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Published on: July 3, 2013
Insulin and growth in chronic renal failure
R H Mak1, G B Haycock, C Chantler
1Department of Pediatrics, Stanford University School of Medicine, CA 94305-5119.
Insights
Children with chronic renal failure experience poor growth, linked to glucose metabolism. Improving glucose disposal and insulin secretion, not just parathyroid hormone (PTH) levels, may enhance growth in these patients.
Area of Science:
- Pediatric Nephrology
- Endocrinology
- Metabolic Research
Background:
- Chronic renal failure (CRF) in children often leads to poor linear growth.
- Glucose metabolism and endocrine factors are implicated in growth impairment in pediatric CRF.
Purpose of the Study:
- To investigate the relationship between glucose metabolism and linear growth in children with CRF.
- To assess the impact of managing hyperparathyroidism on growth and glucose metabolism.
Main Methods:
- Cross-sectional study of 23 children with CRF assessing growth velocity standard deviation score (GVSDS) and glucose metabolism via hyperglycemic technique.
- Longitudinal follow-up of 13 children during medical suppression of hyperparathyroidism.
- Measurements included GVSDS, glucose disposal rate, insulin sensitivity index, insulin secretion, and serum parathyroid hormone (PTH) levels.
Main Results:
- GVSDS correlated with glucose disposal rate in both pubertal and prepubertal children with CRF.
- Following PTH suppression, significant improvements in GVSDS, glucose disposal rate, and insulin secretion were observed.
- Changes in GVSDS correlated with changes in glucose disposal rate and insulin secretion, but not with PTH levels.
Conclusions:
- Glucose metabolism, particularly glucose disposal and insulin secretion, appears crucial in growth failure associated with pediatric CRF.
- Insulin's role may be more significant than PTH in the pathogenesis of growth failure in chronic renal disease.
- Further research is warranted to explore the therapeutic potential of targeting insulin pathways for growth improvement in pediatric CRF.
Abstract:
We studied glucose metabolism using the hyperglycemic technique in a cross-section of 23 children (15 pubertal, 8 prepubertal) with stable chronic renal failure as a possible cause of their poor growth. Linear growth was expressed as growth velocity standard deviation score (GVSDS). GVSDS correlated with glucose disposal rate but not with insulin sensitivity index in the pubertal (r = 0.87, P < 0.001) and prepubertal (r = 0.86, P < 0.02) children with chronic renal failure. Thirteen children were followed longitudinally during medical suppression of hyperparathyroidism with dietary phosphate restriction and high-dose phosphate binders. Following significant suppression of serum parathyroid hormone (PTH) levels back to the normal range (932 +/- 240 ng/l to 199 +/- 50 ng/l), GVSDS, glucose disposal rate and insulin secretion all increased significantly (p < 0.01), with no change in insulin sensitivity index and renal function. The changes in GVSDS correlated with the changes in glucose disposal rate (r = 0.86, P < 0.02) and with the changes in insulin secretion (r = 0.80, P < 0.01). However, the changes in GVSDS did not correlate with the changes in PTH. The hypothesis that insulin may be more important than PTH in the pathogenesis of growth failure in chronic renal disease deserves further investigation.
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