ABSTRACT
BACKGROUND:Long-term use of corticosteroids (hereinafter referred to as hormone) after renal transplantation could obviously lead to adverse reactions. Immunosuppressive regimen with less and no hormone has been a hot focus in the study of renal transplantation al over the world. However, reduction or withdrawal of hormones has a certain risk. At present, there is no unified scheme. Because urine protein can be immediately detected after tubular injury, to monitor urine protein can find the renal dysfunction after transplantation in recipients undergoing renal transplantation, which can gain time for clinical therapy. OBJECTIVE:To discuss the influence of hormone (prednisone) removal on the occurrence of urine protein in recipients undergoing renal transplantation. METHODS:A total of 35 recipients undergoing renal transplantation after removal of prednisone received immunosuppressive regimen of cyclosporine A or tacrolimus+mycophenolate mofetil bivalent. Initial dose of prednisone was 30 mg/d, and then gradual y reduced by 5 mg per week, and withdrawn at 1 month after renal transplantation. There were 16 cases in cyclosporine A group and 19 cases in tacrolimus group. Urine protein was measured and quantified at 3, 6, 12 and 24 months after renal transplantation and 3, 6 and 12 months after addition of prednisone in both groups. Simultaneously, serum creatinine, fasting glucose, body mass increases, the rate of acute rejection, infection, patient/graft survival at 2 years after renal transplantation and urine protein at 24 hours before and after adding hormone were recorded. RESULTS AND CONCLUSION:For the two groups, urineα1-microglobulin started to rise after 6 months of removal of prednisone. Urinary microalbumin, urinaryα1-microglobulin, and urinary transferrin ascended obviously at 12 months. Urinary protein was positive in five cases of cyclosporine A group and in three cases of tacrolimus group. At 24 months, urinary microalbumin, urinaryα1-microglobulin, urinary transferrin and urinary IgG ascended obviously. Urinary protein was positive in cyclosporine A group with 11 cases and in tacrolimus group with 10 cases. 24-hour urinary protein quantity was more than 1 g in every case. On this base, we made the patients to take more prednisone for 6 months, so urineα1-microglobulin and urinary microalbumin began to descend. Each group had one case of positive urinary protein turning to negative. Twelve months after the adjustment of the prednisone, urinary microalbumin, urinaryα1-microglobulin, and urinary transferrin descended respectively. Positive urinary protein turned into negative:in cyclosporine A group with two cases and in tacrolimus group with three cases. 24-hour urinary protein quantity was around 0.7 g. Two years after renal transplantation, serum creatinine and acute rejection rates were higher in the cyclosporine A group than in the tacrolimus group (P<0.05). No significant difference in fasting glucose, body mass increase, infections, and patient/graft survival was detectable between both groups. Results suggested that removal of prednisone greatly affected urine protein in recipients undergoing renal transplantation. In particular, at 2 years after renal transplantation, urinary microalbumin, urinaryα1-microglobulin, urinary transferrin and urinary IgG ascended obviously, and the security needs further research.