Early diagnosis of acute kidney injury by urinary YKL-40 in critically ill patients in ICU: a pilot study

Albeltagy, Eman Salah; Abdul-Mohymen, Abeer Mohammed; Taha, Doaa Refaat Amin

doi:10.1007/s11255-019-02364-2

Cited by 7 publications

(7 citation statements)

References 21 publications

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“…In this multicenter validation study, we found that uCHI3L1 was markedly increased in general ICU patients who developed AKI stage 2 or 3 within a 24-h [15]. This study and previous studies on uCHI3L1 have demonstrated its use as a biomarker for diagnosis of AKI, and this with comparable performance to uNGAL and NephroCheck Risk® [8,9,[17][18][19]. CHI3L1 may also provide mechanistic insights in injury and repair mechanisms in the kidney.…”

Section: Discussionmentioning

confidence: 51%

Urinary cell cycle arrest biomarkers and chitinase 3-like protein 1 (CHI3L1) to detect acute kidney injury in the critically ill: a post hoc laboratory analysis on the FINNAKI cohort

et al. 2020

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Background: Acute kidney injury (AKI) is a frequently occurring syndrome in critically ill patients and is associated with worse outcomes. Biomarkers allow early identification and therapy of AKI which may improve outcomes. Urine chitinase 3-like protein 1 (uCHI3L1) was recently identified as a promising urinary biomarker for AKI. In this multicenter study, we evaluated the diagnostic performance for AKI stage 2 or greater of uCHI3L1 in comparison with the urinary cell cycle arrest biomarkers urinary tissue inhibitor of metalloproteinases-2 (TIMP-2)•insulin-like growth factor-binding protein 7 (IGFBP7) measured by NephroCheck Risk®. Methods: Post hoc laboratory study of the prospective observational FINNAKI study. Of this cohort, we included patients with stored admission urine samples and availability of serum creatinine at day 1 of admission. Patients who already had AKI stage 2 or 3 at ICU admission were excluded. AKI was defined and staged according to the KDIGO definition and staging system. The primary endpoint was AKI stage 2 or 3 at day 1. Biomarker performance was assessed by the area under the curve of the receiver operating characteristic curve (AUC). We assessed individual performance and different combinations of urine biomarkers. Results: Of 660 included patients, 49 (7.4%) had AKI stages 2-3 at day 1. All urine biomarkers were increased at admission in AKI patients. All biomarkers and most combinations had AUCs < 0.700. The combination uCHI3L1•TIMP-2 was best with a fair AUC of 0.706 (0.670, 0.718). uCHI3L1 had a positive likelihood ratio (LR) of 2.25 which was comparable to that of the NephroCheck Risk® cutoff of 2.0, while the negative LR of 0.53 was comparable to that of the NephroCheck Risk® cutoff of 0.3.

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Section: Discussionmentioning

confidence: 51%

Urinary cell cycle arrest biomarkers and chitinase 3-like protein 1 (CHI3L1) to detect acute kidney injury in the critically ill: a post hoc laboratory analysis on the FINNAKI cohort

et al. 2020

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“…In previous work in kidney disease models, a urinary proteomic study has shown that chitinases-like proteins could be candidate biomarkers for S-AKI 65 . Recently, it has been demonstrated to be largely increased in urine from clinical AKI patients 66 . Another study also showed renal Chil3 to be up-regulated at 6…”

Section: Discovery-based Studies Recapitulate Signature Proteins For mentioning

confidence: 99%

Global Proteome and Phosphoproteome Characterization of Sepsis-induced Kidney Injury

