| The refractory nephrotic syndrome is a intractable disease in clinicaltreatment. It's a chronic disease. If the state of disease can't be controlled, itwill be gradually developed chronic renal failure. Recently more and moreresearches enunciated that many factors alone or participate together in thepathogenesis of refractory nephrotic syndrome, including gene mutation,serious hyperlipidemia,immunity mess,phlogistic medium,albuminuria andtraditions cure the medicine etc. factor. Among them, immunity mess andphlogistic traumata take the main function in the pathogenesis of refractorynephrotic syndrome. Therefore, the basic scheme of treatment is restrainimmunity and phlogistic response that it made. Immunosuppressive therapycan alleviate albuminuria and slow down the process of disease,and gainbetter clinic effect. Although the application of immunosuppressive drug suchas cyclophosphamide and cyclosporine A have obtained commendable to getparts of curative effect,it's serious side effect limit it's application. Therefore itis very necessary to study a new immunosuppressive drug with little sideeffect.Objective:To investigate the effect of Tacrolimus(FK506) on thesignificance of IL-2 ,sIL-2R and TGF-β1expression in refractory nephroticsyndrome. And discussion the pathogenesis of refractory nephrotic syndromeand the value of Tacrolimus treatment refractory nephrotic syndrome.Method: The research objects choosed to stay in the hospital from Marchof 2002 to December of 2003 with refractory nephrotic syndrome,divided intopro-treatment and post-treatment.The levels of IL-2,sIL-2R and TGF-β1 weredetected by ELISA. Serum creatinine,serum albumin and lipid all use thefull-automatic bio-chemical analysis instrument measurement. Results : serum IL-2 ,sIL-2R and TGF-β1levels were higher inpre-treatment group than in normal control group(P<0.05), and 24hoursurinary protein,serum lipid level were higher and serum albumin level waslower in pre-treatment group than in normal control group(P<0.01). After thetreatment of FK506 ,the level of IL-2,sIL-2R and TGF-β1 decreased (P<0.05), 24hours urinary protein,serum lipid significantly decreased, andalbumin level significantly increased (P<0.01).Except IL-2,there were nosignificant differences in sIL-2R expression,24hours urinary protein,serumalbumin and lipid in both post-treatment and normal control groups. Discussion: The majority of specialists and scholars considered thatimmunity mess is correlatede with the pathogenesis of refractory nephroticsyndrome. Our study detected that there are significant increased of IL-2 ,sIL-2R expression in refractory nephrotic syndrome(P<0.05).It accordedwith many overseas reports. This indicated that there are unnormal expressionthe activation and multiplication of T lymphocytes. IL-2,sIL-2R participatedin the pathogenesis of refractory nephrotic syndrome.IL-2 is an important cellgene of immune modulation, that has abroad effect of immune buildup. It canaccelerate the activation and multiplication of T lymphocytes, and urge theenhancement of cell gene that T lymphocytes produced and released. At thesame time it has the effect of accelerate growth and differentiation of Blymphocytes and the creation of immunoglobulin. Moreover it also canaccelerate humoral immunity and produce self-antibody that lead to illness,and make self-antibody and immune complex aggradated in kidney, leading todamage of kidney. sIL-2R is also an important cell gene of immunemodulation. There is minim sIL-2R in normal flesh. None but under theconditions of diseases, the level of sIL-2R will significantly increased. Afterthe treatment of FK506, IL-2,sIL-2R levels decreased (P<0.05),and at thesame time decreased urinary protein and increased serum albumin.Consequently, it is an important measure to treat refractory nephroticsyndrome ,including to control IL-2,sIL-2R expression on the refractorynephrotic syndrome and the activation and multiplication of T lymphocytes. Furthermore, Our study also indicated that there were unnormal TGF-β1expression on the refractory nephrotic syndrome. The function of TGF-β1 is toreduce or restrain EMC's disintegration and fibrin's hydrolyze,and acceleratethe sediment of fibrin and the accumulation of EMC in tissue,which willaccelerate glomerular sclerosis. we considered that TGF-β1also participated inthe pathogenesis of refractory nephrotic syndrome. FK506 is a powerful immunosuppressive drug. It can depress the level ofIL-2,sIL-2R,and efficiently depress the activation and multiplication of Tlymphocytes. It also can decrease self-antibody and immune complexaggradated in kidney. Except IL-2,sIL-2R,FK506 decrease TGF-β1level. Itcan reach the aim at preventing glomerular sclerosis.Conclusion:This study demonstrated that there were unnormal activationand multiplication of T lymphocytes and unnormal IL-2 ,sIL-2R andTGF-β1expression on the refractory nephrotic syndrome. This has importantsignificance to study the pathogenesis of refractory nephrotic syndrome.FK506 has the functions of control IL-2,sIL-2R and TGF-β1expression on therefractory nephrotic syndrome. EMC's disintegration and production are inhomeostasis,which preventing glomerular sclerosis.From the clinic curativeeffect, we can see that FK506 reduce 24h urinary protein,serum lipid leveland increase serum albumin level. In conclusion, Tacrolimus could alleviaterefractory nephritic syndrome. |
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