The renal tubular damage marker urinary N-acetyl-β-d-glucosaminidase may be more closely associated with early detection of atherosclerosis than the glomerular damage marker albuminuria in patients with type 2 diabetes

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Abstract

Background

To determine the association between urinary N-acetyl-β- d-glucosaminidase (NAG), a marker of renal tubulopathy, and carotid intima-media thickness (IMT) and plaques in patients with type 2 diabetes mellitus (T2D) and to compare the predictive value of NAG versus albuminuria, a marker of renal glomerulopathy.

Methods

A total of 343 participants were enrolled in this retrospective cross-sectional study. We recruited participants with T2D who were tested for blood glucose parameters, urinary NAG, and urinary albumin-to-creatinine ratio (ACR) and had been checked for carotid ultrasonography.

Results

We classified participants into a below-median urinary NAG group (Group I; n = 172) or an above-median group (Group II; n = 171). Mean, maximum, and mean of maximum carotid IMT and the proportion of patients with carotid plaques were significantly higher in Group II compared with Group I. In multiple linear regression analyses, high urinary NAG (Group II) was significantly associated with carotid IMT, independently of urinary ACR and other confounding factors. In terms of carotid plaques, both urinary NAG and ACR were significantly higher in participants with carotid plaques than in those without carotid plaques. After adjustment for confounding factors, both urinary NAG and ACR were significantly associated with the presence of carotid plaques.

Conclusions

Elevated urinary NAG, a marker of renal tubular damage, was related to increased carotid IMT and the presence of carotid plaques in patients with T2D. Urinary NAG may be a more sensitive biomarker than urinary albumin for early detection of atherosclerosis.

Electronic supplementary material

The online version of this article (doi:10.1186/s12933-017-0497-7) contains supplementary material, which is available to authorized users.

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Most cited references 30

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Mannheim Carotid Intima-Media Thickness and Plaque Consensus (2004–2006–2011)

P.-J. Touboul, M.G. Hennerici, S Meairs … (2012)

Intima-media thickness (IMT) provides a surrogate end point of cardiovascular outcomes in clinical trials evaluating the efficacy of cardiovascular risk factor modification. Carotid artery plaque further adds to the cardiovascular risk assessment. It is defined as a focal structure that encroaches into the arterial lumen of at least 0.5 mm or 50% of the surrounding IMT value or demonstrates a thickness >1.5 mm as measured from the media-adventitia interface to the intima-lumen interface. The scientific basis for use of IMT in clinical trials and practice includes ultrasound physics, technical and disease-related principles as well as best practice on the performance, interpretation and documentation of study results. Comparison of IMT results obtained from epidemiological and interventional studies around the world relies on harmonization on approaches to carotid image acquisition and analysis. This updated consensus document delineates further criteria to distinguish early atherosclerotic plaque formation from thickening of IMT. Standardized methods will foster homogenous data collection and analysis, improve the power of randomized clinical trials incorporating IMT and plaque measurements and facilitate the merging of large databases for meta-analyses. IMT results are applied to individual patients as an integrated assessment of cardiovascular risk factors. However, this document recommends against serial monitoring in individual patients.

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Chronic hypoxia and tubulointerstitial injury: a final common pathway to end-stage renal failure.

Masaomi Nangaku (2006)

