Urine N-acetyl- -D-glucosaminidase - a marker of tubular damage?

Bosomworth, M.; Aparicio, S. R.; Hay, Alastair

doi:10.1093/ndt/14.3.620

Cited by 102 publications

(76 citation statements)

References 17 publications

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“…Plasma and urine creatinine concentrations were measured with the Jaffe reaction, and urinary protein was measured by the pyrogallol red-molybdate protein dyebinding method (SRL, Tokyo, Japan). Concentrations of urinary excretions of NAG, an indicator of tubular damage (Bosomworth et al, 1999), were determined using sodio-3,3'-dichlorophenolsulfonphthaleinyl N-acetyl-␤-D-glucosaminide as a substrate (Shionogi, Osaka, Japan). Urinary concentrations of NAG were normalized to urine creatinine levels.…”

Section: Assay Of Creatinine Protein and N-acetyl-␤-dglucosaminidasmentioning

confidence: 99%

Abnormal Iron Deposition in Renal Cells in the Rat with Chronic Angiotensin II Administration

Ishizaka

Aizawa

Yamazaki

et al. 2002

Laboratory Investigation

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SUMMARY:Acute experimental iron loading causes iron to accumulate in the renal tissue. The accumulation of iron may play a role in enhancing oxidant-induced tubular injury by producing increased amounts of reactive oxygen species. From findings in cells from heme oxygenase-1 (HO-1)-deficient mice, HO-1 is postulated to prevent abnormal intracellular iron accumulation. Recently, it has been reported that HO-1 is induced in the renal tubular epithelial cells, in which iron is deposited after iron loading, and that this HO-1 induction may be involved in ameliorating iron-induced renal toxicity. We previously showed that chronic administration of angiotensin II to rats induces HO-1 expression in the tubular epithelial cells. These observations led us to investigate whether there is a link between iron deposition and HO-1 induction in renal tubular cells in rats undergoing angiotensin II infusion. In the present study, rats were given angiotensin II for continuously 7 days. Prussian blue staining revealed the distinct deposits of iron in the proximal tubular epithelial cells after angiotensin II administration. Electron microscopy demonstrated that iron particles were present in the lysosomes of these cells. Histologic and immunohistochemical analyses showed that stainable iron and immunoreactive ferritin and HO-1 were colocalized in the tubular epithelial cells. Treatment of angiotensin II-infused rats with an iron chelator, deferoxamine, blocked the abnormal iron deposition in kidneys and also the induced expression of HO-1 and ferritin expression. Furthermore, deferoxamine treatment suppressed the angiotensin II-induced increase in the urinary excretion of protein and N-acetyl-␤-D-glucosaminidase, a marker of tubular injury; however, deferoxamine did not affect the angiotensin II-induced decrease in glomerular filtration rate. These results suggest that angiotensin II causes renal injury, in part, by inducing the deposition of iron in the kidney. (Lab Invest 2002, 82:87-96).

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Section: Assay Of Creatinine Protein and N-acetyl-␤-dglucosaminidasmentioning

confidence: 99%

Abnormal Iron Deposition in Renal Cells in the Rat with Chronic Angiotensin II Administration

Ishizaka

Aizawa

Yamazaki

et al. 2002

Laboratory Investigation

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“…NAG is thus exclusively a marker of tubular cell function. 2 Increased urinary NAG activity has been described in various disease states such as heavy metal poisoning and renal diseases. [3][4][5][6][7] Most authors consider increased urinary NAG to be a sensitive marker of tubular injury, 8 related to inflammation and oxidative stress.…”

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confidence: 99%

N-Acetyl-β-D-Glucosaminidase Does Not Enhance Prediction of Cardiovascular or All-Cause Mortality by Albuminuria in a Low-Risk Population

