Development of crescentic membranoproliferative glomerulonephritis after COVID-19 vaccination.

Membranoproliferative glomerulonephritis (MPGN) comprises a histologic pattern of glomerular injury with different underlying diseases. Here we report on a 47-year-old female with rapidly progressive glomerulonephritis (RPGN) on top of a previously diagnosed idiopathic MPGN after receiving the first dose of the Pfizer-BioNTech coronavirus disease 2019 (COVID-19) mRNA vaccine. After aggressive immunosuppression her serum creatinine returned to normal values, along with reduction of proteinuria. Recently, numerous publications have reported an association of glomerular diseases with COVID-19 vaccination. Our case presents to the best of our knowledge the first occurrence of possible association of COVID-19 mRNA vaccination with a crescentic form of MPGN.

Acute viral myositis: profound rhabdomyolysis without acute kidney injury.

BACKGROUND: Acute viral myositis (AVM) may be triggered by influenza A/B, enteroviruses and other viruses. Severe complications including rhabdomyolysis regularly lead to acute kidney injury (AKI). The aim of this short report was to discuss management and differential diagnosis of massive creatine kinase (CK) elevation. PATIENT, MATERIAL AND METHODS: Herein, we report on a 19-year-old Austrian male of African descent with a history of respiratory tract infections and whole-body pain. He further developed acute viral myositis and massive CK elevation up to 440,000 IU/L but without any signs of AKI. A literature search relating AVM, management and differential diagnosis of rhabdomyolysis was conducted in PubMed and UptoDate. RESULTS: A full panel of serological and autoimmune blood work-up including testing for human immunodeficiency virus (HIV), hepatitis, influenza A/B, Epstein-Barr virus (EBV), antinuclear antibodies (ANA) and autoantibodies against various extractable nuclear antigens (ENA) did not reveal evidence for viral originators or autoimmune diseases. This case indicates that in acute viral myositis associated with extreme CK elevation (>400,000 IU/L) AKI might be completely absent. Potential causes for this clinical phenotype, differential diagnosis and management are discussed.

Pulmonary embolism four days after interruption of therapy with rivaroxaban.

Thrombosis after cessation of anticoagulation, also named rebound thrombosis, is a matter of concern and controversy. There are only few published data about occurrence of rebound thrombosis associated with non-vitamin K-antagonist oral anticoagulant drugs (NOACs). We report on a 58-year-old male with paroxysmal atrial fibrillation (AF) with a CHA2DS2VASC score of 4 who developed central pulmonary embolism four days after interruption of rivaroxaban because of parotid surgery. He had received 40 mg enoxaparin/d. The parotid gland was partially resected within 6 hours without blood loss. Pulmonary embolism and AF occurred on the first postoperative day. He recovered with low-molecular-weight heparin in therapeutic dosages and amiodarone and was discharged with phenprocoumon. The relevance of a rivaroxaban rebound phenomenon, manifesting as arterial embolism, stroke or venous thromboembolism should be clarified. It should be assessed if rebound-phenomena also exist for the NOACs dabigatran, apixaban and edoxaban. Thus, the randomized trials and registries investigating patients with AF or venous thromboembolism should be re-analysed and, based on these data, recommendations should be developed for situations in which NOAC-therapy has to be interrupted or ceased.