Objective To observe the change of insulin-like growth factor 1 (IGF-1) before and after glucocorticoid (GC) therapy and to explore the effect of its change on bone metabolism in primary nephrotic syndrome (PNS) patients. Methods A total of 39 PNS patients with mean age of (36.73±12.15) years received GC therapy were selected from January 2008 to August 2009 in our hospital. Serum IGF-1, albumin, calcium, phosphorus, parathormone (PTH), 25 hydroxy vitamin D3, bone gla protein (BGP), degradation products of C-terminal telopeptides of type I collagen (CTx), 24-hour urinary protein excretion and the ratio of urinary calcium to creatinine were measured at five time points—before GC therapy, 4 weeks, 8 weeks, 12 weeks and 24 weeks after the use of GC. BMD was also detected at the same time points. Correlations among indexes were analyzed by Pearson. Results Thirty-six PNS patients fulfilled the follow-up and had complete clinical data, while other 3 patients lost. After GC treatment, serum calcium and 25 hydroxy vitamin D3 were significantly increased in a time-dependent manner and were negatively correlated with 24-hour urinary protein excretion (r=-0.749, r=-0.831, P<0.05, respectively). Serum BGP and IGF-1 were decreased after GC therapy in a time-dependent manner while CTx was significantly increased until week 12 after treatment (P<0.05). Compared with pre-treatment, BMD of various parts had no significant difference at week 4; BMD of lumbar spine (L1-L4) was significantly decreased until week 8 (P<0.05); BMD of femoral neck and femoral shaft was significantly decreased at week 24 (P<0.05). IGF-1 was positively correlated with BGP and BMD (r=0.896, r=0.495, P<0.05) and negatively correlated with serum CTx (r=-0.697, P<0.05 ). Conclusions Serum IGF-1 level decreases in a time-dependent manner after GC treatment, which is correlated to BGP, CTx and BMD. Glucocorticoid treatment affects bone metabolism through IGF-1 pathway possably in patients with PNS. IGF-1 may be used as a new bone biochemical marker of glucocoritcoid-induced osteoporosis.