Autoimmune thyroiditis (AIT) is generally associated with hypothyroidism. It affects ~2% of the female population and 0.2% of the male population. The evidence of thyroid function- and thyroid autoantibody-unrelated microproteinuria in almost half of patients with AIT and sometimes heavy proteinuria as in the nephrotic syndrome point to a link of AIT with renal disease. The most common renal diseases observed in AIT are membranous nephropathy, membranoproliferative glomerulonephritis, minimal change disease, IgA nephropathy, focal segmental glomerulosclerosis, antineutrophil cytoplasmic autoantibody (ANCA) vasculitis, and amyloidosis. Different hypotheses have been put forward regarding the relationship between AIT and glomerulopathies, and several potential mechanisms for this association have been considered. Glomerular deposition of immunocomplexes of thyroglobulin and autoantibodies as well as the impaired immune tolerance for megalin (a thyrotropin-regulated glycoprotein expressed on thyroid cells) are the most probable mechanisms. Cross-reactivity between antigens in the setting of genetic predisposition has been considered as a potential mechanism that links the described association between ANCA vasculitis and AIT.

Background: Vascular intracranial stenosis (IS) is a significant cause of acute ischemic stroke (AIS). This singlecenter study aims to show that symptomatic IS treatment by using the Neuroform Atlas stent (Stryker neurovascular, Kalamazoo, MI, USA) could be effective in reducing vessel stenosis. Methods: Ten patients affected by AIS or TIA, in the vascular territory of high-grade intracranial atherosclerotic lesions (>70% of vessel stenosis), older than 18-year-old, were treated by implanting a Neuroform Atlas stent (diameter of 4.5mm in 80% and 4mm in 20%). 70% of the patients underwent pre-stenting intracranial angioplasty. Results: Patients were between 54.8 and 83 years old (mean 68.46y AE 8.44y), 70% males and 30% females. At admission, 50% of all patients had an AIS and 50% a TIA. Restoration of the stenotic lumen was obtained after the endovascular procedure. The percentage mean of vascular stenosis was 83.7% AE 6.09% before treatment (t0), 52.2% AE 10.42% at the end of treatment (t1) and 46.2% AE 8.28% at the follow-up (t2). The IS percentage mean reduction between t0 and t1 was 31.5% AE 7.31%, and between t1 and t2 was 6% AE 5.47%, t0 and t2 of 37.5% AE 7.38%. Percentage reduction of IS was highly significant between time t0 and t1 (p ¼ 0.005), and t0 and t2 (p ¼ 0.005), also with a significant reduction between t1 and t2 (p ¼ 0.012). No patient had experienced an increase of the ischemic area in the vascular territory of the target vessel at 3 months from the initial assessment. 10% of patients experienced a 3-months negative outcome (mRS ¼ 5), 90% experienced a favorable outcome (mRS 2). Conclusions: Intracranial stenosis endovascular treatment with Neuroform Atlas stent provides encouraging results, with a statistically significant association between the vascular caliber improvement and the endovascular treatment.

BackgroundC3 glomerulonephritis is a rare glomerulopathy characterized at renal biopsy by C3 deposition, alone or with scanty immunoglobulins, as well as by an electron-dense material in mesangium, subendothelial and subepithelial space. An abnormal systemic activation of the alternative pathway of the complement cascade is responsible for the development of the disease if triggered by several possible environmental conditions. We report the first case in literature of a patient affected by cystic fibrosis and C3GN.Case presentationOur case involves a young woman with cystic fibrosis, who had persistent microscopic hematuria, proteinuria and hypocomplementemia C3 for over three months. Renal biopsy confirmed the diagnosis of C3 glomerulopathy. Complement system dysregulation was tested and resulted in a strong terminal pathway activation proved by high levels of sC5b-9 complex, amounting to 1588 ng/ml (normal value < 400 ng/ml). Next generation sequencing (NGS) showed polymorphism in CFH (p.V62I in SCR1) and THBD (p.A473V), already known as pathogenic for C3GN, as well as a mutation in C3 (p.R102G) associated only with age-related macular degeneration (AMD) so far. Treatment was based on ACE inhibitors and kidney function is currently stable (GFR 50 ml/min, serum creatinine 1.7).ConclusionsThe co-existence of C3 glomerulopathy in a patient with CF, which is characterized by chronic infection/inflammation, makes this case an interesting model of chronic altered systemic activation of the alternative pathway of the complement cascade.