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Treatment of Pediatric Chronic Kidney Disease-Mineral and Bone Disorder
Mark R Hanudel1,2, Isidro B Salusky3
1Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. mhanudel@mednet.ucla.edu.
Insights
Chronic kidney disease-mineral and bone disorder (CKD-MBD) in children can cause skeletal problems and cardiovascular issues. Early management of fibroblast growth factor 23 (FGF23) and mineral imbalances is crucial for pediatric CKD patients.
Area of Science:
- Nephrology
- Pediatric Endocrinology
- Skeletal Biology
Background:
- Chronic kidney disease-mineral and bone disorder (CKD-MBD) significantly impacts pediatric patients, leading to fractures, growth impairment, and skeletal deformities.
- Extra-skeletal calcification and cardiovascular complications are serious consequences of CKD-MBD in children.
- Elevated fibroblast growth factor 23 (FGF23) levels are recognized as a primary driver in the pathogenesis of CKD-MBD.
Purpose of the Study:
- To review the pathogenesis and current treatment strategies for CKD-MBD in pediatric populations.
- To highlight the importance of addressing mineral and bone metabolism disorders in children with CKD.
- To discuss the role of FGF23 in CKD-MBD and emerging therapeutic targets.
Main Methods:
- Literature review of pathogenesis and treatment of CKD-MBD.
- Focus on pediatric CKD patient populations.
- Analysis of the role of FGF23 and mineral imbalances.
Main Results:
- CKD-MBD in children leads to significant skeletal and cardiovascular complications.
- Early elevation of FGF23 is a key factor in disease development.
- Current treatments focus on managing hyperphosphatemia and secondary hyperparathyroidism.
Conclusions:
- CKD-MBD is a systemic disorder requiring specialized pediatric care.
- Optimizing skeletal health, growth, and preventing cardiovascular disease are primary treatment goals.
- Further research into FGF23 reduction therapies is ongoing and promising.
Purpose Of Review:
In this paper, we review the pathogenesis and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD), especially as it relates to pediatric CKD patients.
Recent Findings:
Disordered regulation of bone and mineral metabolism in CKD may result in fractures, skeletal deformities, and poor growth, which is especially relevant for pediatric CKD patients. Moreover, CKD-MBD may result in extra-skeletal calcification and cardiovascular morbidity. Early increases in fibroblast growth factor 23 (FGF23) levels play a key, primary role in CKD-MBD pathogenesis. Therapeutic approaches in pediatric CKD-MBD aim to minimize complications to the growing skeleton and prevent extra-skeletal calcifications, mainly by addressing hyperphosphatemia and secondary hyperparathyroidism. Ongoing clinical trials are focused on assessing the benefit of FGF23 reduction in CKD. CKD-MBD is a systemic disorder that has significant clinical implications. Treatment of CKD-MBD in children requires special consideration in order to maximize growth, optimize skeletal health, and prevent cardiovascular disease.
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