The AKI was thought to be due to dehydration, which improved after a few days of fluid management with subsequent normalization of his blood pressure. vasculitis following COVID\19. strong class=”kwd-title” Keywords: COVID\19, diffuse alveolar hemorrhage, P\ANCA vasculitis AbbreviationsAKIacute kidney injuryBALbronchoalveolar lavageBUN/Cr models in mg/dlblood urea nitrogen to creatinine ratioCOVID\19coronavirus disease 2019FFBflexible fiberoptic bronchoscopyFiO2 fraction of inspired oxygenHb/Hct models in gm/dl and percent, respectivelyhemoglobin/hematocritHFNChigh flow nasal cannulaIgGimmunoglobulin GLPMliters per minuteMPOmyeloperoxidaseP\ANCAperinuclear anti\neutrophil cytoplasmic antibodiesPCRpolymerase chain reactionSARS\CoV\2severe acute respiratory syndrome coronavirus 2 1.?CASE DESCRIPTION A seventeen\12 months\old male with a past medical history of obesity and asthma was hospitalized due to COVID\19 pneumonia and respiratory insufficiency, requiring high flow nasal cannula (HFNC) up to 30 LPM, FiO2 50%. Chest X\ray showed moderate bilateral infiltrates. His initial admission Hb/Hct were 9.1/27.5 with a nadir of 7.7/23.8, and BUN/Cr was 9/0.78 during this hospitalization. He was treated with Remdesivir, Dexamethasone, Azithromycin, Beclomethasone inhaled 80?mcg twice daily, and iron supplementation. Before discharge his chest X\ray partly normalized and he was discharged home on room air. One month later, he was readmitted with elevated blood pressure, hematuria, and proteinuria, and diagnosed with acute kidney injury (AKI) with a BUN/Cr of 16/1.30. The patient’s lowest Hb/Hct during this Diethyl aminoethyl hexanoate citrate admission was 7.4/23.0. The AKI was thought to be due to dehydration, which improved after a few days of fluid Diethyl aminoethyl hexanoate citrate management with subsequent normalization of his blood pressure. He was discharged on room air, with Hb/Hct of 7.9/24.8 and a BUN/Cr of 15/0.99. One month after the second hospital admission, he presented to the emergency room with worsening cough, fatigue, exertional dyspnea, and amber\colored urine. SARS\CoV\2 PCR was unfavorable. He developed acute respiratory insufficiency requiring respiratory support with HFNC (40 LPM, FiO2 60%), AKI (BUN/Cr 30/1.52), and was revealed to have significant anemia (Hb/Hct 5.5/16.8). Computed tomography angiography of the chest showed no evidence of pulmonary embolus but did show extensive heterogeneous infiltrates in both lungs with an unusual fluffy central distribution concerning for diffuse alveolar hemorrhage (DAH) (Physique?1). Flexible fiberoptic bronchoscopy with bronchoalveolar lavage (FFB/BAL) exhibited DAH as evidenced by the BAL return color and RBC presence, along with positive hemosiderin\laden macrophages. Respiratory culture and PCR respiratory panel from BAL were unfavorable for an infectious etiology including unfavorable SARS\CoV\2 PCR. He then disclosed that he had a yearlong knee & lower back pain as well as generalized body aches, which were intensified after initial COVID\19 contamination. Rheumatologic evaluation revealed antinuclear antibody, Diethyl aminoethyl hexanoate citrate perinuclear anti\neutrophil cytoplasmic antibodies (P\ANCA), and myeloperoxidase (MPO) antibody positivity, culminating in a diagnosis of ANCA positive vasculitis. Renal biopsy showed necrotizing glomerulonephritis with limited immune complex deposition. Open in a separate Diethyl aminoethyl hexanoate citrate window Physique 1 CT angiography noting extensive heterogeneous infiltrates in both lungs with an unusual fluffy central distribution concerning for diffuse alveolar hemorrhage He was initially treated with methylprednisolone (1?g/day) for 72?h and was simultaneously started on plasmapheresis which he received for 5 consecutive days. Following plasmapheresis, he was started on cyclophosphamide infusions 10?mg/kg IV every 2 weeks and methylprednisolone was slowly weaned to 0.85?mg/kg/day over 7 days, and then was transitioned to oral steroids. DAH and AKI resolved, and he was discharged on room air without need for outpatient dialysis. 2.?DISCUSSION The precise etiology of autoimmune disorders is yet unclear, though there is growing evidence that there is a role for both genetic Diethyl aminoethyl hexanoate citrate predisposition and environmental factors. 1 It is proposed that infections with bacterial or viral organisms trigger an exaggerated host immune response via molecular mimicry and activation of pre\primed autoreactive T cells and proinflammatory mediators. 1 This in turn may lead to tissue damage and multisystem organ dysfunction. 1 SARS\CoV\2 has been shown to share similar pathogenic mechanisms driving an exaggerated immune response. 2 Rabbit Polyclonal to COPS5 There is a growing evidence to suggest an association between prior SARS\CoV\2 contamination and subsequent development of autoimmune disordersprimarily in the adult populationsuch as Systemic Lupus Erythematosus, GuillainCBarr syndrome, Kawasaki disease, and Rheumatoid Arthritis. 2 In the pediatric.
The AKI was thought to be due to dehydration, which improved after a few days of fluid management with subsequent normalization of his blood pressure
Previous articleUse of the CNC minimizes nonspecific interactions (which modify the PL) between conjugated polyelectrolytes and biopolymersNext article Along with inhalation of oxygen, the patient was subjected to methylprednisolone pulse therapy (1000?mg daily for 3?days) followed by prednisolone treatment (30?mg daily), which resulted in the regression of pulmonary lesions, and facilitated the tapering of prednisolone dose