Relationship between leukotrienes and clinical, pathological features of Henoch-Schoenlein purpura nephritis in children

Abstract

To investigate the role of leukotrienes (LTs) in the progress of children's Henoch-Schoenlein purpura (HSP) nephritis (HSPN), and to provide an experimental basis for clinical application of leukotrienes antagonists in treatment of HSPN. The serum and urine samples were collected from 34 patients with HSPN 18 of them received renal biopsy, 27 cases with HSP and 16 healthy children as control. The level of LTB4 in the serum and urine was tested by enzyme-linked immunosorbent assay (ELISA) and LTE4 in urine in each group by enzyme immunoassay (EIA). The extent of expression of LTC4 synthase was detected by indirect immune fluorescence (IIF) in the renal tissue of 18 HSPN cases who received renal needle biopsy. Meanwhile, 3 cases with thin basement membrane nephropathy (TBMN) and 4 cases with simple hematuria were enrolled as controls. The results of pathological examination of the 4 cases with simple hematuria was normal by light microscope or electron microscope. At the same time, total urine protein in 24 hours was determined in 24 HSPN patients. (1) The level of serum and urinary LTB4 in the children with HSPN was (1164.33 +/- 300.28) ng/L and (841.19 +/- 115.23) ng/L, respectively. The level of serum and urinary LTB4 in those with HSP was (559.60 +/- 180.23) ng/L and (574.42 +/- 101.17) ng/L, respectively. The level of serum and urinary LTB4 in the control group was (211.95 +/- 67.72) ng/L and (227.33 +/- 76.12) ng/L, respectively. There was significant difference in the LTB4 level between HSPN group and HSP group (P < 0.01) while there was statistically significant difference in the LTB4 level between HSPN group and control group (P < 0.01). The urinary LTE4 was (1252.31 +/- 251.62) ng/L, (805.93 +/- 185.52) ng/L and (149.51 +/- 33.66) ng/L for HSPN group, HSP group and control group, respectively, and the differences were significant (P < 0.01). (2) The increase of serum and urinary LTB4 and urinary LTE4 was closely relative to the severity of histopathological changes. (3) Serum and urinary LTB4, urinary LTE4 increased in parallel to the enhancement of urine protein in HSPN patients (P < 0.01 or P < 0.05). (4) Markedly significant difference of LTC4 synthase by IIF existed between HSPN groups and control group. LTs can promote the progress of children's HSPN. There is a close relationship between LTs expression in renal tissues, the pathological severity of HSPN and proteinuria.