Solbu

Toft

Løchen

et al. 2016

Journal of the American Society of Nephrology

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Albuminuria is a well known risk factor for cardiovascular disease and mortality, but focus on renal tubular dysfunction as a potential risk factor is growing also. The association between the urinary activity of N-acetylb-D-glucosaminidase (NAG) and cardiovascular risk has been assessed mostly in cross-sectional studies. We studied the cross-sectional associations between urinary NAG and cardiovascular risk factors and the longitudinal associations between NAG, cardiovascular disease, and all-cause mortality in a general population. Urinary NAG/creatinine ratio (NAG ratio) and albumin/creatinine ratio (ACR) were measured in 6834 participants of the Tromsø Study in 1994-1995. During the median 17.5 years of follow-up, 958 myocardial infarctions, 726 ischemic strokes, and 2358 deaths were registered. In multivariable analyses adjusted for albuminuria and cardiovascular risk factors, a baseline NAG ratio in the highest quartile was associated with an increased risk of myocardial infarction (hazard ratio [HR], 1.43; 95% confidence interval [95% CI], 1.16 to 1.76), ischemic stroke (HR, 1.41; 95% CI, 1.10 to 1.80), and all-cause mortality (HR, 1.60; 95% CI, 1.39 to 1.84). Combined, ACR and NAG ratio above median associated with a 48%-80% increased risk for the three end points. However, the NAG ratio did not add significantly to the baseline risk-prediction models when assessed by area under the receiver operating characteristics curve or net reclassification improvement. In conclusion, the nonsignificant improvement of risk prediction does not support the clinical use of NAG ratio in cardiovascular risk assessment in a low-risk group.

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“…Lysosomal enzyme NAG (EC3.2.1.30) is one of the markers of tubular damage that is mentioned most (18), because NAG assays are sensitive enough to allow dilution of the urine, overcoming any enzyme inhibition. The effects of varied urine concentration can be minimized by expressing NAG activity per mmol creatinine (19). It has been suggested (20) that urinary NAG activity may have raised urinary NAG activity in some patients with essential hypertension.…”

Section: Discussionmentioning

confidence: 99%

Clinical value of urinary kidney biomarkers for estimation of renal impairment in elderly Chinese with essential hypertension

Fang

et al. 2008

Clinical Laboratory Analysis

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The purpose of this work was to observe the excretion of specific types of urinary proteins and urinary enzymes in elderly essential hypertension patients, for early detection and targeted treatment of hypertensive nephropathy in the elderly. A total of 120 elderly essential hypertensive patients and 38 healthy elderly volunteers were involved. The urinary excretion rate of retinal-binding protein (RBP), transferrin (Tf), albumin (Alb), and urinary enzyme N-acetyl-beta-D-glucosaminidase (NAG) activity were determined. Patients were divided into two groups according to their creatinine clearance (Cockroft-Gault formula). There were 88 patients in group A, whose glomerular filtration rate (GFR) was Z80 mL/min, and 32 patients in group B with a GFR o80 mL/min. Among the essential hypertensive patients, urinary excretion rates of RBP, Alb, Tf, and NAG were increased in both groups compared with the healthy controls. But the amount of urinary protein differed between group A and group B. The excretion rate of specific urinary protein and urinary enzyme had a positive relationship with the duration of course of hypertension. We believe that specific types of urinary proteins and urinary enzymes may be useful markers for early diagnosis of hypertensive nephropathy; they can also be regarded as a clinical indicator of the progression of hypertensive nephropathy, serving in the assessment of therapeutic effects.

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Urine N-acetyl- -D-glucosaminidase - a marker of tubular damage?

Abstract: This animal model demonstrates that an increase in lysosomal turnover and hence urine NAG activity, occurs when increased protein is presented to the tubular cells. Urine NAG activity is thus a measure of altered function in the renal tubules and not simply an indicator of damage.

Cited by 102 publications

References 17 publications

Abnormal Iron Deposition in Renal Cells in the Rat with Chronic Angiotensin II Administration

Abnormal Iron Deposition in Renal Cells in the Rat with Chronic Angiotensin II Administration

N-Acetyl-β-D-Glucosaminidase Does Not Enhance Prediction of Cardiovascular or All-Cause Mortality by Albuminuria in a Low-Risk Population

Clinical value of urinary kidney biomarkers for estimation of renal impairment in elderly Chinese with essential hypertension

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