All Title Author
Keywords Abstract


Association between Urinary N-Acetyl-Beta-D-Glucosaminidase and Microalbuminuria in Diabetic Black Africans

DOI: 10.1155/2012/235234

Full-Text   Cite this paper   Add to My Lib

Abstract:

Diabetes mellitus is the commonest cause of ESRD worldwide and third most common cause in Nigeria. Recent reports from Nigeria indicate the prevalence of diabetic nephropathy as an aetiology of ESRD is increasing necessitating early diagnosis of diabetic nephropathy. We measured the urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), NAG/creatinine ratio, urinary protein-creatinine ratio and calculated eGFR in 30 recently diagnosed nonhypertensive diabetics and 67 controls. The age and sex distribution, systolic blood pressure, serum and urinary creatinine were similar for both groups. There was higher urinary excretion of NAG (304 versus 184?μmol/h/L, ?? < 0 . 0 0 1 ) and NAG/creatinine ratio (21.2 versus 15.7?μmol/h/L/mmolCr, ?? < 0 . 0 0 1 ) in the diabetics than controls. There was a strong correlation between NAG/creatinine ratio and albumin/creatinine ratio ( ?? = 0 . 7 4 , ?? < 0 . 0 0 1 ). A multivariate linear regression model showed a significant linear relationship between NAG/creatinine ratio and albumin/creatinine ratio after adjusting for the effect of blood pressure, age, sex, and serum creatinine. The strong association found between albumin/creatinine ratio and NAG/creatinine ratio perhaps indicates the need for further investigation of the clinical utility of NAG/creatinine ratio as a screening tool for early nephropathy in African diabetics. 1. Introduction End-stage renal disease is on the increase worldwide. However, it is difficult to appropriately compare international data on the aetiology, incidence, and prevalence because of differences in how data for various registries are derived, different patient demographics, and quality of healthcare among others. Diabetes mellitus (DM) is still recognized in the US and Europe as the commonest cause of end-stage renal disease (ESRD). Indeed recent data from the US Renal Data System suggests that the rates of ESRD due to DM and hypertension rose by 2.2% and 2.7%, respectively, in 2009 with overall prevalent ESRD estimated at 1,738 per million population [1]. African Americans were in the majority. Reports from Europe and Asia have also shown a rise in the incidence of ESRD over the years [2–4]. In Nigeria, many hospital-based reports put diabetic nephropathy as the third most common cause of ESRD [5–7], but it appears that the proportion of ESRD caused by diabetic nephropathy is increasing [8]. In the last two decades, studies have focused on the role of glomerular injury in early diabetic nephropathy (as measured by the onset of persistent microalbuminuria), but attention is now

