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Metabolic bone loss after urinary diversion in children
Terry W Hensle1, Gerald Mingin, Mina Fam
1aColumbia University College of Physicians & Surgeons' New York, New York bThe University of Vermont, Burlington, Vermont cRutgers New Jersey Medical School, Newark, New Jersey, USA.
Insights
Pediatric urinary diversion and enterocystoplasty can cause bone loss due to metabolic acidosis. Bone demineralization aids compensation, allowing for normal linear growth despite increased bone cell activity.
Area of Science:
- Pediatric Urology
- Pediatric Nephrology
- Pediatric Endocrinology
Background:
- Bone loss is a known complication in children undergoing urinary diversion and enterocystoplasty.
- The multifactorial causes of bone loss and its impact on growth in these children require further understanding.
Purpose of the Study:
- To review recent evidence on the causes of bone loss in children undergoing urinary diversion and/or enterocystoplasty.
- To investigate the link between bone demineralization and growth retardation in this patient population.
Main Methods:
- Literature review of recent publications.
- Analysis of evidence regarding bone mineralization, metabolic acidosis, and linear growth.
Main Results:
- Decreased bone mineralization in normal individuals does not typically affect final adult height.
- Bone demineralization facilitates compensation for metabolic acidosis over time.
- Increased osteoclastic and osteoblastic activity are observed.
Conclusions:
- Enterocystoplasty in childhood frequently leads to metabolic acidosis.
- Bone buffering plays a role in compensating for acidosis.
- Bone demineralization, driven by increased bone cell activity, is a consequence of metabolic compensation that permits normal linear growth.
Purpose Of Review:
It has been widely known for some time that bone loss can be seen in certain subpopulations of children undergoing urinary diversion and/or enterocystoplasty. This review will hopefully look at the recent evidence in the field and help understand the multifactorial cause of bone loss in this group of individuals, as well as look at evidence for this phenomenon in growth retardation in certain groups of these individuals.
Recent Findings:
Most of the recent publications indicate that in normal individuals, decreased bone mineralization does not appear to affect final growth or adult height. It would appear that over time, demineralization allows compensation of the acidosis. However, it should be noted that it does lead to an increase in both osteoclastic and osteoblastic activity.
Summary:
It is very likely that enterocystoplasty in childhood can lead to significant metabolic acidosis and that compensation with bone buffering does take place. It would appear that the bone demineralization secondary to increased osteoblastic and osteoclastic activity is the price paid for metabolic compensation and continued normal and near normal linear growth.
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