Abstractand interstitial collagen IV (r=0.588, P<0.01). In addition, the number of interstitial a-SMA+ cells and Background. The cellular and humoral factors involved in the pathogenesis of glomerulosclerosis and the extent of immunostain for collagen IV were positively correlated with the final serum creatinine (r= renal fibrosis following a crescentic glomerulonephritis have not been fully elucidated. Myofibroblasts and 0.517, P<0.05 and r=0.612, P<0.01 respectively) and partially predicted functional outcome (R2=26.7% and transforming growth factor-b ( TGF-b) have been implicated in the development of experimental and 37.5% respectively) as well as the response to treatment.An association was observed between periglomerular clinical renal fibrosis. We have attempted to identify these mediators in crescentic glomerulonephritis and myofibroblasts and the generation of fibrotic and fibrocellular crescents. determine their role in the progression of the disease. Patients and methods. We studied retrospectively 21 Conclusion. These observations suggest a causal link between myofibroblasts and fibrotic crescent formapatients with crescentic and necrotizing glomerulonephritis (CNG) with emphasis on the renal expression tion. We also believe that interstitial myofibroblasts are actively involved in the pathogenesis of interstitial (detected by immunohistochemistry) of myofibroblasts (a-smooth muscle actin+ cells), TGF-b and collagen fibrosis in CNG.(III and IV ) as well as their relationship with the clinical outcome of these patients. In situ hybridization Key words: Myofibroblasts; TGF-b; crescentic necrotizhistochemistry was applied to determine the site of ing glomerulonephritis synthesis of TGF-b1 and collagen III. All the patients were treated by immunosuppression and followed up for a median period of 14 months.

Wegener’s granulomatosis (WG) is a necrotizing vasculitis that mainly affects the respiratory tract and kidneys. Of note, involvement of the heart is being increasingly recognized in these patients. Cardiac manifestations can arise from the coronary arteries, pericardium, myocardium, endocardium, valves, conduction system and great vessels, but in most cases cardiac involvement is clinically silent. Consequently, a regular cardiovascular evaluation, including echocardiography, should be performed in every patient with WG, while patients with WG flare should be closely monitored for cardiac complications even in the absence of specific symptoms.

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An unusually large number of cases of tuberculosis, often of miliary or disseminated form, have been reported in patients receiving infliximab therapy for rheumatoid arthritis or Crohn's disease. We describe a patient with rheumatoid arthritis who was treated with infliximab and became systemically ill with Mycobacterium tuberculosis-disseminated infection. Patients who are candidates for treatment with tumour necrosis factor-alfa inhibitors should be evaluated for the presence of latent or active