References

[1]  US Renal Data System, “USRDS 2011 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States,” National Institute of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Md, USA, 2011.
[2]  R. Steenkamp, C. Castledine, T. Feest, and D. Fogarty, “UK renal registry 13th annual report (December 2010): chapter 2: UK RRT prevalence in 2009: national and centre-specific analyses,” Nephron Clinical Practice, vol. 119, supplement 2, pp. c27–c52, 2011.
[3]  P. Van Dijk, K. J. Jager, B. Stengel, C. Gr?nhagen-Riska, T. G. Feest, and J. D. Briggs, “Renal replacement therapy for diabetic end-stage renal disease: data from 10 registries in Europe (1991–2000),” Kidney International, vol. 67, no. 4, pp. 1489–1499, 2005.
[4]  K. Wakai, S. Nakai, K. Kikuchi et al., “Trends in incidence of end-stage renal disease in Japan, 1983–2000: age-adjusted and age-specific rates by gender and cause,” Nephrology Dialysis Transplantation, vol. 19, no. 8, pp. 2044–2052, 2004.
[5]  O. R. Adetunji, J. O. Adeleye, N. O. Agada, and B. L. Salako, “Microalbuminuria and clinical correlates in black African patients with type 2 diabetes,” West African Journal of Medicine, vol. 25, no. 4, pp. 279–283, 2006.
[6]  C. O. Alebiosu, O. O. Ayodele, A. Abbas, and I. A. Olutoyin, “Chronic renal failure at the Olabisi Onabanjo University teaching hospital, Sagamu, Niigeria,” African Health Sciences, vol. 6, no. 3, pp. 132–138, 2006.
[7]  U. E. Ekrikpo, A. I. Udo, E. E. Ikpeme, and E. E. Effa, “Haemodialysis in an emerging centre in a developing country: a two year review and predictors of mortality,” BMC Nephrology, vol. 12, article 50, 2011.
[8]  C. O. Alebiosu and O. E. Ayodele, “The increasing prevalence of diabetic nephropathy as a cause of end stage renal disease in Nigeria,” Tropical Doctor, vol. 36, no. 4, pp. 218–219, 2006.
[9]  M. Dunlop, “Aldose reductase and the role of the polyol pathway in diabetic nephropathy,” Kidney International, vol. 58, supplement 77, pp. S3–S12, 2000.
[10]  M. C. Thomas, W. C. Burns, and M. E. Cooper, “Tubular changes in early diabetic nephropathy,” Advances in Chronic Kidney Disease, vol. 12, no. 2, pp. 177–186, 2005.
[11]  A. Matheson, M. D. Willcox, J. Flanagan, and B. J. Walsh, “Urinary biomarkers involved in type 2 diabetes: a review,” Diabetes/Metabolism Research and Reviews, vol. 26, no. 3, pp. 150–171, 2010.
[12]  M. Mazaheri, A. Samaie, and V. Semnani, “Renal tubular dysfunction measured by N-acetyl-beta glucosaminidase/creatinine activity index in children receiving antiepileptic drugs: a randomized controlled trial,” Italian Journal of Pediatrics, vol. 37, article 21, 2011.
[13]  M. P. Bosomworth, S. R. Aparicio, and A. W. Hay, “Urine N-acetyl-β-D-glucosaminidase—a marker of tubular damage?” Nephrology Dialysis Transplantation, vol. 14, no. 3, pp. 620–626, 1999.
[14]  C. Bazzi, C. Petrini, V. Rizza et al., “Urinary N-acetyl-β-glucosaminidase excretion is a marker of tubular cell dysfunction and a predictor of outcome in primary glomerulonephritis,” Nephrology Dialysis Transplantation, vol. 17, no. 11, pp. 1890–1896, 2002.
[15]  A. Piwowar, M. Knapik-Kordecka, I. Fus, and M. Warwas, “Urinary activities of cathepsin B, N-acetyl-β-D-glucosaminidase, and albuminuria in patients with type 2 diabetes mellitus,” Medical Science Monitor, vol. 12, no. 5, pp. CR210–CR214, 2006.
[16]  A. Kalansooriya, I. Holbrook, P. Jennings, and P. H. Whiting, “Serum cystatin C, enzymuria, tubular proteinuria and early renal insult in type 2 diabetes,” British Journal of Biomedical Science, vol. 64, no. 3, pp. 121–123, 2007.
[17]  A. Mohammadi-Karakani, S. Asgharzadeh-Haghighi, M. Ghazi-Khansari, and R. Hosseini, “Determination of urinary enzymes as a marker of early renal damage in diabetic patients,” Journal of Clinical Laboratory Analysis, vol. 21, no. 6, pp. 413–417, 2007.
[18]  K. T. Koh, K. S. Chia, and C. Tan, “Proteinuria and enzymuria in non-insulin-dependent diabetics,” Diabetes Research and Clinical Practice, vol. 20, no. 3, pp. 215–221, 1993.
[19]  UK Prospective Diabetes Study Group, “UK Prospective Diabetes Study (UKPDS). IX: relationships of urinary albumin and N-acetylglucosaminidase to glycaemia and hypertension at diagnosis of type 2 (non-insulin-dependent) diabetes mellitus and after 3 months diet therapy,” Diabetologia, vol. 36, no. 9, pp. 835–842, 1993.
[20]  W. J. Fu, S. L. Xiong, Y. G. Fang et al., “Urinary tubular biomarkers in short-term type 2 diabetes mellitus patients: a cross-sectional study,” Endocrine, vol. 41, no. 1, pp. 82–88, 2012.
[21]  E. F. Kern, P. Erhard, W. Sun, S. Genuth, and M. F. Weiss, “Early urinary markers of diabetic kidney disease: a nested case-control study from the Diabetes Control and Complications Trial (DCCT),” American Journal of Kidney Diseases, vol. 55, no. 5, pp. 824–834, 2010.
[22]  C. T. Yuen, P. R. Kind, R. G. Price, P. F. Praill, and A. C. Richardson, “Colorimetric assay for N-acetyl-β-D-glucosaminidase (NAG) in pathological urine using the ω-nitrostyryl substrate: the development of a kit and the comparison of manual procedure with the automated fluorimetric method,” Annals of Clinical Biochemistry, vol. 21, no. 4, pp. 295–300, 1984.
[23]  A. S. Levey, J. Coresh, T. Greene et al., “Using standardized serum creatinine values in the modification of diet in renal disease study equation for estimating glomerular filtration rate,” Annals of Internal Medicine, vol. 145, no. 4, pp. 247–254, 2006.
[24]  F. N. Ziyadeh and S. Goldfarb, “The renal tubulointerstitium in diabetes mellitus,” Kidney International, vol. 39, no. 3, pp. 464–475, 1991.
[25]  R. Lorini, A. Scaramuzza, L. Cortona, G. Valenti, G. d'Annunzio, and G. V. Melzi d'Eril, “Increased urinary N-acetyl-β-glucosaminidase (NAG) excretion in young insulin-dependent diabetic patients,” Diabetes Research and Clinical Practice, vol. 29, no. 2, pp. 99–105, 1995.
[26]  T. Basturk, Y. Altunta?, A. Kurklu, L. Aydin, N. Eren, and A. Unsal, “Urinary N-acetyl B glucosaminidase as an earlier marker of diabetic nephropathy and influence of low-dose perindopril/indapamide combination,” Renal Failure, vol. 28, no. 2, pp. 125–128, 2006.
[27]  G. F. Watts, M. A. Vlitos, R. W. Morris, and R. G. Price, “Urinary N-acetyl-β-D-glucosaminidase excretion in insulin-dependent diabetes mellitus: relation to microalbuminuria, retinopathy and glycaemic control,” Diabete et Metabolisme, vol. 14, no. 5, pp. 653–658, 1988.
[28]  V. S. Vaidya, M. A. Niewczas, L. H. Ficociello et al., “Regression of microalbuminuria in type 1 diabetes is associated with lower levels of urinary tubular injury biomarkers, kidney injury molecule-1, and N-acetyl-β-D-glucosaminidase,” Kidney International, vol. 79, no. 4, pp. 464–470, 2011.
[29]  K. Jung, A. Hempel, K. D. Grutzmann, R. D. Hempel, and G. Schreiber, “Age-dependent excretion of alanine aminopeptidase, alkaline phosphatase, γ-glutamyltransferase and N-acetyl-β-D-glucosaminidase in human urine,” Enzyme, vol. 43, no. 1, pp. 10–16, 1990.

Full-Text

comments powered by Disqus

Contact Us

service@oalib.com

QQ:3279437679

微信:OALib Journal