Plasma levels of soluble CD30 are increased in children with chronic renalfailure and with primary growth deficiency and decrease during treatment with recombination human growth hormone

Citation
G. Barbano et al., Plasma levels of soluble CD30 are increased in children with chronic renalfailure and with primary growth deficiency and decrease during treatment with recombination human growth hormone, NEPH DIAL T, 16(9), 2001, pp. 1807-1813
Citations number
23
Categorie Soggetti
Urology & Nephrology
Journal title
NEPHROLOGY DIALYSIS TRANSPLANTATION
ISSN journal
09310509 → ACNP
Volume
16
Issue
9
Year of publication
2001
Pages
1807 - 1813
Database
ISI
SICI code
0931-0509(200109)16:9<1807:PLOSCA>2.0.ZU;2-H
Abstract
Background. Previous studies have suggested that in vivo Th2 lymphocyte act ivation is related to increased soluble CD30 (sCD30) plasma levels. As vari ous hormones (dehydroepiandrosterone, glucocorticoids, progesterone) can re gulate the Th1/Th2 balance, and because growth hormone (GH) enhances lympho cyte function, we measured sCD30 plasma levels, before and after treatment with recombinant human GH (rhGH), in children with growth failure due to ch ronic renal failure (CRF) or to isolated GH deficiency in order to evaluate the potential effects of rhGH treatment on Th1/Th2 balance. Methods. sCD30 plasma levels were determined by ELISA assay in 30 children with CRF (mean age 10.7 +/- 3.7 years), in five children with isolated GH d eficiency (mean age 11.4 +/- 2.6 years), and in 10 normal controls (mean ag e 10.1 +/- 3.5 years). Results. sCD30 levels were higher in the 30 children with CRF than in the 1 0 controls (179.8 +/- 79.4 vs 11.3 +/- 10.9 U/ml, P < 0.001) exhibiting an inverse correlation with glomerular filtration rate (GFR) (r=-0.7860, P < 0 .001). In 11 children with CRF, after 19.9 +/- 16.7 months of rhGH treatmen t, a decrease of sCD30 plasma level (170 +/- 50 vs 134 +/- 49 U/ml, P < 0.0 1) was observed. The five children with primary GH deficiency had higher sC D30 plasma level than controls (mean 147 +/- 105 vs 11 +/- 10U/ml, P < 0.00 4) and sCD30 plasma levels decreased to 95.2 +/- 109.6 U/ml after rhGH trea tment. Conclusions. The finding that rhGH treatment decreased sCD30 plasma levels in children with CRF, and that children with primary GH deficiency had high er sCD30 plasma levels than controls, suggest that GH may regulate CD30 exp ression and possibly the balance of Th1/Th2. Whether the uraemia-induced in crease in sCD30 is due to decreased renal excretion, to overproduction or b oth, remains to be determined.