Fractional Excretion of Survivin, Extracellular Matrix Metalloproteinase Inducer, and Matrix Metalloproteinase 7 in Children with Chronic Kidney Disease - European Medical Journal

Fractional Excretion of Survivin, Extracellular Matrix Metalloproteinase Inducer, and Matrix Metalloproteinase 7 in Children with Chronic Kidney Disease

Nephrology
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Authors:
Agnieszka Bargenda, *Kinga Musiał, Danuta Zwolińska
Disclosure:

The authors have declared no conflicts of interest.

Received:
11.01.16
Accepted:
24.05.16
Citation:
EMJ Nephrol. ;4[1]:113-119. DOI/10.33590/emjnephrol/10311462. https://doi.org/10.33590/emjnephrol/10311462.
Keywords:
Epithelial–mesenchymal transition (EMT), fibrosis, tubular damage, E-cadherin, transforming growth factor beta 1 (TGF-β1)

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.

Abstract

Background: Epithelial–mesenchymal transition (EMT) is defined as a transformation of tubular epithelial cells into mesenchymal ones. These cells migrate through the extracellular matrix and change into active myofibroblasts, which are responsible for excessive matrix deposition. Such changes may lead to tubular dysfunction and fibrosis of the renal parenchyma, characteristic of chronic kidney disease (CKD). However, there are no data on potential EMT markers in children with CKD. The aim of our study was to assess the usefulness of fractional excretion (FE) of survivin, E-cadherin, extracellular matrix metalloproteinase inducer (EMMPRIN), matrix metalloproteinase (MMP)7, and transforming growth factor beta 1 (TGF-β1) as potential markers of CKD-related complications such as tubular damage and fibrosis.

Methods: Forty-one pre-dialysis children with CKD Stages 3–5 and 23 age-matched controls were enrolled in the study. The serum and urine concentrations of analysed parameters were assessed by an enzyme-linked immunosorbent assay test.

Results: Tubular reabsorption of all analysed parameters was >99% in the control group. All FE values rose significantly in children with CKD, yet they remained <1% in the case of E-cadherin and TGF-β1. The highest FE values in CKD children were those of survivin, EMMPRIN, and MMP7: >1%.

Conclusions: FE of the examined markers may become a useful tool in the assessment of tubular dysfunction during the course of CKD. The FE of survivin, EMMPRIN, and MMP7 warrant further research as potential independent markers of kidney-specific EMT.

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