Neutrophil Gelatinase–Associated Lipocalin (NGAL) as a Marker of Kidney Damage

脂质运载蛋白 医学 肾病科 肾脏疾病 急性肾损伤 中性粒细胞明胶酶相关脂蛋白 多囊肾病 泌尿系统 内科学 免疫学 生物信息学 生物
作者
Davide Bolignano,Valentina Donato,Giuseppe Coppolino,Susanna Campo,Antoine Buemi,Antonio Lacquaniti,Michele Buemi
出处
期刊:American Journal of Kidney Diseases [Elsevier BV]
卷期号:52 (3): 595-605 被引量:564
标识
DOI:10.1053/j.ajkd.2008.01.020
摘要

Neutrophil gelatinase–associated lipocalin (NGAL) is a protein belonging to the lipocalin superfamily initially found in activated neutrophils, in accordance with its role as an innate antibacterial factor. However, it subsequently was shown that many other types of cells, including in the kidney tubule, may produce NGAL in response to various injuries. The increase in NGAL production and release from tubular cells after harmful stimuli of various kinds may have self-defensive intent based on the activation of specific iron-dependent pathways, which in all probability also represent the mechanism through which NGAL promotes kidney growth and differentiation. NGAL levels predict the future appearance of acute kidney injury after treatments potentially detrimental to the kidney and even the acute worsening of unstable nephropathies. Furthermore, recent evidence also suggests that NGAL somehow may be involved in the pathophysiological process of chronic renal diseases, such as polycystic kidney disease and glomerulonephritis. NGAL levels clearly correlate with severity of renal impairment, probably expressing the degree of active damage underlying the chronic condition. For all these reasons, NGAL may become one of the most promising next-generation biomarkers in clinical nephrology and beyond. Neutrophil gelatinase–associated lipocalin (NGAL) is a protein belonging to the lipocalin superfamily initially found in activated neutrophils, in accordance with its role as an innate antibacterial factor. However, it subsequently was shown that many other types of cells, including in the kidney tubule, may produce NGAL in response to various injuries. The increase in NGAL production and release from tubular cells after harmful stimuli of various kinds may have self-defensive intent based on the activation of specific iron-dependent pathways, which in all probability also represent the mechanism through which NGAL promotes kidney growth and differentiation. NGAL levels predict the future appearance of acute kidney injury after treatments potentially detrimental to the kidney and even the acute worsening of unstable nephropathies. Furthermore, recent evidence also suggests that NGAL somehow may be involved in the pathophysiological process of chronic renal diseases, such as polycystic kidney disease and glomerulonephritis. NGAL levels clearly correlate with severity of renal impairment, probably expressing the degree of active damage underlying the chronic condition. For all these reasons, NGAL may become one of the most promising next-generation biomarkers in clinical nephrology and beyond. NGAL in Acute Kidney Injury: From Serendipity to UtilityAmerican Journal of Kidney DiseasesVol. 52Issue 3PreviewThe incidence of acute kidney injury (AKI) has reached epidemic proportions, affecting an estimated 7% of hospitalized patients, in whom it is an independent predictor of mortality and morbidity.1,2 In the critical care setting, the prevalence of AKI requiring dialysis is about 6%, with a mortality rate exceeding 60%.3 Once established, the treatment of AKI is largely supportive, at an annual cost surpassing $8 billion in the United States alone.4 The diagnosis currently depends on detection of reduced kidney function by the rise in serum creatinine concentration, which is a woefully inadequate measure in the acute setting for a multitude of reasons. Full-Text PDF
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