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.

Methylene-blue-treated fresh-frozen plasma is safer than the untreated product even in patients who require large quantities of plasma transfusion.

We report for the first time a patient with ADPKD who is heterozygous for a de novo PKD1 variant and homozygous for a novel PKD2 mutation.

Measurement of the cerebral ventricular system, by means of computerized tomography, was performed in 25 patients suffering from end-stage chronic renal failure (ESCRF) and in 45 undergoing chronic hemodialysis (CH), in order to estimate the degree of brain atrophy. Significant enlargement of the ventricular size was found in both groups in comparison with the controls, with the greatest enlargement in the group of patients undergoing hemodialysis. This ventricular enlargement expresses the degree of brain atrophy, which in the patients with ESCRF may be due to the metabolic factors of the renal disease and in the hemodialysed patients, to aluminum toxicity.