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Updated: Oct 7, 2025

Use of Ultra-high Field MRI in Small Rodent Models of Polycystic Kidney Disease for In Vivo Phenotyping and Drug Monitoring
Published on: June 23, 2015
Is autosomal dominant polycystic kidney disease an early sweet disease?
Angélique Dachy1,2,3, Jean-Paul Decuypere1, Rudi Vennekens4
1PKD Research Group, GPURE, Department of Development and Regeneration, KU Leuven, Leuven, Belgium.
Insights
Autosomal dominant polycystic kidney disease (ADPKD) may be worsened by obesity. This review explores glucose metabolism
Area of Science:
- Nephrology
- Metabolic Disorders
- Pediatric Research
Background:
- Autosomal dominant polycystic kidney disease (ADPKD) has early childhood onset.
- Overweight and obesity are linked to faster ADPKD progression in adults.
- Metabolic reprogramming and glucose metabolism defects are implicated in ADPKD.
Purpose of the Study:
- To review the role of glucose metabolism in ADPKD pathophysiology.
- To highlight the risks of overweight and obesity in ADPKD, particularly in children.
- To discuss potential metabolic therapeutic targets for ADPKD.
Main Methods:
- Literature review of studies on ADPKD, glucose metabolism, and obesity.
- Analysis of current and emerging metabolic interventions for ADPKD.
- Examination of pediatric obesity trends and their implications for ADPKD.
Main Results:
- Accumulating evidence supports early nephron-protective strategies and lifestyle changes for ADPKD.
- Defective glucose metabolism pathways are potential therapeutic targets in ADPKD.
- Childhood obesity crisis presents risks for pediatric ADPKD patients' cardiovascular and renal health.
Conclusions:
- Understanding glucose metabolism is crucial for managing ADPKD.
- Overweight and obesity pose significant risks to ADPKD prognosis, especially long-term cardiovascular and renal outcomes.
- Further research is needed on metabolic interventions for pediatric ADPKD.
Abstract:
The clinical course of autosomal dominant polycystic kidney disease (ADPKD) starts in childhood. Evidence of the beneficial impact of early nephron-protective strategies and lifestyle modifications on ADPKD prognosis is accumulating. Recent studies have described the association of overweight and obesity with rapid disease progression in adults with ADPKD. Moreover, defective glucose metabolism and metabolic reprogramming have been reported in distinct ADPKD models highlighting these pathways as potential therapeutic targets in ADPKD. Several "metabolic" approaches are currently under evaluation in adults, including ketogenic diet, food restriction, and metformin therapy. No data are available on the impact of these approaches in childhood thus far. Yet, according to World Health Organization (WHO), we are currently facing a childhood obesity crisis with an increased prevalence of overweight/obesity in the pediatric population associated with a cardio-metabolic risk profile. The present review summarizes the knowledge about the role of glucose metabolism in the pathophysiology of ADPKD and underscores the possible harm of overweight and obesity in ADPKD especially in terms of long-term cardiovascular outcomes and renal prognosis.
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