Recent studies emphasize the role of chronic hypoxia in the tubulointerstitium as a final common pathway to end-stage renal failure. When advanced, tubulointerstitial damage is associated with the loss of peritubular capillaries. Associated interstitial fibrosis impairs oxygen diffusion and supply to tubular and interstitial cells. Hypoxia of tubular cells leads to apoptosis or epithelial-mesenchymal transdifferentiation. This in turn exacerbates fibrosis of the kidney and subsequent chronic hypoxia, setting in train a vicious cycle whose end point is ESRD. A number of mechanisms that induce tubulointerstitial hypoxia at an early stage have been identified. Glomerular injury and vasoconstriction of efferent arterioles as a result of imbalances in vasoactive substances decrease postglomerular peritubular capillary blood flow. Angiotensin II not only constricts efferent arterioles but, via its induction of oxidative stress, also hampers the efficient utilization of oxygen in tubular cells. Relative hypoxia in the kidney also results from increased metabolic demand in tubular cells. Furthermore, renal anemia hinders oxygen delivery. These factors can affect the kidney before the appearance of significant pathologic changes in the vasculature and predispose the kidney to tubulointerstitial injury. Therapeutic approaches that target the chronic hypoxia should prove effective against a broad range of renal diseases. Current modalities include the improvement of anemia with erythropoietin, the preservation of peritubular capillary blood flow by blockade of the renin-angiotensin system, and the use of antioxidants. Recent studies have elucidated the mechanism of hypoxia-induced transcription, namely that prolyl hydroxylase regulates hypoxia-inducible factor. This has given hope for the development of novel therapeutic approaches against this final common pathway.

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Preventing cardiovascular disease and diabetes: a call to action from the American Diabetes Association and the American Heart Association.

H Eckel, Richard Kahn, Rose Marie Robertson … (2006)

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Author and article information

Contributors

So Ra Kim: mdsrkim12@yuhs.ac

Yong-ho Lee: yholee@yuhs.ac

Sang-Guk Lee: comforter6@yuhs.ac

Eun Seok Kang: edgo@yuhs.ac

Bong-Soo Cha: bscha@yuhs.ac

Byung-Wan Lee: bwanlee@yuhs.ac

Journal

Journal ID (nlm-ta): Cardiovasc Diabetol

Journal ID (iso-abbrev): Cardiovasc Diabetol

Title: Cardiovascular Diabetology

Publisher: BioMed Central (London )

ISSN (Electronic): 1475-2840

Publication date (Electronic): 26 January 2017

Publication date PMC-release: 26 January 2017

Publication date Collection: 2017

Volume: 16

Electronic Location Identifier: 16

Affiliations

[1 ]ISNI 0000 0004 0470 5454, GRID grid.15444.30, Division of Endocrinology and Metabolism, Department of Internal Medicine, Graduate School, , Yonsei University College of Medicine, ; 50-1, Yonsei-ro, Seodaemun-gu, Seoul, 03722 South Korea

[2 ]ISNI 0000 0004 0636 3064, GRID grid.415562.1, , Severance Hospital, ; 50-1, Yonsei-ro, Seodaemun-gu, Seoul, 03722 South Korea

[3 ]ISNI 0000 0004 0470 5454, GRID grid.15444.30, Department of Laboratory Medicine, , Yonsei University College of Medicine, ; 50-1, Yonsei-ro, Seodaemun-gu, Seoul, 03722 South Korea

Article

Publisher ID: 497

DOI: 10.1186/s12933-017-0497-7

PMC ID: 5267389

PubMed ID: 28122570

SO-VID: 94b7ddcd-7899-47db-9d03-b1d0ac7db294

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 5 October 2016

Date accepted : 13 January 2017

Custom metadata

ScienceOpen disciplines: Endocrinology & Diabetes

Keywords: n-acetyl-β-d glucosaminidase,carotid intima-media thickness,carotid plaque,type 2 diabetes mellitus

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ScienceOpen disciplines: Endocrinology & Diabetes

Keywords: n-acetyl-β-d glucosaminidase, carotid intima-media thickness, carotid plaque, type 2 diabetes mellitus

The renal tubular damage marker urinary N-acetyl-β-d-glucosaminidase may be more closely associated with early detection of atherosclerosis than the glomerular damage marker albuminuria in patients with type 2 diabetes

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Abstract

Background

Methods

Results

Conclusions

Electronic supplementary material

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Journal of the ASEAN Federation of Endocrine Societies

Most cited references 30

Mannheim Carotid Intima-Media Thickness and Plaque Consensus (2004–2006–2011)

Chronic hypoxia and tubulointerstitial injury: a final common pathway to end-stage renal failure.

Preventing cardiovascular disease and diabetes: a call to action from the American Diabetes Association and the American Heart Association.

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