Clinical And Pathological Study Of Leukotrienes And Henoch-Schoenlein Purpura Nephritis In Children

Henoch-Schoenlein purpura nephritis(HSPN) is a very frequentsecondary nephritic disease in children. Its etiology and pathogenesis are notcompletely clarified and there is no specific therapy for it at present.Leukotrienes(LTs) are potent inflammatory factors which involve in a series ofinflammatory or allergic diseases such as asthma, inflammatory enteric diseases andso on. Some study showed that LTs play the most important role in the maintein ofthe glomeruli function and structure integrality. They can stimulate the contraction ofvascular smooth muscle and mesangeall cell, resulting in the decrease of renal bloodflow and glomerular filtration rate, leading the increase of the cell adhesion, that is,capillary endothelial cell, mesangial cell and leucocyte, and provoking theproliferation of mesangeall cells. In this experiment, we detect the expression of LTsin the serum, urine and kidney tissue for searching the relationship between them andthe clinical and pathologic features in HSPN children, and for identifying the etiologyand pathogenesis of HSPN.Method: The serum and urine samples were collected from 34 patients withHSPN (18 of them received renal biopsy), 27 cases with HPS and 16 healthycontrol (all from the department of health care of the Yuying children hospitalaffiliated to Wenzhou medical college ). All samples were centrifugated andcryopreservated. The level of LTB4 in the serum and urine was tested byEnzyme-linked immunosorbent assay(ELISA) and LTE4 in urine in each group byenzyme immunoassay (EIA). The expression degree of LTC4 synthase was detectedby Indirect immune fluorescence(IIF) in the renal tissue of 18 HSPN cases receivingrenal needle biopsy. Meanwhile,3 cases with thin basement membrane nephropathy(TBMN) and 4 cases with simple hematuria were control. The pathologicalexamination of the 4 cases with simple hematufia was normal by light microscope orelectron microscope. At same time, total protein in 24 hours in 24 HSPNpathients. Finally, all data were statistically analyze. Result: 1. LTB4 in urinary and serum among the HSPN group, HSP groupand control grouop: The level of serum and urinary LTB4 in the children withHSPN was 1164.338±300.288 pg/ml and 841.195±115.231 pg/ml, respectively.The level of serum and urinary LTB4 in those with HSP was 559. 608±180.238pg/ml and 574.420±101.173pg/ml, respectively.The level of serum and urinary LTB4in the control grouop was 211.955±67.720 pg/ml and 227.330±76.122 pg/mlrespectively. There was obvious statistical difference of the LTB4 level betweenHSPN group and HSP group(P＜0.01) while there was markedly obvious statisticaldifference of the LTB4 level between HSPN group and control group(P＜0.01). Thecriteria for Pathological classification of patients with HSPN was referral to ISKDC.Of them, 2 cases were classⅡa, whose serum LTB4 was 954.410±98.995 pg/ml andurinary LTB4 was 629.817±56.569 pg/ml. 4 cases with classⅡb was1009.484±127.802pg/ml for serum LTB4 and 678.491±58.878pg/ml for urinaryLTB4. 6 cases with pathologic classⅢa had serum LTB4 up to 1289.752±110.454pg/ml and urinary LTB4 to 747.456±73.212 pg/ml. 4 cases were pathologic classⅢbwith serum LTB4 up to 1456.214±179.815 pg/ml and urinary LTB4 up to816.273±91.287pg/ml. Pathologic classⅣa andⅣb was only one case, respectively.In the former, his serum and urinary LTB4 was 1568.123pg/ml and 937.564pg/ml,respectively and in the later, his serum and urinary LTB4 was 1868.245pg/ml and1058.274pg/ml respectively. The increase of serum and urinary LTB4 was closelyrelative to the severity of histological pathologic changes. In ten cases withpathologic classeⅢ, serum LTB4 was1356.337±157.939pg/ml and urinary LTB4 was774.983±83.776pg/ml. 6 cases with pathologic classeⅢhad 991.126±112.111pg/mlof serum LTB4 and 662.266±57.895pg/ml of urinary LTB4.2 cases with pathologicclasseⅣhad 1718.184±212.218pg/ml and 997.819±85.213pg/ml for the serum andurinary LTB4, respectively. Serum and urinary LTB4 in those with pathologicclasseⅢwas markly higher than pathologic classeⅡ(P＜0.01,P＜0.05) butsignificantly less than those with pathologic classeⅣ(P＜0.01).2. Results of urinary LTE4: The urinary LTE4 was 1252.313±251.624pg/ml,805.936±185.522 pg/ml and 149.513±33.664 pg/ml for HSPN group, HSP group andcontrol grouop, respectively. There was significant differences of urinary LTE4between HSPN group and HSP group, P＜0.01. Of 18 HSPN cases received renal biopsy.2 cases were pathologic classeⅡa with urinary LTE4 of 879.214±84.853pg/ml. 4 cases were classeⅡb, whose urinary LTE4 was 918.341±135.401pg/ml. 6 cases classeⅢa had urinary LTE4 up to 1178.256±115.931pg/ml. 4 caseswere classeⅢb with urinary LTE4 up to 1364.795±129.099 pg/ml. One case wasclasseⅣa with urinary LTE4 of 1576.605pg/ml and still one case was classeⅣbwith urinary LTE4 of 1687.395pg/ml. The increase of serum and urinary LTB4 wasclosely relative to the severity of histological pathologic changes.10 cases withpathologic classⅢhad 1252.872±149.336pg/ml for urinary LTE4 and 6 cases werepathologic classⅡwith urinary LTE4 up to 905.299±113.350pg/ml. 2 cases withpathologic classⅣpossessed urinary LTE4 approaching to 1633.000±79.755pg/ml.The urinary LTE4 in those with pathologic classⅢwas markedly higher than thosewith pathologic classⅡ, but being significantly less than those with pathologicclassiv (P＜0.01).3. results of LTC4 synthase by Indirect immune fluorescence(IIF) in renaltissue: Markedly significant difference of LTC4 synthase by IIF existed betweenHSPN groups and control group.4. The comparision of urinary LTE4 and LTB4 of HSPN patients withdifferent urine protein: Serum and urinary LTB4, urinary LTE4 increasedparalleling to the enhancement of urine protein in HSPN patients. Of them, those withtotal urine protein up to 0.2～1.0g/24hr had higher serum and urinary LTB4, urinaryLTE4 than those with urine protein less than 0.2g/24hr, but less than those with urineprotein more than 1.0g/24hr.Serum and urinary LTB4,urinary LTE4 of those withurine protein 0.2～1.0g/24hr was 1196.561±403.935 pg/ml, 867.688±249.094pg/mland 735.200±287.895 pg/ml, respectively. Serum and urinary LTB4, urinary LTE4 inthose with urine protein＜0.2g/24hr was 524.041±174.302 pg/ml,582.772±42.208pg/ml and 252.193±41.960 pg/ml, respectively. Serum and urinary LTB4,urinary TE4of those with urine protein＞1.0g/24hr was1323.851±368.290 pg/ml,1281.951±699.604pg/ml and 1320.237±50.227pg/ml, respectively.Conclusions: LTs can promote the progress of Children's HSPN.There is aclose relationship between LTs expression in renal tissues,the pathological severity ofHSPN and proteinuria. They will be hopeful to become a effective therapy target of HSPN by Leukotrienes antagonists.