A 53-year-old male with no past medical history presented to a private clinic with flu-like symptoms. He underwent investigations in a private clinic and was discharged on an antibiotic, anti-pyretic and a cough syrup for 5 days with no improvement. He presented again to the emergency department with a one-week history of fever and intermittent chills. He also had productive cough with thick mucoid sputum. He was tachypneic with mild shortness of breath and complained of myalgia and general malaise. He had no history of recent travel, but he mentioned that his spouse had the same symptoms.
On admission, he had a temperature of 39°C with a regular heart rate of 90 bpm and a blood pressure of 128/70 mmHg. His respiratory rate was 28 breaths per minute, and his peripheral oxygen saturation was 94% on room air. Arterial blood gas (ABG) was sent on room air, and a partial oxygen (PO2) of 62 mmHg (normal 75 to 100 mmHg), PCO2 of 35 mmHg (normal 35-45) mmHg, lactic acid of 0.5 (normal 0.5-1 mmol/L), and inflammatory marker were as follows: C reactive protein (CRP) was 50.1 mg/L (normal range 0–10 mg/L), and procalcitonin (PCT) was 0.11 ng/mL (minor 0.10 – 0.49 ng/mL). All blood electrolytes were within the normal range. The patient’s serum creatinine and urea levels were normal on admission, as were his transaminases, bilirubin and albumin. His creatinine clearance was > 60 ml/min on with no history of renal disease.
Moreover, his chest examination showed normal breath sounds with left side crackles and no wheezes. His chest X-ray image showed multifocal patchy areas of airspace opacities, with the bronchogram noted bilaterally predominantly in the lower zones. obscuration of the left costophrenic angle (CP) angle noted. (Figure 1. A)
The patient was assessed as having a lower respiratory tract infection, viral in origin. COVID-19 was suspected. Therefore, the patient was kept under airborne and contact isolation. Nasopharyngeal aspirate was sent, and the results were positive for severe respiratory syndrome coronavirus 2. The case was confirmed as COVID-19 pneumonia, and he was admitted to the medical intensive care unit (MICU).
He was started on the treatment suggested by the local protocol for the management of COVID-19, which consists of azithromycin, hydroxychloroquine, cobicistat boosted with darunavir and oseltamivir with concomitant antibiotics. (figure 2)
On day 4 of treatment, his fever subsided, and the patient began to improve. He was able to move around with mild tachypnea. The patient was discharged from the MICU to the medical unit, but he still required oxygen on and off through noninvasive ventilation. On day 5 of treatment, chest X-ray was repeated, which showed slight progression of perivascular infiltrates/airspace opacities prominent at the right lung field and left lower lungs. (Figure 1. B)
An abrupt rise in the patient’s serum creatinine occurred on day 9 of treatment. His serum creatinine increased from 87 μmol/L to 113, 162 and 365 μmol/L on days 9, 10 and 11 of treatment, respectively. He was considered a case of acute kidney injury. His serum creatinine continued to trend until it reached 571 μmol/L. Upon worsening of renal functions, the patient was oliguric and complained of symptoms of nausea and vomiting. He was encouraged to drink water, and intravenous fluid was administered. Oseltamivir and ampicillin-sulbactam were discontinued due to his condition.
Ultrasound for the kidney was performed, and based on the report, the right kidney measured 11.6x5.1 cm in length, and the left kidney measured 11x5.6 cm. No masses, cysts, calculi, or hydronephrosis were seen. There was a mild bilateral increase in renal cortical echogenicity. The urinary bladder was distended with urine and showed normal wall thickness without masses. The prostate was normal sized (25 cc) with normal echogenicity. Therefore, the impression was a mild bilateral increase in renal parenchymal echogenicity, and there was no sign of obstructive uropathy. (Figure 3)
At the time of rise in serum creatinine, the urine protein creatinine ratio was 76.00 mg/mmol (normal range <15 mg/mmol), urine eosinophils were negative, creatine kinase came 160 U/L, myoglobin was 193 ng/mL, urine sodium was 32 mmol/L and fractional excretion of sodium (FENa) was 1.9%, indicating the cause of intrinsic acute kidney injury (AKI).
The next day, after stopping darunavir on day 10, the patient’s symptoms were settling, and a repeated serum creatinine level had come down to 333 μmol/L, fluid intake 4.3 L and urine output 4.2 L, patient acute kidney injury recovered and decreased gradually to reach 119 μmol/L. He completed his COVID-19 treatment without further problems and had good clinical improvement. Then, he was transferred to the isolation point to complete a total of 28 days from the first positive PCR result. Virologic clearance was reached after 22 days of treatment.