The coronavirus disease 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2). Infection by the SARS-CoV-2 increases the risk for systematic multi-organ complications and venous, arterial thromboembolism. The need for an effective vaccine to combat the pandemic prompted the Centers for Disease Control and Prevention (CDC) and Food and Drug Administration (FDA) to approve a nationwide distribution of the Ad26.COV2.S vaccine manufactured by Johnson & Johnson (J&J). The use of the vaccine was halted after reported cases of cerebral venous sinus thrombosis (CVST) and thrombocytopenia among recipients. Researchers have postulated these rare occurrences as potentially immune-triggered responses associated with complement-mediated thrombotic microangiopathy (TMA). Thrombotic complications and thrombocytopenia increase the risk for blood clot growth due to the inflammation of immune complexes by pro-thrombotic activation of anti-platelet antibodies.A 52-year-old man presented to the intensive care unit (ICU) with severe dyspnea. He required bilevel positive airway pressure (BiPAP) for supplemental oxygen therapy. Endotracheal intubation was performed due to his worsened respiratory deterioration. Lab results suggested respiratory failure due to decreased partial pressure of oxygen (pO 2 ) and increased partial pressure of carbon dioxide (pCO 2 ). Findings of elevated D-dimer levels with decreased fibrinogen and thrombocytopenia with prolonged prothrombin clotting time were consistent for disseminated intravascular coagulation (DIC). Chest radiography displayed moderate to heavy bilateral airspace consolidations, consistent with multifocal pneumonia suspicious for COVID-19. A computed tomography angiogram (CTA) revealed a mildly enlarged right ventricle and interventricular septum consistent for right heart strain due to a saddle pulmonary embolism (PE) that extended into the main pulmonary lobar segmental arteries bilaterally. The patient was transferred to a higher-level (tertiary) care for radiology intervention to remove the pulmonary embolism found on his lungs.This patient presented with severe dyspnea secondary to massive PE and deep venous thrombosis (DVT) due to SARS-CoV2 infection following the administration of the J&J vaccine. Bilateral thrombus opacities and pulmonary emboli are consistent among COVID-19 patients by intravascular coagulation with increased prothrombin time and D-dimer concentration with a low platelet count. Adverse emboli growths with increased D-dimer and thrombocytopenia strikes a similarity in recipients of the AstraZeneca vaccine due to vaccine-induced immune thrombotic thrombocytopenia (VITT). Administrative use of the J&J vaccine resumed in May 2021. The FDA's reassurance stemmed from their conclusive findings that the vaccine's benefits far outweigh these rare developments, which account for less than 0.01% of the total recipient population. Nevertheless, a further detailed analysis must be conducted on the adverse thrombotic manifestations...

Since its initial reporting in December 2019, the novel coronavirus SARS-CoV-2 has emerged as a global health problem after its official declaration as a pandemic by the World Health Organization, with an estimated 346 million cases and over 5.9 million fatalities as of January 22, 2022. Studies on the prevalence of COVID-19 among severe cases have shown that comorbidities and risk factors such as obesity, increased aging, and chronic cardiovascular and respiratory diseases play a role in the severity of SARS-CoV-2 infections. The interactions between such factors and their involvement with the progression of infection and mortality remain unclear.While it is known that SARS-CoV-2 damages the lungs, various morbidities such as acute kidney disease and thyroid dysregulation have recently emerged in symptomatic COVID-19 patients. Conditions that alter thyroid hormones, which play a critical role in regulating metabolic pathways, have a role in the level of infectivity of the SARS-CoV-2. The capability of the SARS-CoV-2 to invade and affect any organ system is dependent on its access to the angiotensin-converting enzyme II (ACE2) commonly expressed among various host cells. This binding puts any system at high risk of direct viral injury, inevitably creating an excessively high concentration of anti-inflammatory mediators and cytokines to predispose COVID-19 patients to a state of severe immunosuppression. This case report describes a 62-year-old female who tested positive for COVID-19, with a medical history of hypothyroidism, who presented with a unique combination of acute bacterial hemorrhagic pyelonephritis and ureteral obstruction. She experienced intermittent dysuria, urinary urgency, and hematuria over the past five days. She developed chills, diaphoresis, nausea, and vomiting after administering acetaminophen for her headache. Ageusia and anosmia accompanied her respiratory illnesses despite receiving the Pfizer double dose vaccine six months before her arrival. A computerized tomography (CT) scan revealed severe to moderate inflammation surrounding the enlarged kidney with a 1 mm ureteral stone. Blood and urine cultures showed the growth of Escherichia coli gram-negative bacilli. Chest X-rays displayed a patchy appearance in the right infrahilar airspace, reflecting atelectasis in part for the diagnosis of COVID-19 with additional laboratory findings of profoundly elevated C-reactive protein, fibrinogen, and d-dimer levels. Abdominal CT scans revealed a hemorrhagic ureteral obstruction and massive swelling of the renal parenchyma persistent to pyelonephritis and hydronephrosis.