They are traditionally classified by the size of the vessels involved and in many cases there is an autoimmune aetiology. We present a case of a patient with a medium vessel vasculitis affecting multiple

vascular beds and causing renal infarction. Case Report: A 44-year-old Italian male presented to the Emergency Department on three occasions over 4 days with severe left flank pain. Initial investigations including a renal tract ultrasound were normal and he was discharged with analgesia. On his third presentation a CT angiogram was performed due to persisting pain, which demonstrated infarction of his left kidney as well as thickening of the anterior branch Vorinostat of left renal artery and complete occlusion with focal intimal dissection of the celiac artery. His ANCA was negative. A medium vessel vasculitis was suspected and confirmed on PET-CT, which also revealed increased metabolic activity involving the right internal mammary selleck and celiac arteries. Treatment with pulse methylprednisolone was commenced followed by a tapering prednisolone regimen. There was a rapid reduction in his inflammatory indices and 18 months later his renal function remains normal off all immunosuppression. Conclusion: In younger patients, without significant atherosclerotic disease or other risk factors for arterial occlusion (such as atrial fibrillation),

vasculitis should be considered in the differential diagnosis. Outcomes may be favourable following prompt treatment with immunosuppression. “
“Aim:  Activation of protein kinase C (PKC) has been SB-3CT implicated in the pathogenesis of diabetic nephropathy where therapy targeting the β isoform of this enzyme has been examined. However, PKC-β is also increased in various forms of human glomerulonephritis, including IgA nephropathy.

Accordingly, we sought to examine the effects of PKC-β inhibition in the Thy1.1 model of mesangial proliferative glomerulonephritis. Methods:  Following administration of monoclonal OX-7, anti-rat Thy-1.1 antibody, Male Wistar rats were randomized to receive either the PKC-β inhibitor, ruboxistaurin (10 mg/kg per day in chow) or vehicle. Animals were then examined 6 days later. Results:  PKC-β inhibition was associated with reductions in mesangial cellularity and extracellular matrix deposition. Proteinuria was, however, unaffected. In vitro, PKC-β inhibition showed modest, dose-dependent reductions in mesangial cell 3H-thymidine and 3H-proline incorporations, indices of cell proliferation and collagen synthesis, respectively. Conclusion:  The amelioration of the pathological findings of experimental mesangial proliferative glomerulonephritis by PKC-β inhibition suggests the potential clinical utility of this approach as a therapeutic strategy in non-diabetic glomerular disease.