本文检验了40例肾虚病人外周血 NK 细胞活性以及单个核细胞产生 IL—2和 IL—2受体表达能力,结果:肾虚病人 NK 活性、IL—2和 IL—2受体活性均较正常对照显著降低(P<0.01);正常对照 NK 活性与 IL—2活性呈直线正相关,而肾虚病人无明...本文检验了40例肾虚病人外周血 NK 细胞活性以及单个核细胞产生 IL—2和 IL—2受体表达能力,结果:肾虚病人 NK 活性、IL—2和 IL—2受体活性均较正常对照显著降低(P<0.01);正常对照 NK 活性与 IL—2活性呈直线正相关,而肾虚病人无明显相关性。展开更多
The release of proinfammatory cytokines during infam-mation represents an attempt to respond to injury, but it may produce detrimental effects. The infammasome is a large, multiprotein complex that drives proinfammato...The release of proinfammatory cytokines during infam-mation represents an attempt to respond to injury, but it may produce detrimental effects. The infammasome is a large, multiprotein complex that drives proinfammatory cytokine production in response to infection and tissue injury; the best-characterized inflammasome is the nod-like receptor protein-3 （NLRP3）. Once activated, infammasome leads to the active form of caspase-1, the enzyme required for the maturation of interleukin-1beta. Additional mechanisms bringing to renal inflammatory, systemic diseases and fibrotic processes were recently reported, via the activation of the inflammasome that consists of NLRP3, apoptosis associated speck-like protein and caspase-1. Several manuscripts seem to identify NLRP3 infammasome as a possible therapeutic target in the treatment of progressive chronic kidney disease. Serum amyloid A （SAA）, as acute-phase protein with also proinfammatory properties, has been shown to induce the secretion of cathepsin B and infammasome components from human macrophages. SAA is a well recognised potent activator of the NLRP3. Here we will address our description on the involvement of the kidney in autoinflammatory diseases driven mainly by secondary, or reactive, AA amyloidosis with a particular attention on novel therapeutic approach which has to be addressed in suppressing underlying inflammatory disease and reducing the SAA concentration.展开更多
Circulating toxins namely： free radicals, cytokines and metabolic products induce glomerular endothelial dys-function, hemodynamic maladjustment and chronic ischemic state;this leads to tubulointerstitial fbrosis in ...Circulating toxins namely： free radicals, cytokines and metabolic products induce glomerular endothelial dys-function, hemodynamic maladjustment and chronic ischemic state;this leads to tubulointerstitial fbrosis in chronic kidney disease （CKD）. Altered vascular homeo-stasis observed in late stage CKD revealed defective angiogenesis and impaired nitric oxide production ex-plaining therapeutic resistance to vasodilator treatment in late stage CKD. Under current practice, CKD patients are diagnosed and treated at a rather late stage due to the lack of sensitivity of the diagnostic markers avail-able. This suggests the need for an alternative thera-peutic strategy implementing the therapeutic approachat an early stage. This view is supported by the normal or mildly impaired vascular homeostasis observed in early stage CKD. Treatment at this early stage can potentially enhance renal perfusion, correct the renal ischemic state and restore renal function. Thus, this alternative therapeutic approach would effectively pre-vent end-stage renal disease.展开更多
文摘The release of proinfammatory cytokines during infam-mation represents an attempt to respond to injury, but it may produce detrimental effects. The infammasome is a large, multiprotein complex that drives proinfammatory cytokine production in response to infection and tissue injury; the best-characterized inflammasome is the nod-like receptor protein-3 （NLRP3）. Once activated, infammasome leads to the active form of caspase-1, the enzyme required for the maturation of interleukin-1beta. Additional mechanisms bringing to renal inflammatory, systemic diseases and fibrotic processes were recently reported, via the activation of the inflammasome that consists of NLRP3, apoptosis associated speck-like protein and caspase-1. Several manuscripts seem to identify NLRP3 infammasome as a possible therapeutic target in the treatment of progressive chronic kidney disease. Serum amyloid A （SAA）, as acute-phase protein with also proinfammatory properties, has been shown to induce the secretion of cathepsin B and infammasome components from human macrophages. SAA is a well recognised potent activator of the NLRP3. Here we will address our description on the involvement of the kidney in autoinflammatory diseases driven mainly by secondary, or reactive, AA amyloidosis with a particular attention on novel therapeutic approach which has to be addressed in suppressing underlying inflammatory disease and reducing the SAA concentration.
基金Thailand Research FundNational Research Council Fund of Thailandthe Royal Institute of Thailand
文摘Circulating toxins namely： free radicals, cytokines and metabolic products induce glomerular endothelial dys-function, hemodynamic maladjustment and chronic ischemic state;this leads to tubulointerstitial fbrosis in chronic kidney disease （CKD）. Altered vascular homeo-stasis observed in late stage CKD revealed defective angiogenesis and impaired nitric oxide production ex-plaining therapeutic resistance to vasodilator treatment in late stage CKD. Under current practice, CKD patients are diagnosed and treated at a rather late stage due to the lack of sensitivity of the diagnostic markers avail-able. This suggests the need for an alternative thera-peutic strategy implementing the therapeutic approachat an early stage. This view is supported by the normal or mildly impaired vascular homeostasis observed in early stage CKD. Treatment at this early stage can potentially enhance renal perfusion, correct the renal ischemic state and restore renal function. Thus, this alternative therapeutic approach would effectively pre-vent end-stage renal disease.
