Background and Aims Antineutrophil cytoplasmatic antibody (ANCA)- associated vasculitis (AAV) is a small vessel vasculitis hallmarked by the presence of antibodies against antigens in cytoplasmic granules of neutrophils. Vaccines per se stimulate the immune system, including the innate and the adaptive immune response. Therefore, it is possible that an excess of autoimmunity is observed after vaccine administration. Vaccination (notably influenza) is a recognized trigger for the relapse of ANCA-associated vasculitis. ANCA associated vasculitis and autoimmune reactions have been reported with COVID-19 infection and following vaccination. Results We report the case of a Caucasian, 62 year-old-man, with a previous history of type 2 diabetes mellitus, hypertension and atrial fibrillation. Blood analysis one year before presentation showed preserved renal function and normal urinalysis. He received the first dose of Pfizer-BioNTech COVID-19 vaccine and two weeks later routine blood analysis showed acute kidney injury with serum Creatinine 1.75 mg/dL with de novo hematuria, a protein to creatinine ratio (RPC) 1.1 mg/g and candersartan (4 mg twice daily) was started. The patient received the second dose of COVID-19 vaccine 21 days after the first injection. Two weeks later he developed anorexia, nausea and de novo hematuria. He was admitted at the emergency department with deteriorating renal function with a sCr of 5.5 mg/dL, worsening hematuria with dysmorphic red blood cells and proteinuria (RPC 2.9 mg/g). Renal ultrasound was normal. Immunological studies revealed an elevated ANCA-MPO titer of 561. A kidney biopsy was performed and showed a crescentic necrotizing glomerulonephritis. Immunofluorescence confirmed pauciimmune glomerulonephritis. He was diagnosed with renal limited myeloperoxidase (MPO) ANCA AAV. He started 3 pulses of 500mg I.V methylprednisolone followed by prednisolone 1 mg/kg/day after that. He also started rituximab (4 doses of 500mg I.V once week apart). Despite the immunosuppression, the patient never recovered renal function and remained dialysis dependent. Conclusion Whether autoimmune diseases can be triggered after vaccination remains a matter of discussion among experts. ANCA associated vasculitis and autoimmune reactions have been reported with COVID-19 infection and following vaccination, which prompts the question whether this response could be a direct reaction to the RNA present in the vaccine. While an association with de novo ANCA vasculitis and COVID-19 vaccine may be possible, further investigation is necessary.

Background and Aims Cytomegalovirus (CMV) infection is an opportunistic pathogen in immunocompromised patients and its management is well described after solid organ/bone marrow transplant or in HIV patients. Although less common, since Systemic Lupus Erythemathous (SLE) is a chronic auto immune disease often requiring intense immunosuppression to induce remission of disease exacerbation, SLE patients are also prone to it. Besides complicating the course of the disease, it may be a life-threatening infection. Due to the heterogeneity of SLE manifestations, usually is difficult to distinguish between a SLE flare and CMV active infection, making the diagnose challenging. It has also been described in the literature as an exacerbating SLE factor. We report the case of an Asian, 27-year-old woman, with a recent SLE diagnosis that was admitted with a SLE flare while developing a CMV encephalitis. She was previously admitted due to a nephrotic syndrome. Immunological studies revealed an ANA title of 1:640 and a positive anti dsDNA Ab with diminished C3 and C4 levels, nephrotic range proteinuria and a diagnose of SLE was made. Renal biopsy revealed class IV lupus nephritis. She started high dose intravenous methylprednisolone (3 pulses of 500mg) and mycophenolate mofetil (MMF) at a dose of 2g per day. She was discharged taking 60 mg of oral prednisolone and the same dose of MMF. Two weeks after being discharged, she was readmitted due to worsening anaemia (Hb 6.8 g/dL), thrombocytopenia (Pl 27 000/µL) and deteriorating renal function with a sCr of 5.5 mg/dL with de novo haematuria. It was admitted a severe SLE flare and she was given another 3 pulses of 500mg I.V methylprednisolone and cyclophosphamide (CYC) was started (1 pulse of 500mg I.V). At the same time, she started to complain of myalgias and malaise, generalized hypotonia, developed fever, leukopenia with neutropenia and seizures. Serum CMV viremia was 71 000 copies and CMV polymerase chain reaction was positive in cerebrospinal fluid. She was started on I.V Ganciclovir, CYC was suspended and clinical improvement was observed. Conclusion Studies about the risk of different treatment drugs and other risk factors on the development of CMV disease in SLE are lacking. These studies will be useful for establishing guidelines on the institution of prophylaxis or pre-emptive treatment of CMV infection in SLE patients. Protocols for screening and prevention in this population should be implemented to account for this emerging problem. Given the rising prevalence of CMV infection in the past few years, the authors recommend that patients recently diagnosed with SLE while taking high doses of corticosteroids, which appears to be a risk factor for CMV reactivation, should be routinely tested for CMV viremia. There should be a low threshold for suspicion, hence treatment should be started as soon as possible given the high morbidity and mortality in severe cases.

