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

Abstract

Background. Previous studies have suggested that in vivo Th2 lymphocyte activation is related to increased soluble CD30 (sCD30) plasma levels. As various hormones (dehydroepiandrosterone, glucocorticoids, progesterone) can regulate the Th1/Th2 balance, and because growth hormone (GH) enhances lymphocyte function, we measured sCD30 plasma levels, before and after treatment with recombinant human GH (rhGH), in children with growth failure due to chronic 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 deficiency (mean age 11.4±2.6 years), and in 10 normal controls (mean age 10.1±3.5 years). Results. sCD30 levels were higher in the 30 children with CRF than in the 10 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 treatment, a decrease of sCD30 plasma level (170±50 vs 134±49 U/ml, P < 0.01) was observed. The five children with primary GH deficiency had higher sCD30 plasma level than controls (mean 147±105 vs 11±10 U/ml, P < 0.004) and sCD30 plasma levels decreased to 95.2±109.6 U/ml after rhGH treatment. Conclusions. The finding that rhGH treatment decreased sCD30 plasma levels in children with CRF, and that children with primary GH deficiency had higher sCD30 plasma levels than controls, suggest that GH may regulate CD30 expression and possibly the balance of Th1/Th2. Whether the uraemia-induced increase in sCD30 is due to decreased renal excretion, to overproduction or both, remains to be determined.