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      Serum Cystatin C and Tubular Urinary Enzymes as Biomarkers of Renal Dysfunction in Type 2 Diabetes Mellitus

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          Abstract

          Renal tubulointerstitium plays an important role in the development and progression of diabetic nephropathy. The aim of this study was to assess serum cystatin C and 2 renal tubular enzymes, neutrophil gelatinase associated lipocalin (NGAL) and N-acetyl-beta-D-glucosaminidase (NAG), as screening markers for early renal dysfunction in patients with type 2 diabetes mellitus (T2DM). ROC curve analysis showed that urinary NAG is the most sensitive marker of microalbuminuria and early renal damage with sensitivity of 83.3%, while serum cystatin C was the most sensitive and specific marker of macroalbuminuria and damage progress with sensitivity of 70.8% and specificity of 83.3% versus 70.6% and 83.3% for uNGAL; and 64.7% and 66.7% for NAG, respectively. Our data indicate that urinary NAG is the most sensitive marker for early renal damage in diabetic patients. However, for damage progress, serum cystatin C is the most sensitive and specific marker for follow-up and monitoring renal dysfunction.

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          NGAL is an early predictive biomarker of contrast-induced nephropathy in children.

          Russel Hirsch, Catherine Dent, Holly Pfriem … (2007)
          We hypothesized that neutrophil gelatinase-associated lipocalin (NGAL) is an early predictive biomarker of contrast-induced nephropathy (CIN). We prospectively enrolled 91 children (age 0-18 years) with congenital heart disease undergoing elective cardiac catheterization and angiography with contrast administration (CC; Ioversol). Serial urine and plasma samples were analyzed in a double-blind fashion by NGAL enzyme-linked immunosorbent assay (ELISA). CIN, defined as a 50% increase in serum creatinine from baseline, was found in 11 subjects (12%), but detection using increase in serum creatinine was only possible 6-24 h after CC. In contrast, significant elevation of NGAL concentrations in urine (135 +/- 32 vs. 11.6 +/- 2 ng/ml without CIN, p < 0.001) and plasma (151 +/- 34 vs. 36 +/- 4 without CIN, p < 0.001) were noted within 2 h after CC in those subjects. Using a cutoff value of 100 ng/ml, sensitivity, specificity, and area under the receiver-operating characteristic (ROC) curve for prediction of CIN were excellent for the 2-h urine NGAL (73%, 100%, and 0.92, respectively) and 2-h plasma NGAL (73%, 100%, and 0.91, respectively). By multivariate analysis, the 2-h NGAL concentrations in the urine (R (2) = 0.52, p < 0.0001) and plasma (R (2) = 0.72, p < 0.0001) were found to be powerful independent predictors of CIN. Patient demographics and contrast volume were not predictive of CIN.
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            Urinary biomarkers for sensitive and specific detection of acute kidney injury in humans.

            Vishal Vaidya, Sushrut S Waikar, Michael A H Ferguson … (2008)
            Acute kidney injury (AKI) is associated with high morbidity and mortality. The lack of sensitive and specific injury biomarkers has greatly impeded the development of therapeutic strategies to improve outcomes of AKI.The unique objective of this study was to evaluate the diagnostic performance of nine urinary biomarkers of AKI-kidney injury molecule-1 (KIM-1), neutrophil gelatinase associated lipocalin (NGAL), interleukin-18 (IL-18), hepatocyte growth factor (HGF), cystatin C (Cys), N-acetyl-beta-D-glucosaminidase (NAG), vascular endothelial growth factor (VEGF), chemokine interferon-inducible protein 10 (IP-10; CXCL10), and total protein-in a cross-sectional comparison of 204 patients with or without AKI.Median urinary concentrations of each biomarker were significantly higher in patients with AKI than in those without AKI (p 5.72 and HGF > 0.17) + 2.93*(PROTEIN > 0.22) -2*(KIM < 0.58)] was greater (0.94) than individual biomarker AUC-ROCs. Age-adjusted levels of urinary KIM-1, NAG, HGF, VEGF, and total protein were significantly higher in patients who died or required renal replacement therapy (RRT) when compared to those who survived and did not require RRT.Our results demonstrate the comparative value of multiple biomarkers in the diagnosis and prognosis of AKI.
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              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.

              Julie A C Johnson, James Warram, Linda H. Ficociello … (2011)
              Elevated urinary albumin excretion in patients with type 1 diabetes reverts to normoalbuminuria in a majority of patients but advances toward proteinuria in some. In order to gain valuable insights into the early pathophysiology of diabetic nephropathy we evaluated the association of kidney tubular injury biomarkers with changes in albuminuria in patients with type 1 diabetes mellitus. Urine levels of kidney injury molecule-1 (KIM-1), N-acetyl-β-D-glucosaminidase (NAG), and some inflammatory markers were determined in 38 healthy individuals and 659 patients with type 1 diabetes mellitus having varying degrees of albuminuria. Urinary interleukin-6, CXCL10/IP-10, NAG, and KIM-1 levels were very low in healthy individuals, increased in type 1 patients with normoalbuminuria, and were highest in diabetic patients that had microalbuminuria. Low baseline concentrations of urinary KIM-1 and NAG both individually and collectively were significantly associated with the regression of microalbuminuria over the subsequent 2 years; an effect independent of clinical characteristics. Progression and regression of microalbuminuria were unrelated to urinary levels of interleukins 6 and 8, CXCL10/IP-10, and monocyte chemoattractant protein-1. Thus our results show that lower urinary KIM-1 and NAG levels were associated with the regression of microalbuminuria in type 1 diabetes mellitus. Hence, tubular dysfunction is a critical component of the early course of diabetic nephropathy.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Med Insights Endocrinol Diabetes
                Journal ID (iso-abbrev): Clin Med Insights Endocrinol Diabetes
                Journal ID (publisher-id): Clinical Medicine Insights: Endocrinology and Diabetes
                Title: Clinical Medicine Insights. Endocrinology and Diabetes
                Publisher: Libertas Academica
                ISSN (Electronic): 1179-5514
                Publication date Collection: 2013
                Publication date (Electronic): 31 July 2013
                Volume: 6
                Pages: 7-13
                Affiliations
                [1 ]Department of Internal Medicine, Medical Research Division, National Research Centre, Egypt.
                [2 ]Department of Clinical and Chemical Pathology, Medical Research Division, National Research Centre, Cairo, Egypt.
                Author notes
                Corresponding author email: d_lebedy@ 123456yahoo.co.uk
                Article
                Publisher ID: cmed-6-2013-007
                DOI: 10.4137/CMED.S12633
                PMC ID: 3738377
                PubMed ID: 23966807
                SO-VID: f3c0f64d-dd03-43f7-a0e0-5e0e79999c62
                Copyright © © 2013 the author(s), publisher and licensee Libertas Academica Ltd.
                License:

                This is an open access article published under the Creative Commons CC-BY-NC 3.0 license.

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                Categories
                Subject: Original Research

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: diabetic nephropathy,neutrophil gelatinase-associated lipocalin,n-acetyl-beta-d-glucosaminidase,cystatin c
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: diabetic nephropathy, neutrophil gelatinase-associated lipocalin, n-acetyl-beta-d-glucosaminidase, cystatin c

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