Aim: To explore the underlying mechanism of low-molecular-weight heparin calcium therapy on Henoch-Schö nlein purpura nephritis (HSPN). Methods: Eighty-nine children with severe HSPN were randomized into control group (treated with conventional therapy, n ¼ 45) and treatment group (treated with conventional therapy plus low-molecular-weight heparin calcium, n ¼ 44). The concentrations of plasma fibrinogen (Fg), D-dimer and fibrin degradation products (FDPs) were detected before and after treatment. The urinary red blood cell (RBC) and 24 h proteinuria were determined weekly for assessing the children's kidney function. Results: Two groups were well-matched at baseline. After 8 weeks of treatment, the clinical outcomes of HSPN and outcome of proteinuria of the treatment group were better than the control group (p50.05); the content of Fg, D-dimer and FDP in plasma of the treatment group were lower than the control group (p50.05); but there was no difference about the curative effect of hematuria and the coagulation function between the two groups (p40.05). Conclusions: Fibrinolytic system may participate in the kidney injury of HSPN children and low-molecularweight heparin calcium could correct blood hypercoagulability through inhibiting hyperfibrinolysis, and thus improving the blood supply of kidney. KeywordsFibrinolytic system, Henoch-Schö nlein purpura nephritis (HSPN), low-molecular-weight heparin calcium History
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