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ATP5B and ETFB metabolic markers in children with congenital hydronephrosis
Qi Zhao1, Yi Yang1, Changlin Wang1
1Department of Pediatric Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Insights
Congenital obstructive nephropathy in children involves mitochondrial dysfunction. Increased levels of β-F1-ATPase (ATP5B) and electron transfer flavoprotein β subunit (ETFB) indicate worsening kidney injury and may serve as novel biomarkers.
Area of Science:
- Pediatric Nephrology
- Mitochondrial Biology
- Biomarker Discovery
Background:
- Congenital obstructive nephropathy is a leading cause of pediatric chronic renal failure.
- Mitochondrial energy metabolism disorders are implicated in tubular cell apoptosis in hydronephrosis.
- ATP5B and ETFB are key metabolic markers in mitochondrial energy pathways.
Purpose of the Study:
- To investigate the presence and expression of ATP5B and ETFB in pediatric hydronephrotic kidneys.
- To determine the association between ATP5B and ETFB levels and hydronephrosis progression.
- To evaluate ATP5B and ETFB as potential diagnostic markers for hydronephrosis.
Main Methods:
- Comparative analysis of gene and protein expression using reverse transcription-quantitative polymerase chain reaction and immunoblotting.
- Study cohort included 20 children with severe hydronephrosis (grades III-IV) and 20 controls (nephroblastoma patients).
- Correlation and receiver-operator curve analyses were employed to assess marker association with renal function.
Main Results:
- Gene and protein expression of ATP5B and ETFB were significantly upregulated in hydronephrotic kidneys compared to controls.
- Higher protein levels of ATP5B and ETFB correlated negatively with split renal function (SRF), indicating poorer kidney function.
- ETFB protein demonstrated diagnostic potential for identifying hydronephrosis with abnormal SRF (<45%).
Conclusions:
- Elevated ATP5B and ETFB levels are associated with increased renal injury in pediatric hydronephrosis.
- ATP5B and ETFB represent promising novel biomarkers for hydronephrosis.
- Further research is warranted to validate ATP5B and ETFB as clinical markers for hydronephrosis.
Abstract:
Congenital obstructive nephropathy is the primary cause of chronic renal failure in children. Disorders of mitochondrial energy metabolism may be a primary factor underlying tubular cell apoptosis in hydronephrosis. The β-F1-ATPase (ATP5B) and electron transfer flavoprotein β subunit (ETFB) metabolic markers are involved in mitochondrial energy metabolism in other diseases. The aim of the present study was to evaluate whether ATP5B and ETFB are represented in the hydronephrotic kidney, and whether they are associated with the progression of hydronephrosis. The cohort examined consisted of 20 children with hydronephrosis, graded III and IV using the Society for Fetal Urology grading system, and a control group consisting of 20 patients with nephroblastoma. Reverse transcription‑quantitative polymerase chain reaction and immunoblot analyses were used to investigate the differential expression of genes and proteins in the two groups. The gene and protein expression levels of ATP5B and ETFB were upregulated in the hydronephrosis group. Correlation analyses revealed negative correlations between ATP5B, ETFB protein and split renal function (SRF). Receiver‑operator curve analysis found a diagnostic profile of the ETFB protein in identifying children with hydronephrosis with abnormal SRF (<45%). These results suggested that increasing levels of ATP5B and ETFB were associated with worsening renal injury. ATP5B and ETFB may be novel markers in hydronephrosis and require further detailed investigation.
