[Clinical effect and mechanism of total glucosides of paeony in the adjuvant therapy for children with Henoch-Schönlein purpura nephritis: a prospective randomized controlled study].

OBJECTIVE

To study the clinical effect and mechanism of total glucosides of paeony (TGP) in the adjuvant therapy for children with Henoch-Schönlein purpura nephritis (HSPN).

METHODS

Sixty-four HSPN children with moderate proteinuria were divided into a TGP treatment group (=34) and a routine treatment group (=30) using a random number table. Thirty healthy children who underwent physical examination were enrolled as the healthy control group. The children in the routine treatment group were given conventional treatment alone, and those in the observation group were given TGP in addition to the conventional treatment. The two groups were compared in the clinical outcome after 4 weeks of treatment. The proportion of follicular helper T (Tfh) cells in peripheral blood and the plasma levels of interleukin-21 (IL-21) and interleukin-4 (IL-4) were measured in the healthy control group and the two HSPN groups. The changes in serum cystatin C (CysC) level and urinary alpha 1-microglobulin (A1M) concentration were compared before and after treatment in the two HSPN groups.

RESULTS

Compared with the healthy children before treatment, the children with HSPN had higher proportion of Tfh cells and expression levels of IL-21 and IL-4 ( < 0.01). The TGP treatment group had a higher overall response rate to treatment than the routine treatment group (94% vs 67%, < 0.05). After treatment, both groups had reductions in the proportion of Tfh cells in peripheral blood, the expression levels of IL-21, IL-4, serum CysC, and urinary A1M concentration. The TGP treatment group had greater reductions in these indices than the routine treatment group ( < 0.01).

CONCLUSIONS

TGP has a marked clinical effect in the treatment of HSPN and can reduce the inflammatory response of the kidney and exert a protective effect on the kidney by inhibiting the proliferation of Tfh cells and downregulating the expression of IL-21 and IL-4 in plasma.