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.

Nephrology (Carlton, Vic.)
|September 30, 2025
PubMed

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.
Abstract

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