Prerenal acute kidney injury diagnosed by urinary indices in a COVID-19 patient: A critical care case report.

Coronavirus Disease 2019 (COVID-19) primarily affects the respiratory system but can also cause acute kidney injury (AKI). Infection-related circulatory disturbances driven by systemic inflammation, cytokine release, and reduced effective blood volume play a central role in prerenal AKI. The diagnostic challenge in infection-associated AKI is distinguishing functional hypoperfusion from intrinsic renal injury, particularly when relying solely on serum creatinine. Laboratory investigations showed elevated blood urea nitrogen (BUN) (51 mg/dL) and serum creatinine (2.7 mg/dL), with reduced estimated glomerular filtration rate (eGFR) of 32.5 mL/min. Targeted urinary indices (low urine sodium, high osmolality, and FeNa <1%) were instrumental in identifying a reversible perfusion-related etiology, minimizing the risk of diagnostic misclassification. Renal ultrasonography showed normal kidney size and architecture. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection was confirmed by reverse transcription polymerase chain reaction (RT-PCR). The patient received oxygen therapy, IV Ringer's lactate, furosemide for diuresis, low-molecular-weight heparin for thromboprophylaxis, and ceftriaxone for secondary infection prevention. Potassium imbalance was corrected with intravenous and oral supplementation of potassium chloride. Urine output improved within 48 h, and renal function recovered (eGFR 61 mL/min/1.73 m²) without renal replacement therapy. Two consecutive negative RT-PCR tests confirmed viral clearance. The patient was discharged in stable condition with outpatient follow-up.