Performance of urinary kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, and N-acetyl-β-D-glucosaminidase to predict chronic kidney disease progression and adverse outcomes

Abstract

Urinary biomarkers can predict the progression of chronic kidney disease (CKD). In this study, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and N-acetyl-β-D-glucosaminidase (NAG) were correlated with the stages of CKD, and the association of these biomarkers with CKD progression and adverse outcomes was determined. A total of 250 patients, including 111 on hemodialysis, were studied. Urinary KIM-1, NGAL, and NAG were measured at baseline. Patients not on dialysis at baseline who progressed to a worse CKD stage were compared with those who did not progress. The association of each biomarker and selected covariates with progression to more advanced stages of CKD, end-stage kidney disease, or death was evaluated by Poisson regression. NGAL was moderately correlated (rs=0.467, P<0.001) with the five stages of CKD; KIM-1 and NAG were also correlated, but weakly. Sixty-four patients (46%) progressed to a more advanced stage of CKD. Compared to non-progressors, those patients exhibited a trend to higher levels of KIM-1 (P=0.064) and NGAL (P=0.065). In patients not on dialysis at baseline, NGAL was independently associated with progression of CKD, ESKD, or death (RR=1.022 for 300 ng/mL intervals; CI=1.007-1.037, P=0.004). In patients on dialysis, for each 300-ng/mL increase in urinary NGAL, there was a 1.3% increase in the risk of death (P=0.039). In conclusion, urinary NGAL was associated with adverse renal outcomes and increased risk of death in this cohort. If baseline urinary KIM-1 and NGAL predict progression to worse stages of CKD is something yet to be explored.

Urinary Kidney Injury Molecule 1 (U-KIM-1) as a Predictor of Lupus Nephritis

“…Lobato et al, study detected a trend toward increased baseline levels of KIM-1 and NGAL in patients with renal impairment who progressed to more advanced stages of CKD [40] . Therefore elevations in U Kim-1 levels are not specific to nephritis in SLE; However,this does not detract from a potentially valuable role for Kim-1 in lupus patients as suggested by the results of our study, in the initial diagnosis of kidney involvement, or in subsequent monitoring of disease activity.…”

Peer Review #2 of "Metabolomic and biochemical characterization of a new model of the transition of acute kidney injury to chronic kidney disease induced by folic acid (v0.2)"

“…Other proteins including kidney injury molecule-1 (KIM-1), neutrophil gelatinase associated with lipocalin (NGAL) and cystatin C (Cys-C) also have a major impact on the development of kidney disease. KIM-1, NGAL and Cys-C were originally proposed as markers of AKI, but recently have been used to describe the evolution of CKD (Gil et al 2016;Lobato et al 2017). In addition, the omics sciences allow us to evaluate globally the different molecules of a family, rather than a single protein or metabolite, in such a way that the physiological state of an organism can be described by the presence or absence of these molecules (Amaro et al 2016).…”

Clinical Factors and Anticoagulation Level That Determine the Sudden Loss of Kidney Function in Patients Long-Taking Warfarin (A 5-Year Prospective, Observational Study)

“…Все это обусловливает актив-ный интерес к биомаркерам раннего поврежде-ния почки, которые отвечали бы требованиям высокой чувствительности и специфичности, будучи при этом простыми и неивазивными. Среди новых биомаркеров активно изучаются ассиметричный диметиларгинин, симметрич-ный диметиларгинин, уромодулин, молекула повреждения почки-1, липокалин, ассоцииро-ванный с нейтрофильной желатиназой [7][8][9][10][11][12][13][14][15]. Все они в наибольшей степени изучены как пре-дикторы острого почечного повреждения (ОПП).…”

“…Перспективным в отношении оценки про-грессирования ХБП также кажется липокалин, ассоциированный с нейтрофильной желатина-зой. Повышение его уровня в результате ише-мии-реперфузии канальцев позволяет говорить о нем как о высокоспецифичном маркере ОПП в результате острых соматических катастроф, так и о маркере развития контраст-индуциро-ванной нефропатии [14,15]. Этот биомаркер легко секретируется с мочой, при этом его появление в моче ассоциировано с поврежде-нием именно проксимальных канальцев.…”

“…Этот биомаркер легко секретируется с мочой, при этом его появление в моче ассоциировано с поврежде-нием именно проксимальных канальцев. Ряд исследований говорят о возможности исполь-зования мочевого липокалина, ассоциирован-ного с нейтрофильной желатиназой, как мар-кера ухудшения функции почек по сравнению со стабильной ХБП [14,15].…”