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Association Between Multicystic Dysplastic Kidney and the Local Renin-Angiotensin-Aldosterone System: A Pilot Study
Shingo Ishimori1, Shinya Ishiko2, Junya Fujimura3
1Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan.
Insights
Local renin-angiotensin-aldosterone system (RAAS) activation may be linked to persistent multicystic dysplastic kidney (MCDK) in children. Higher urinary angiotensinogen (AGT) levels were observed in children with residual MCDK, suggesting a potential role in disease persistence.
Area of Science:
- Pediatric nephrology
- Renal physiology
- Biomarker research
Background:
- Multicystic dysplastic kidney (MCDK) is a congenital kidney malformation.
- The natural history of MCDK can involve persistence or spontaneous regression.
- The role of local renin-angiotensin-aldosterone system (RAAS) activity in MCDK progression is not well understood.
Purpose of the Study:
- To investigate the association between local RAAS activity and the clinical course of multicystic dysplastic kidney (MCDK) in children.
- To evaluate urinary angiotensinogen (AGT) as a biomarker for local RAAS activity in the kidney.
Main Methods:
- A multicentre, cross-sectional study involving children with unilateral MCDK, solitary kidneys, and age/sex-matched controls.
- Urinary angiotensinogen (AGT) to creatinine ratio was measured as a marker of intrarenal RAAS activity.
- Comparison of urinary AGT levels across different kidney conditions.
Main Results:
- Children with persistent MCDK showed significantly higher urinary AGT/creatinine ratios compared to those with regressed MCDK, solitary kidneys, or controls.
- Hypertension was present in children with residual or regressed MCDK.
- Urinary AGT/creatinine was a significant independent predictor of MCDK regression.
Conclusions:
- Local RAAS activation may be associated with the persistence of MCDK in children.
- The study design does not allow for causal inference regarding RAAS activation and MCDK pathogenesis.
- Further research is needed to determine if RAAS activation contributes to MCDK development or if AGT is secreted by the dysplastic kidney itself.
Aim:
To examine the relationship between children with multicystic dysplastic kidney (MCDK) that persists or spontaneously regresses over time and local renin-angiotensin-aldosterone system (RAAS) activity in children.
Methods:
We conducted a multicentre, cross-sectional study of patients who were diagnosed with unilateral MCDK or a solitary kidney. The controls were age- and sex-matched children who underwent evaluation for short stature without any clinical kidney symptoms. We evaluated urinary angiotensinogen (AGT) as a biomarker of local RAAS activity, which acts specifically within the kidneys and differs from systemic RAAS.
Results:
We included 52 children who were divided into the following four groups: 11 children with residual MCDK (MCDK persisted), 11 with regressed MCDK (MCDK spontaneously regressed), 12 with a solitary kidney and 18 were controls. Hypertension was identified in six patients, all of whom were in the residual or regressed MCDK groups. The urinary AGT/creatinine ratio was significantly higher in children in the residual MCDK group than in those in the regressed MCDK, solitary and control groups (p = 0.02, p < 0.01, p < 0.01, respectively). A logistic regression model showed that the only significant independent factor for regression of MCDK was urinary AGT/creatinine (odds ratio: 16.0, p < 0.01).
Conclusion:
Our data suggest that local RAAS activation could be associated with persistence of MCDK, but causality cannot be inferred because of the cross-sectional study design. Whether RAAS activation in residual MCDK is involved in the pathogenesis of MCDK or AGT is secreted from the MCDK kidney itself remains unknown.
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