NGAL, also called lipocalin 2 (LCN2), is the most evaluated candidate biomarker of kidney damage in the literature. It is a protein identified in the early 1990s, consisting of 178 amino acids and with a molecular weight of approximately 25 kDa. It belongs to the lipocalin family and is expressed not only by neutrophil granulocytes and their precursors but also by many tissues, including the liver, lungs, trachea, salivary glands, prostate, uterus, stomach, and, above all, renal tubular cells. All these tissues express NGAL in minimal amounts, but stimuli such as oxidative stress, acute phase with cytokine accumulation, infections, cancer, intoxication, and other conditions leading to cell necrosis, apoptosis, and death induce NGAL overexpression. Its main biological action is bacteriostatic through iron sequestration. During the early stages of AKI, NGAL is massively synthesized by cells in Henle’s loop and in the distal and collector tubules (renal NGAL pool); at the same time, AKI induces an increase in NGAL synthesis also in organs such as the liver and lungs (systemic NGAL pool) and, for this reason, in the early stages of AKI, NGAL increases both in the circulation and in the urine. Both clinical and experimental studies in animal models and in human cells in vitro have unequivocally demonstrated that, just 3–6 h after the onset of ischemia or anoxia, tubule cells express amounts of NGAL increased by approximately 10-fold from the base line. Unfortunately, NGAL is affected by some issues that have so far limited its use in clinical practice. First, NGAL is a protein expressed by various tissues and organs, as highlighted above, and, therefore, can increase in circulation even in many extrarenal pathologies. Clinical pictures such as systemic infections and sepsis are associated with increased NGAL due to hyperactivity of neutrophil granulocytes. Moreover, “noxae” of the tubule, such as ischemia, anoxia, oxidative stress, etc., cause not only the increased synthesis of NGAL by tubular cells but also the recall of inflammatory cells and, more specifically, of neutrophil polymorphonucleates, which, in turn, express NGAL. Therefore, the amount of NGAL detectable in the tubular interstitium, and, thus, also in the urine, derives from both the tubule and the neutrophils. There are three molecular isoforms of NGAL: monomers (MW ≅ 25 kDa), dimers formed by the binding of two monomers (MW ≅ 45 kDa), and heterodimers formed by the binding of a monomer to neutrophil matrix metalloproteinase-9 or gelatinase (NGAL-MMP-9, MW ≅ 135 kDa). Monomers and dimers are expressed and released by neutrophils, whereas monomers and heterodimers are isoforms expressed and released by renal tubule cells. It follows that a heterodimer can be considered tubule-specific, and its presence in the urine or in the circulation identifies release by tubular cells, excluding the share of NGAL from neutrophils or other cell types or tis sues. Since 2010, automated methods for the determination of NGAL also in urine have been developed, which allow the test to be introduced in clinical laboratories on an urgent/emergency basis. Unfortunately, these methods use mixtures of antibodies that recognize the epitopes common to the three isoforms, and this prevents the differentiation of the isoform corresponding to the heterodimer. In a restricted population of healthy adult subjects (n = 174), the 95th percentile urinary NGAL concentration was 107 μg/L; distinguishing the population into men (n = 100) and women (n = 74), the 95th per centile was 91 and 129 μg/L, respectively. To reduce intra- and interindividual variability, it is recommended to express NGAL in urine in relation to creatininuria.

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قسم الصيانة ينفذ أعمال إدامة لإحدى المدارس في محافظة النجف الأشرف

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كيف يمكن لعادات القيادة السيئة أن تؤثر على قيمة سيارتك

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هكذا يسرق "قراصنة الذكاء الاصطناعي" المليارات بطرق بسيطة

فيديو لانفجار كرة نارية في سماء اليابان.. ما تفسير ذلك؟

المزيد

مواضيع ذات صلة

Biomarkers of Tubulo-Interstitial Injury

Low-Molecular-Weight Plasma Proteins

Immunofluorescence Assay (IFA)

Enzyme-Linked Fluorescent Assay (ELFA)

Diagnostic Evaluation of Lyme disease

red blood cell count (RBC count, Erythrocyte count)

rabies-neutralizing antibody test

prothrombin time (PT, Protime, International normalized ratio [INR])

Estimation of the Glomerular Filtration Rate by Equations

Creatinine test for Diagnosis of Kidney Diseases

Urea test for Diagnosis of Kidney Diseases

Standard Urine Test for Diagnosis of Kidney Diseases