Plasma Concentrations' Changes And Significance Of Plasminogen Activator, Plasminogen Activator Receptor And Plasminogen Activator Inhibitor-1 In Chronic Glomerulonephritis And The Intervenient Research On Them

As a result of over deposition of extracellular matrix (ECM),glomerulosclerosis and renal fibrosis appears as the common pathway of finalstage. Plasminogen activator inhibitor lype 1(PAI-1) and tissue plasminogenactivator (tPA) are the major regulators of plasmin generation. GlomerularPAI-1/tPA balance is involved in extracellular matrix tumover, as well asfibrin deposition in glomeruli. We explore the plasmac concentrations'changes of tissue-type plasminogen activator (tPA), urokinasetypeplasminogen activator (uPA), urokinasetype plasminogen activator receptor(uPAR) and plasminogen activator inhibitor-1(PAI-1) in chronicglomerulonephritis (CGN) and the effect of treatment with angiotensionconverting enzyme inhibitor (ACEI).ELISA method was used to measure the plasma levels of tPA, uPA,uPAR and PAI-1 in 78 patients suffered CGN. We compared their plasmacconcentrations of tPA, uPA, uPAR and PAI-1 with them of healthy person,and observed the changes after eight weeks' treatment with ACEI(monopril,10-20mg per day for 8 weeks). We find: the plasmac concentration of uPAR increased obviously in the CGN patients compared with that in the healthypeople (p＜0.05); the plasmac concentration of PAI-1 increased obviously inthe CGN patients compared with that in the healthy people (p＜0.01); and theplasmac concentrate ion of PAI-1 decreased obviously in the CGN patientswho received the treatment of ACEI after 8 weeks, compared with that inCGN patients who did not received such treatment (p＜0.05). So we conclude:the plasmac concentration of PAI-1 increases obviously in the CGN patientsso that the tumover of extracellular matrix (ECM) is inhibited. Meanwhile thetreatment of ACEI can accelerate the tumover of ECM by decreasing theplasmac concentration of PAI-1, so as to retard renal fibrosis.