N-Acetyl-glucosaminidase

N-Acetyl-glucosaminidase kit (96 determinations)Order button

European Union Price €295,- (As per 01-01-2017)

Inquire for a quotation if you are located outside the European Union.

 

Description

N-acetyl-glucoseaminidase (NAG) is excreted into the urine following injury to the tubular system of the kidney. This injury may occur after renal ischemia or may be induced by an inflammatory reaction. A quantitative measure of tubular damage can be obtained after simultaneous measurement of urea, to correct for dilution. NAG is determined by means of a substrate conversion assay. Under appropriate conditions, NAG present in a urine sample converts a chromogenic substrate. After development of the color the optical density is determined. The concentration [U/L] is quantified by applying standards with known concentrations of the enzyme.

 

Application

Measuring N-acetyl-glucosaminidase activity. This kit is intended for laboratory research use only and is not for use in diagnostic or therapeutic procedures. The analysis should be performed by trained laboratory professionals.

 

Principle

The enzyme N-acetyl-glucosaminidase (NAG) can be used as a marker for kidney proximal tubulus damage. The samples are incubated with a chromogenic substrate. After one hour of incubation at low pH, a basic stop solution is added and the optical density at 400 nm is measured. Because the samples may contain components which can result in a high background signal, for every sample a blank value is determined in which the stop solution is added prior to the reaction, instead of after the reaction. The concentration of NAG is expressed in units/liter [U/L]. One unit of enzyme can convert 1 mmol of substrate per minute at a pH of 4,25 and a temperature of 25°C.

 

Storage and Stability

Product is stable at -20 °C for one year.

 

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References

Gerritsen KG, Leeuwis JW, Koeners MP, Bakker SJ, van Oeveren W, Aten J, Tarnow L, Rossing P, Wetzels JF, Joles JA, Kok RJ, Goldschmeding R, Nguyen TQ. Elevated Urinary Connective Tissue Growth Factor in Diabetic Nephropathy Is Caused by Local Production and Tubular Dysfunction. J Diabetes Res. 2015;2015:539787.

 

Vermeulen Windsant IC, de Wit NC, Sertorio JT, van Bijnen AA, Ganushchak YM, Heijmans JH, Tanus-Santos JE, Jacobs MJ, Maessen JG, Buurman WA. Hemolysis during cardiac surgery is associated with increased intravascular nitric oxide consumption and perioperative kidney and intestinal tissue damage. Front Physiol. 2014 Sep 8;5:340.

 

de Haan JJ, Windsant IV, Lubbers T, Hanssen SJ, Hadfoune M, Prinzen FW, Greve JW, Buurman WA. Prevention of hemolysis-induced organ damage by nutritional activation of the vagal anti-inflammatory reflex*. Crit Care Med. 2013 Nov;41(11):e361-7.

 

van Wijck K, Lenaerts K, van Loon LJ, Peters WH, Buurman WA, Dejong CH. Exercise-induced splanchnic hypoperfusion results in gut dysfunction in healthy men. PLoS One. 2011;6(7):e22366.

 

Nauta FL, Boertien WE, Bakker SJ, van Goor H, van Oeveren W, de Jong PE, Bilo H, Gansevoort RT. Glomerular and tubular damage markers are elevated in patients with diabetes. Diabetes Care. 2011 Apr;34(4):975-81.

 

Snoeijs MG, van Bijnen A, Swennen E, Haenen GR, Roberts LJ 2nd, Christiaans MH, Peppelenbosch AG, Buurman WA, Ernest van Heurn LW. Tubular epithelial injury and inflammation after ischemia and reperfusion in human kidney transplantation. Ann Surg. 2011 Mar;253(3):598-604.

 

Meijer E, Boertien WE, Nauta FL, Bakker SJ, van Oeveren W, Rook M, van der Jagt EJ, van Goor H, Peters DJ, Navis G, de Jong PE, Gansevoort RT. Association of urinary biomarkers with disease severity in patients with autosomal dominant polycystic kidney disease: a cross-sectional analysis. Am J Kidney Dis. 2010 Nov;56(5):883-95.

 

Vermeulen Windsant IC, Snoeijs MG, Hanssen SJ, Altintas S, Heijmans JH, Koeppel TA, Schurink GW, Buurman WA, Jacobs MJ. Hemolysis is associated with acute kidney injury during major aortic surgery. Kidney Int. 2010 May;77(10):913-20.

 

Morariu AM, Schuurs TA, Leuvenink HG, van Oeveren W, Rakhorst G, Ploeg RJ. Early events in kidney donation: progression of endothelial activation, oxidative stress and tubular injury after brain death. Am J Transplant. 2008 May;8(5):933-41.

 

Huybregts RA, Morariu AM, Rakhorst G, Spiegelenberg SR, Romijn HW, de Vroege R, van Oeveren W. Attenuated renal and intestinal injury after use of a mini-cardiopulmonary bypass system. Ann Thorac Surg. 2007 May;83(5):1760-6.