F, Goodsaid F. Renal biomarker qualification submission: a dialog between the FDA-EMEA and Predictive Safety Testing Consortium. Nat Biotechnol, 2010, 28(5): 455-462.
[26]Zhang CF, Wang HJ, Tong ZH. The diagnostic and prognostic values of serum and urinary kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin in sepsis induced acute renal injury patients. Eur Rev Med Pharmacol Sci, 2020, 24(10): 5604-5617.