A 32-year-old fully vaccinated, non-smoker male patient with unremarkable past medical history presents to the hospital with a complaint of rash and joint pain. His symptoms started 2 weeks ago, with unilateral conjunctival injection, sinus congestion, and migratory polyarthralgia. The patient had been seen earlier at an urgent care facility and started on a course of amoxicillin, methylprednisolone, and a steroid shot without any improvements. He also complained of nonproductive cough and purpura on both hands and feet for 1 week, which started with multiple tiny red spots on his legs and gradually increased in size. He reported associated splinter hemorrhages of multiple fingernails, significant night sweats, body aches, fatigue, headache, migratory arthralgias, and poor appetite for a few days. He had no history of sexually transmitted diseases or alcohol or drug use. His family history was notable for lupus in his mother, a prothrombin gene mutation, and factor-V Leiden mutation with a history of blood clots in multiple family members.
The patient's SARS-CoV-2 antigen and PCR test were positive. Initial lab work showed hyponatremia (121), hyperkalemia (5.9), elevated blood urea nitrogen, elevated creatinine (5.5), decreased glomerular filtration rate (14 mL/min), and elevated erythrocyte sedimentation rate, c-reactive protein, lactate dehydrogenase, d-dimer, and ferritin. Initial evaluation revealed multiple abnormalities, including sepsis, COVID-19 infection, acute renal failure, and features suggestive of vasculitis. Chest X-ray showed mixed density perihilar opacities in both lungs. Computed tomography (CT) of the chest showed extensive airspace opacities in both lungs, suggesting COVID-19 multifocal, multilobar pneumonitis.
He was initially started on broad-spectrum antibiotics (cefepime and vancomycin) for sepsis and underwent extensive workup for concomitant infections, which were negative, including a transthoracic echocardiogram. QuantiFERON-TB was indeterminate. He also had to undergo intermittent hemodialysis briefly for acute renal failure. Renal ultrasound was normal; however, renal biopsy indicated limited thrombotic microangiopathy and tubulointerstitial nephritis, for which he was started on steroids, and his renal functions gradually improved.
The purpuric rash was a diffuse leukocytoclastic rash with macular erythema distributed on both hands and feet. He tested positive for C-ANCA during an immune workup, and antinuclear antibody testing was negative. The rash worsened initially for a few days and improved gradually after the immunosuppressive therapy started. X-rays of the wrist and knee, along with right knee arthrocentesis done for joint pain and swelling, did not show any abnormalities.
The patient developed a non-occlusive thrombus in the proximal segment of the left superficial femoral vein, and he was initiated on a heparin infusion. Two days later, he developed left flank pain and was diagnosed with left renal hemorrhage with active extravasation noted on CT angiogram. Most likely, the cause of his left renal hematoma was status post renal biopsy. Heparin was discontinued, and he was given protamine zinc. Embolization was performed by interventional radiology. He also developed acute blood loss anemia secondary to renal hemorrhage, and he was transfused PRBC. Repeat venous Doppler did not show any further evidence of deep venous thrombosis. Repeat renal ultrasound did not show hematoma.
His hospital course was very complicated, requiring the involvement of various specialists, including infectious disease, nephrology, hematology/oncology, rheumatology, dermatology, orthopedics, pulmonology, and interventional radiology. In brief, the patient's creatinine improved during the hospital course. His acute kidney injury was thought to be due to interstitial nephritis from recent antibiotic use or an immunologic reaction. The patient had a confusing picture, and the exact cause of his vasculitis or nephritis was unknown. His inflammatory markers improved throughout the hospital course, and he was cleared for discharge on a steroid taper for nephritis, with outpatient follow-up by all the consultants. He was discharged with a steroid taper for nephritis.
Once the taper reached less than 10 mg/day, he developed acute scleritis and a new pulmonary cavitary lesion of 6 cm. The biopsy via bronchoscopy revealed acute inflammatory cells with hemosiderin-laden macrophages and negative cultures, including bacterial, fungal, and acid-fast bacilli. He was restarted on systemic steroids for scleritis after failing topical steroids, which incidentally also reduced the size of the cavitary lesion, indicating an immune component.