To this end we developed a novel bilateral renal ablation model that was staged by the level of proteinuria. In order to differentiate hypertensive effects of superoxide and H2O2, we studied acute effects of the SOD mimetic Tempol or PEG-catalase on blood pressure and renal hemodynamics in rats with established CKD and agematched sham-operated control rats. Furthermore, we investigated the effect of both these interventions on oxidative stress in CKD and control rats. The main novel finding of this study is that in established CKD, MAP and RVR do not depend on ROS. This was demonstrated by the failure to alter MAP in CKD rats by acute scavenging of superoxide with Tempol. Reducing H2O2 with PEG-catalase did not normalize MAP in CKD rats. Furthermore, in CKD rats, Tempol had no effect on TBARS excretion while PEG-catalase reduced it. Parameters of oxidative stress are increased and antioxidant enzyme activities are decreased in patients with various degrees of CKD. Important endogenous antioxidant enzymes are SOD that convert superoxide to H2O2, which is in turn disposed of by two other enzymes, catalase and glutathione peroxidase. In experimental CKD a marked down-regulation of hepatic and renal cytoplasmic and mitochondrial SOD was found as well as down-regulation of renal catalase and glutathione peroxidase protein abundance and catalase activity. Tuberculosis is an infectious disease with chronic evolution, and its etiological agent is the intracellular bacterium Mycobacterium tuberculosis . Toll-like receptor 2 is the main receptor for mycobacterial constituents, recognizing lipoarabinomannan; its precursor, phosphatidylinositol mannoside; and 19-kDa lipoprotein. TLR4 is a receptor for exogenous ligands, such as LPS from Gramnegative bacteria, and can recognize endogenous ligands, such as heat shock protein 60/65, which is released by mycobacteria. Studies have shown that the recognition of mycobacterial products by TLRs leads to NF-kB activation and BAY 73-4506 consequently to gene transcription that produces pro-inflammatory cytokines, such as IL-12, TNF-a, IL-1b and nitric oxide. The recognition of M. tuberculosis by TLRs induces phagocytosis by alveolar phagocytes and the production of IL-12 by macrophages and dendritic cells. IL-12 stimulates natural killer cells and Th1 responses that produce IFN-c. Which in synergy with IFN-c, acts to increase phagocytosis and microbicidal activity through the production of reactive nitrogen and oxygen intermediates involved in the growth inhibition and death of mycobacteria. TNF-a is also essential for forming and maintaining granulomas. Studies have suggested that protective immunity against M. tuberculosis and Th1 responses require Th17, mainly at the start of infection. IL-17 has proinflammatory properties that induce the expression of cytokines, chemokines and metalloproteinases, which are important in neutrophil recruitment, activation and migration. Despite the protective effect of Th1 and Th17 responses against tuberculosis, the elevated expression of pro-inflammatory cytokines is related to disease immunopathogenesis.