The Predictive Role of the Biomarker Kidney Molecule-1 (KIM-1) in Acute Kidney Injury (AKI) Cisplatin-Induced Nephrotoxicity

Tănase, Daniela Maria; Gosav, Evelina Maria; Radu, Smaranda; Costea, Claudia Florida; Ciocoiu, Manuela; Cărăuleanu, Alexandru; Lǎcǎtusu, C.M.; Mărănducă, Minela Aida; Floria, Mariana; Rezuş, Ciprian

doi:10.3390/ijms20205238

Cited by 103 publications

(68 citation statements)

References 160 publications

(201 reference statements)

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“…Similar histopathologic changes have been reported in diabetic nephropathy and acute kidney injury (Chen et al, 2014;Yan et al, 2014). KIM-1 is a transmembrane glycoprotein whose extracellular segments can be shed, and the levels in urine are often detected in clinical or experimental studies to diagnose acute kidney injury or early kidney damage (Khreba et al, 2019;Tanase et al, 2019;Zhang et al, 2017). In this study, the signi cant increase of KIM-1 protein expression in serum and KIM-1 mRNA expression in kidney tissues were observed after PM 2.5 exposure in vivo experiment (Fig.2B-D).…”

Section: Discussionmentioning

confidence: 53%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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Abstract Background: Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro.Results: In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the concentrated PM2.5 (PM2.5) group and the filtered air (FA) group. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure activated the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, activation of P62 and beclin-1. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure. Conclusions: Taken together, our findings indicated that PM2.5-induced renal function impairment via the activation of the autophagic pathway in renal tubular epithelial cells.

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Section: Discussionmentioning

confidence: 53%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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“…Murine primary tubular epithelial cells (mTECs) were isolated from above described wt and Lcn-2 −/− mice as previously described [48,49]. In brief, after kidney removal, the tissue was minced and digested with a collagenase/dispase suspension.…”

Section: Isolation and Culture Of Murine Proximal Tubular Epithelial mentioning

confidence: 99%

Macrophage-Secreted Lipocalin-2 Promotes Regeneration of Injured Primary Murine Renal Tubular Epithelial Cells

Urbschat

Thiemens

Mertens

et al. 2020

IJMS

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Lipocalin-2 (Lcn-2) is rapidly upregulated in macrophages after renal tubular injury and acts as renoprotective and pro-regenerative agent. Lcn-2 possesses the ability to bind and transport iron with high affinity. Therefore, the present study focuses on the decisive role of the Lcn-2 iron-load for its pro-regenerative function. Primary mouse tubular epithelial cells were isolated from kidney tissue of wildtype mice and incubated with 5 µM Cisplatin for 24 h to induce injury. Bone marrow-derived macrophages of wildtype and Lcn-2−/− mice were isolated and polarized with IL-10 towards an anti-inflammatory, iron-release phenotype. Their supernatants as well as recombinant iron-loaded holo-Lcn-2 was used for stimulation of Cisplatin-injured tubular epithelial cells. Incubation of tubular epithelial cells with wildtype supernatants resulted in less damage and induced cellular proliferation, whereas in absence of Lcn-2 no protective effect was observed. Epithelial integrity as well as cellular proliferation showed a clear protection upon rescue experiments applying holo-Lcn-2. Notably, we detected a positive correlation between total iron amounts in tubular epithelial cells and cellular proliferation, which, in turn, reinforced the assumed link between availability of Lcn-2-bound iron and recovery. We hypothesize that macrophage-released Lcn-2-bound iron is provided to tubular epithelial cells during toxic cell damage, whereby injury is limited and recovery is favored.

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“…KIM-1 and NGAL had found to appear early in acute renal tubular injury. [22][23][24][25][26] Many researches had improved them as markers for injury in chronic kidney disease. 15,22,27,28 Urinary NGAL was a noninvasive biomarker of normoalbuminuria renal in type 2 diabetes.…”

Section: Discussionmentioning

confidence: 99%

<p>Evaluation of Urinary Neutrophil Gelatinase Associated Lipocalin and Kidney Injury Molecule-1 as Diagnostic Markers for Early Nephropathy in Patients with Type 2 Diabetes Mellitus</p>

Quang¹,

Nguyet²,

Thao³

et al. 2020

DMSO

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The purpose of this study was evaluating the early diagnostic value of two specific tubular markers neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) in diabetes nephropathy. Patients and Methods: Cross-sectional study was carried in three groups of patients from 10/2017 to 10/2018 in Military Hospital 103. Group I included 30 healthy peoples with estimated glomerular filtration rate (eGFR) >60 mL/min/1.73 m 2 and urine albumin creatinine ratio (uACR) <30 mg/g. Group II included 30 type 2 diabetic patients having uACR <30 mg/g, eGFR >60 mL/min/1.73 m 2. Group III included 30 type 2 diabetic patients having uACR >30 mg/g, eGFR >60 mL/min/1.73 m 2. Results: Urine KIM-1 and NGAL increased progressively from control group (57.29 ± 25.91 pg/mL; 25.71 ± 13.69 ng/mL) to the group of diabetic patients with uACR <30 mg/g (167.06 ± 44.01 pg/mL; 37.42 ± 10.89 ng/mL) and the group of diabetic patients with uACR ≥30 mg/g) (p < 0.05). There were moderate correlations between KIM-1 (r = 0.48, p < 0.05) and NGAL (r = 0.45, p < 0.05) with uACR. There was a mild correlation between KIM-1 and NGAL (r = 0.29, p < 0.05). KIM-1 and NGAL are the independent tests to detect diabetic nephropathy. The sensivity and specificity of KIM-1 with cutoff value of 174.95 pg/mL were 62.37% and 73.48%, respectively; the sensivity and specificity of NGAL with cutoff value of 35.2 ng/mL were 60.45% and 70.37%, respectively. Conclusion: KIM-1 and NGAL in urine are independent markers for early diagnostic diabetic nephropathy.

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The Predictive Role of the Biomarker Kidney Molecule-1 (KIM-1) in Acute Kidney Injury (AKI) Cisplatin-Induced Nephrotoxicity

Cited by 103 publications

References 160 publications

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Macrophage-Secreted Lipocalin-2 Promotes Regeneration of Injured Primary Murine Renal Tubular Epithelial Cells

<p>Evaluation of Urinary Neutrophil Gelatinase Associated Lipocalin and Kidney Injury Molecule-1 as Diagnostic Markers for Early Nephropathy in Patients with Type 2 Diabetes Mellitus</p>

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