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      NGAL as an Early Predictive Marker of Diabetic Nephropathy in Children and Young Adults with Type 1 Diabetes Mellitus

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          Abstract

          Aims

          Type 1 diabetes (T1D) is often associated with early microvascular complications. Previous studies demonstrated that increased systolic (SAP) and diastolic arterial blood pressures (DAP) are linked to microvascular morbidity in T1D. The aim of the study was to investigate the predictive role of neutrophil gelatinase-associated lipocalin (NGAL) in unravelling early cardio-renal dysfunction in T1D.

          Methods

          Two T1D patient groups participating in two-centre prospective cohorts were studied. Group A consisted of 57 participants aged 13.9 years (SD: 3.1) and group B consisted of 59 patients aged 28.0 years (SD: 4.4). Forty-nine healthy children [age: 10.5 years (SD: 6.6)] and 18 healthy adults [age 27.7 years (SD: 4.2)] served as controls. Serum concentrations of NGAL (ELISA) were determined, and SAP and DAP were examined (SAP and DAP also expressed as z-scores in the younger group).

          Results

          NGAL correlated positively with SAP in both patient groups ( P = 0.020 and P = 0.031, resp.) and SAP z-score ( P = 0.009) (group A) and negatively with eGFR in both groups ( P < 0.001 and P < 0.001, resp.).

          Conclusions

          NGAL may be proposed as a biomarker of early renal dysfunction even in nonalbuminuric T1D patients, since it was strongly associated with renal function decline and increasing systolic arterial pressure even at prehypertensive range in people with T1D, in a broad age range.

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          Dual action of neutrophil gelatinase-associated lipocalin.

          Kai M Schmidt-Ott, Kiyoshi Mori, Jau Yi Li … (2007)
          Neutrophil gelatinase-associated lipocalin (NGAL) is expressed and secreted by immune cells, hepatocytes, and renal tubular cells in various pathologic states. NGAL exerts bacteriostatic effects, which are explained by its ability to capture and deplete siderophores, small iron-binding molecules that are synthesized by certain bacteria as a means of iron acquisition. Consistently, NGAL deficiency in genetically modified mice leads to an increased growth of bacteria. However, growing evidence suggests effects of the protein beyond fighting microorganisms. NGAL acts as a growth and differentiation factor in multiple cell types, including developing and mature renal epithelia, and some of this activity is enhanced in the presence of siderophore:iron complexes. This has led to the hypothesis that eukaryotes might synthesize siderophore-like molecules that bind NGAL. Accordingly, NGAL-mediated iron shuttling between the extracellular and intracellular spaces may explain some of the biologic activities of the protein. Interest in NGAL has been sparked by the observation that NGAL is massively upregulated after renal tubular injury and may participate in limiting kidney damage. This review summarizes the current knowledge about the dual effects of NGAL as a siderophore:iron-binding protein and as a growth factor and examines the role of these effects in renal injury.
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            Early Progressive Renal Decline Precedes the Onset of Microalbuminuria and Its Progression to Macroalbuminuria

            Andrzej Krolewski, Monika A Niewczas, Jan Skupien … (2013)
            OBJECTIVE Progressive decrease in the glomerular filtration rate (GFR), or renal decline, in type 1 diabetes (T1D) is observed in patients with macroalbuminuria. However, it is unknown whether this decline begins during microalbuminuria (MA) or normoalbuminuria (NA). RESEARCH DESIGN AND METHODS The study group (second Joslin Kidney Study) comprises patients with T1D and NA (n = 286) or MA (n = 248) who were followed for 4–10 years (median 8 years). Serial measurements (median 6, range 3–16) of serum creatinine and cystatin C were used jointly to estimate GFR (eGFRcr-cys) and assess its trajectories during follow-up. RESULTS Renal decline (progressive eGFRcr-cys loss of at least 3.3% per year) occurred in 10% of the NA and 35% of the MA (P < 0.001). In both groups, the strongest determinants of renal decline were baseline serum concentrations of uric acid (P < 0.001) and tumor necrosis factor receptor 1 or 2 (TNFR-1 or -2, P < 0.001). Other significant risk factors included baseline HbA1c, age/diabetes duration, and systolic blood pressure. Relative impacts of these determinants were similar in NA and MA. Renal decline was not associated with sex or baseline serum concentration of TNF-α, IL-6, IL-8, IP-10, MCP-1, VCAM, ICAM, Fas, or FasL. CONCLUSIONS Renal decline in T1D begins during NA and it is determined by multiple factors, similar to MA. Thus, this early decline is the primary disease process leading to impaired renal function in T1D. Changes in albumin excretion rate, such as the onset of MA or its progression to macroalbuminuria, are either caused by or develop in parallel to the early renal decline.
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              Neutrophil gelatinase-associated lipocalin as a biomarker of acute kidney injury: a critical evaluation of current status.

              Anja Haase-Fielitz, Michael Haase, Prasad Devarajan (2014)
              The early prediction of acute kidney injury (AKI) by current clinical and laboratory methods remains inadequate. Neutrophil gelatinase-associated lipocalin (NGAL) has emerged as a promising non-invasive biomarker of kidney injury. We systematically reviewed the utility of plasma and urine NGAL measurements for the prediction of AKI in humans.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Diabetes Res
                Journal ID (iso-abbrev): J Diabetes Res
                Journal ID (publisher-id): JDR
                Title: Journal of Diabetes Research
                Publisher: Hindawi
                ISSN (Print): 2314-6745
                ISSN (Electronic): 2314-6753
                Publication date (Print): 2017
                Publication date (Electronic): 15 May 2017
                Volume: 2017
                Electronic Location Identifier: 7526919
                Affiliations
                1Department of Endocrinology, Department of Medical and Health Sciences, Linkoping University, Linkoping, Sweden
                2Diabetes Centre, Department of Endocrinology, Diabetes and Metabolism, First Department of Pediatrics, National and Kapodistrian University of Athens, Aghia Sophia Children's Hospital, Thivon, 115 27 Athens, Greece
                3Department of Clinical Biochemistry, Aghia Sophia Children's Hospital, Thivon, 115 27 Athens, Greece
                Author notes
                *Nektaria Papadopoulou-Marketou: papadopoulounektaria@ 123456gmail.com

                Academic Editor: Feng Wang

                Author information
                http://orcid.org/0000-0002-6719-7923
                http://orcid.org/0000-0002-2126-3251
                Article
                DOI: 10.1155/2017/7526919
                PMC ID: 5460379
                PubMed ID: 28620620
                SO-VID: 0468df5a-b8b7-4743-92de-4d037a70690e
                Copyright © Copyright © 2017 Nektaria Papadopoulou-Marketou et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 1 September 2016
                Date accepted : 3 April 2017
                Categories
                Subject: Research Article

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