BACKGROUND AND AIMS Antineutrophil cytoplasmatic antibody (ANCA) associated vasculitis (AAV) is a small vessel vasculitis hallmarked by the presence of antibodies against antigens in cytoplasmic granules of neutrophils. Vaccines per se stimulate the immune system, including the innate and the adaptive immune response. Therefore, it is possible that an excess of autoimmunity is observed after vaccine administration. Vaccination (notably influenza) is a recognized trigger for the relapse of ANCA-associated vasculitis. ANCA associated vasculitis and autoimmune reactions have been reported with COVID-19 infection and following vaccination. We report the case of a Caucasian, 62-year-old-man, with a previous history of type 2 diabetes mellitus, hypertension and atrial fibrillation. Blood analysis 1 year before presentation showed preserved renal function and normal urinalysis. He received the first dose of Pfizer-BioNTech COVID-19 vaccine and 2 weeks later routine blood analysis showed acute kidney injury with serum Creatinine 1.75 mg/dL with de novo hematuria, a protein-to-creatinine ratio (RPC) 1.1 mg/g and candersartan (4 mg twice daily) was started. The patient received the second dose of COVID-19 vaccine 21 days after the first injection. Two weeks later, he developed anorexia, nausea and de novo hematuria. He was admitted at the emergency department with deteriorating renal function with a sCr of 5.5 mg/dL, worsening hematuria with dysmorphic red blood cells and proteinuria (RPC 2.9 mg/g). Renal ultrasound was normal. Immunological studies revealed an elevated ANCA-MPO titer of 561. A kidney biopsy was performed and showed a crescentic necrotizing glomerulonephritis. Immunofluorescence confirmed pauci-immune glomerulonephritis. He was diagnosed with renal limited myeloperoxidase (MPO) ANCA AAV. He started three pulses of 500 mg I.V methylprednisolone followed by prednisolone 1 mg/kg/day after that. He also started rituximab (four doses of 500 mg I.V. once a week apart). Despite the immunosuppression, the patient never recovered renal function and remained dialysis dependent. CONCLUSION Whether autoimmune diseases can be triggered after vaccination remains a matter of discussion among experts. ANCA-associated vasculitis and autoimmune reactions have been reported with COVID-19 infection and following vaccination, which prompts the question whether this response could be a direct reaction to the RNA present in the vaccine. While an association with de novo ANCA vasculitis and COVID-19 vaccine may be possible, further investigation is necessary.

Background and Aims Vascular calcification is a common complication of chronic kidney disease (CKD), particularly in end-stage-renal disease (ESRD) and is predictive of subsequent cardiovascular disease and mortality. The aim of the present study was to evaluate the relationship between arterial calcification assessed by doppler ultrasound (DUS) performed by the same observer and biochemical parameters of CKD-MBD as well as the standard-of-care therapy for CKD-MBD. Method We present a retrospective study of 454 patients who were evaluated by DUS for pre-surgical vascular mapping from 2018 to 2021. Both arms brachial, radial and cubital arteries were analyzed, and vascular calcification was classified as absent, mild or moderate/severe (presence of acoustic shadowing). Laboratory serum analysis of PTH, serum Calcium (sCa), serum phosphorous (sPi) and serum magnesium (sMg) were collected (with a maximum interval of 6 months from DUS evaluation). Mortality was also registered during follow-up period. Results The demographics and biochemistry of the study population are summarized in Table 1. Arterial calcification was observed in 91.6% (n = 416) of the patients, 62.3% (n = 259) had mild calcification and 37.7% (n = 157) presented moderate/severe calcification. In univariate analysis, male gender (OR 2.2, p < 0.023), age (OR 1.03, p < 0.003), phosphate binders (OR 0.55, p value < 0.03) and cinacalcet use (OR 0.28, p < 0.019) were independently associated with the presence of arterial vascular calcification. Presence of vascular calcification on DUS was associated to mortality. In patients with vascular calcifications, moderate/severe calcification was associated with diabetes mellitus (OR 2.85, p<0.000), male gender (OR 1.69, p < 0.012), PAD (OR 2.43, p <0.001) and hemodialysis therapy for more than 5 years (OR 3.00, p< 0.010). Cinacalcet, phosphate binders, serum calcium, phosphorous, PTH and mortality did not correlate with calcification severity. In the multivariate logistic regression analysis adjusted to age, gender, PAD and serum calcium and magnesium, we found that serum PTHi (OR 1.00, p<0.040), hemodialysis for more than one year (OR 4.44, p< 0.040) and diabetes mellitus (OR 3.95, p< 0.001) were associated with moderate/severe vascular disease. Conclusion Concerning CKD-MBD related markers our study showed that only phosphate binders and cinacalcet use were predictive of absence of vascular calcifications, however no causality could be advanced with these data. For serious calcification, in our multivariable model, only PTH had statistical significance. It is widely recognized the importance of monitoring serum PTH, calcium and Pi to reduce the adverse clinical events associated with CKB-MBD. Widespread implementation of DUS in pre-surgical mapping for VA construction is also an opportunity for vascular study and features as calcifications can be a surrogate of CKD-MBD and cardiovascular burden.