A 63-year-old man with past medical history of diabetes mellitus, hypertension, and hyperlipidemia was hospitalized for COVID-19 pneumonia after being diagnosed with COVID-19 10 days before. He was improving initially, but a few days prior to admission, he experienced worsening shortness of breath and generalized myalgia. Upon presentation, he was hypoxic and required high flow oxygen via a nasal cannula. He was given dexamethasone, baricitinib, and remdesivir. Despite the treatments, his respiratory status deteriorated and, on hospital day 7, he required intubation and mechanical ventilation. In the subsequent week, he became increasingly septic and hypotensive that required vasopressors. Urine output decreased significantly and, on hospital day 15, he became oliguric with total urine output less than 100 ml in 24 hours. Nephrology consultation was requested.
Physical examination was significant for diminished lung sounds and diffuse anasarca in his upper and lower extremities. He was intubated and required 100% FiO2. Arterial blood gas showed severe respiratory acidosis due to hypercapnia with a component of gap metabolic acidosis. Arterial blood gas showed a pH of 7.10, PaCO2 71 mm Hg with serum CO2 21 mmol/L. The rest of the laboratory tests showed:
Serum creatinine 3.1 mg/dL (baseline 0.8 mg/dL)
Blood urea nitrogen (BUN) 83 mg/dL
Serum sodium 135 mmol/L, potassium 3.8 mg/dL, chloride 98 mmol/L, and calcium 8.7 mg/dL
White blood cell count 18 x 109 cells/L
Hemoglobin 8.3 mg/dL
D-dimer 4.69 (normal ≤0.49 mcg FEU/mL)
Urine microscopy showed many muddy brown casts and non-dysmorphic red blood cells.
A dialysis catheter was placed in the internal jugular vein. Continuous kidney replacement therapy (CKRT) was initiated. Continuous venovenous hemofiltration (CVVH) with sodium bicarbonate replacement was used as the CKRT modality.