Insulin and growth in chronic renal failure.
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.
Mak
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RH
Department of Pediatrics, Stanford University School of Medicine, CA 94305-5119.
Haycock
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GB
Chantler
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C
D000293:Adolescent; D001786:Blood Glucose / Q000378:metabolism; D002648:Child; D005919:Glomerular Filtration Rate; D006130:Growth Disorders / Q000209:etiology / Q000378:metabolism*; D006801:Humans; D006961:Hyperparathyroidism / Q000378:metabolism; D007328:Insulin / Q000378:metabolism*; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000378:metabolism
D001786:Blood Glucose; D007328:Insulin; D010281:Parathyroid Hormone