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Prospective Study on Several Urinary Biomarkers as Indicators of Renal Damage in Children with CAKUT
Fabio Bartoli1, Valentina Pastore1, Isabella Calè2
1Pediatric Surgery Unit, University of Foggia, Foggia, Italy.
Insights
Children with congenital anomalies of kidney and urinary tract (CAKUT) show increased urinary monocyte chemotactic protein-1 (MCP-1), indicating chronic inflammation and poor kidney regeneration. This suggests a higher risk of progressive renal damage in these patients.
Area of Science:
- Pediatric Nephrology
- Urology
- Biomarker Discovery
Background:
- Congenital anomalies of the kidney and urinary tract (CAKUT) are a leading cause of chronic kidney disease in children.
- Children with CAKUT are at risk for glomerular hyperfiltration syndrome and progressive renal damage.
- Early identification of disease progression markers is crucial for timely intervention.
Purpose of the Study:
- To investigate urinary levels of monocyte chemotactic protein-1 (MCP-1), epidermal growth factor (EGF), β-2-microglobulin (β2M), and FAS-ligand (FAS-L) in children with CAKUT.
- To assess the potential of these biomarkers in predicting renal damage and regenerative response in CAKUT patients.
- To evaluate the diagnostic utility of urinary EGF/MCP-1 and EGF/β2M ratios.
Main Methods:
- A prospective, multicentric study enrolled 80 children with various CAKUT conditions (hypodysplasia, agenesis, multicystic kidney, post-nephrectomy).
- Urine samples were analyzed using enzyme-linked immunosorbent assay (ELISA) for MCP-1, EGF, β2M, and FAS-L.
- Urinary ratios of EGF/MCP-1 and EGF/β2M were calculated and compared to 30 healthy controls.
Main Results:
- Urinary MCP-1 levels were significantly overexpressed in all CAKUT patient groups compared to controls.
- Both urinary EGF/MCP-1 and EGF/β2M ratios were significantly downregulated in CAKUT patients, indicating reduced regenerative capacity and increased tubular damage.
- FAS-L levels were not explicitly detailed in the abstract's results summary.
Conclusions:
- Elevated urinary MCP-1 suggests chronic renal inflammation mediated by monocytes is a key factor in CAKUT progression.
- Downregulated EGF/MCP-1 and EGF/β2M ratios indicate a poor regenerative response and ongoing tubular damage in children with CAKUT.
- These findings support the hypothesis that CAKUT patients are susceptible to progressive renal damage and underscore the need for monitoring inflammatory and regenerative markers.
Purpose:
The aim of the study was to investigate urinary levels of monocyte chemotactic protein-1 (MCP-1), epidermal growth factor (EGF), β-2-microglobulin (β2M), and FAS-ligand (FAS-L) in children with congenital anomalies of kidney and urinary tract (CAKUT) disease at risk of developing glomerular hyperfiltration syndrome. For this reason, we selected patients with multicystic kidney, renal agenesia and renal hypodysplasia, or underwent single nephrectomy.
Materials And Methods:
This prospective, multicentric study was conducted in collaboration between the Pediatric Surgery Unit in Foggia and the Pediatric Nephrology Unit in Bari, Italy. We enrolled 80 children with CAKUT (40 hypodysplasia, 22 agenetic; 10 multicystic; 8 nephrectomy) who underwent extensive urological and nephrological workup. Exclusion criteria were recent urinary tract infections or pyelonephritis, age > 14 years, presence of systemic disease, or hypertension. A single urine sample was collected in a noninvasive way and processed for measuring by enzyme-linked immunosorbent assay urine levels of MCP-1, EGF, β2M, and FAS-L. As control, urine samples were taken from 30 healthy children.Furthermore, we evaluated the urinary ratios uEGF/uMCP-1 (indicator of regenerative vs inflammatory response) and uEGF/uβ2M (indicator of regenerative response vs. tubular damage).
Results:
These results suggest that urinary levels of MCP-1 are overexpressed in CAKUT patients. Furthermore, our findings clearly demonstrated that both uEGF/uMCP-1 and uEGF/uβ2M ratios were significantly downregulated in all patient groups when compared with the control group.
Conclusion:
These findings further support that CAKUT patients may, eventually, experience progressive renal damage and poor regenerative response. The increased urinary levels of MCP-1 in all groups of CAKUT patients suggested that the main factor responsible for the above effects is chronic renal inflammation mediated by local monocytes.
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