Key result
Active nephrotic syndrome in children linked to ~63% lower serum IGF-I and reduced IGFBP-3 versus controls.
Why the study?
Growth failure is a major problem in steroid-resistant nephrotic children, and altered serum IGF and IGFBP profiles have been reported in renal diseases but not well characterized in nephrotic syndrome.
Observational (n=22)
Low serum IGF-I and IGFBP-3 levels in children with nephrotic syndrome are associated with increased urinary losses of IGF-IGFBP complexes, potentially contributing to growth failure.
Altered IGFBP profiles may contribute to growth failure in nephrotic children; leaves open causal mechanisms and need for prospective studies.
Growth failure appears to be a major problem for nephrotic children who fail to respond to steroid therapy. Recently altered serum insulin-like growth factor (IGF) and IGF-binding protein (IGFBP) profiles are reported in renal failure and glomerulonephritis. In this study, the serum IGFBP profile was evaluated by Western ligand blot and RIA in 22 patients with the nephrotic syndrome. Serum IGFBP-3 was decreased, whereas IGFBP-2 was increased in most patients with the nephrotic syndrome. The mean serum IGFBP-3 level was 2123 +/- 531 ng/mL in active states and was increased to a normal level (3593 +/- 407 ng/mL) in remission states. We also measured serum IGF-I by RIA. The serum concentration of IGF-I (mean +/- SD) was 67.4 +/- 23.2 ng/mL in active states and was increased to 127.1 +/- 21.8 ng/mL in remission states, but was still lower than that in control subjects (180.4 +/- 15.8 ng/mL). IGF-I and IGFBP-3 levels were not correlated with primary renal diseases or the amount of proteinuria. For serum IGF-IGFBP complexes, 150-kDa complexes were significantly decreased in patients with the nephrotic syndrome compared with those in control subjects. In urine from nephrotic syndrome patients, 150- and 50-kDa complexes were found, whereas these complexes did not exist in the urine of control subjects. We speculate that low serum IGF-I and IGFBP-3 levels would be partially due to the increased urinary losses of serum IGF-IGFBP complexes, especially that of 150 kDa, and these changes may contribute to growth failure in persistent nephrotic syndrome.
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Lee et al. (1996) conducted an observational in Nephrotic syndrome (n=22). Active nephrotic syndrome vs. Remission state and healthy controls was evaluated on Serum IGF-I concentration. Active nephrotic syndrome in children was associated with lower serum IGF-I (67.4 vs 180.4 ng/mL in controls) and IGFBP-3 levels, which increased during remission but remained below normal.
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