Lin

Platt

et al. 2020

Molecular & Cellular Proteomics

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Sepsis-induced acute kidney injury (S-AKI) is the most common complication in hospitalized and critically ill patients, highlighted by a rapid decline of kidney function occurring a few hours or days after sepsis onset. Systemic inflammation elicited by microbial infections is believed to lead to kidney damage under immunocompromised conditions. However, while AKI has been recognized as a disease with long-term sequelae, partly due to the associated higher risk of chronic kidney disease (CKD), the understanding of kidney pathophysiology at the molecular level and the global view of dynamic regulations in situ after S-AKI, including the transition to CKD, remains limited. Existing studies of S-AKI mainly focus on deriving sepsis biomarkers from body fluids. In the present study, we constructed a mid-severity septic murine model using cecal ligation and puncture (CLP), and examined the temporal changes to the kidney proteome and phosphoproteome at day 2 and day 7 after CLP surgery, corresponding to S-AKI and the transition to CKD, respectively, by employing an ultrafast and economical filter-based sample processing method combined with the label-free quantitation approach. Collectively, we identified 2,119 proteins and 2,950 phosphosites through multi-proteomics analyses. Among them, we identified an array of highly promising candidate marker proteins indicative of disease onset and progression accompanied by immunoblot validations, and further denoted the pathways that are specifically responsive to S-AKI and its transition to CKD, which include regulation of cell metabolism regulation, oxidative stress, and energy consumption in the diseased kidneys. Our data can serve as an enriched resource for the identification of mechanisms and biomarkers for sepsis-induced kidney diseases.

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“…Elevated YKL-40 concentrations have been observed in numerous inflammatory conditions, most notably asthma, chronic obstructive pulmonary disease (COPD), sepsis, diabetes mellitus (DM), acute pancreatitis (AP), chronic pancreatitis (CP), acute and chronic liver diseases, IBD, acute kidney injury (AKI), CKD, RA, Alzheimer disease (AD), multiple sclerosis (MS), and coronary artery disease (CAD). Higher serum concentrations of YKL-40 are associated with severe forms of the inflammatory diseases and consequently poorer prognosis, implicating its potential role as a biological marker in the prediction of the inflammatory response severity ( 37 , 45 - 57 ). Results of recent human studies in patients and healthy controls are presented in Figure 2 .…”

Section: Laboratory Methods and Measurement Of Ykl-40mentioning

confidence: 99%

“…Two times increased YKL-40 concentrations were identified both in urine and plasma of the patients with AKI compared with controls, predominantly referring to hospitalized patients or those with preexisting CKD. Plasma YKL-40 concentration was in the linear correlation to the severity of AKI and proinflammatory markers, with a cut-off concentration > 142 µg/L being predictor of adverse outcomes and mortality ( 37 , 91 ). In patients developing AKI as a consequence of an acute hantavirus infection, elevated plasma concentrations of YKL-40 (32 µg/L (3-213 µg/L)) persisted for a year after the hospitalization, possibly due to prolonged endothelial dysfunction (ED) after hantavirus induced vasculitis ( 91 ).…”

Section: Urinary Systemmentioning

confidence: 98%

YKL-40 as a biomarker in various inflammatory diseases: A review

Hrabar,

Bakula,

Vrkljan

et al. 2023

Biochem. med. (Online)

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YKL-40 or Chitinase-3-Like Protein 1 (CHI3L1) is a highly conserved glycoprotein that binds heparin and chitin in a non-enzymatic manner. It is a member of the chitinase protein family 18, subfamily A, and unlike true chitinases, YKL-40 is a chitinase-like protein without enzymatic activity for chitin. Although its accurate function is yet unknown, the pattern of its expression in the normal and disease states suggests its possible engagement in apoptosis, inflammation and remodeling or degradation of the extracellular matrix. During an inflammatory response, YKL-40 is involved in a complicated interaction between host and bacteria, both promoting and attenuating immune response and potentially being served as an autoantigen in a vicious circle of autoimmunity. Based on its pathophysiology and mechanism of action, the aim of this review was to summarize research on the growing role of YKL-40 as a persuasive biomarker for inflammatory diseases’ early diagnosis, prediction and follow-up (e.g., cardiovascular, gastrointestinal, endocrinological, immunological, musculoskeletal, neurological, respiratory, urinary, infectious) with detailed structural and functional background of YKL-40.

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Early diagnosis of acute kidney injury by urinary YKL-40 in critically ill patients in ICU: a pilot study

Cited by 7 publications

References 21 publications

Urinary cell cycle arrest biomarkers and chitinase 3-like protein 1 (CHI3L1) to detect acute kidney injury in the critically ill: a post hoc laboratory analysis on the FINNAKI cohort

Urinary cell cycle arrest biomarkers and chitinase 3-like protein 1 (CHI3L1) to detect acute kidney injury in the critically ill: a post hoc laboratory analysis on the FINNAKI cohort

Global Proteome and Phosphoproteome Characterization of Sepsis-induced Kidney Injury

YKL-40 as a biomarker in various inflammatory diseases: A review

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