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COVID-19–Associated Prerenal Acute Kidney Injury: Hemodynamic Instability and Renal Hypoperfusion
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Background: COVID-19 not only primarily affects the respiratory system, but renal involvement is increasingly recognized. Prerenal acute kidney injury (AKI) is a common and potentially reversible complication driven by hypovolemia, hypoxia, systemic inflammation, and hemodynamic instability.Case Presentation: A 60-year-old male presented with fever, dry cough, dyspnea, oliguria, and generalized weakness. Laboratory findings revealed elevated blood urea nitrogen and serum creatinine, a high BUN/creatinine ratio, low urine sodium (18 mmol/L), high urine osmolality (650 mOsm/kg), and a low fractional excretion of sodium (0.67%), consistent with prerenal AKI. Chest imaging suggested viral pneumonia, and RT-PCR confirmed COVID-19 infection. Renal ultrasonography showed normal kidney structure with reduced renal perfusion. The patient was diagnosed with stage II prerenal AKI secondary to COVID-19. Management included oxygen therapy, prompt fluid resuscitation with lactated Ringer’s solution, anticoagulation, and supportive care. Renal function and urine output improved within 48 hours without the need for renal replacement therapy.Conclusion: COVID-19 can precipitate prerenal AKI through hypovolemia, hypoxia, and inflammation-mediated hemodynamic disturbances. Early diagnosis using urinary biomarkers and prompt fluid resuscitation can lead to complete renal recovery.
Title: COVID-19–Associated Prerenal Acute Kidney Injury: Hemodynamic Instability and Renal Hypoperfusion
Description:
Background: COVID-19 not only primarily affects the respiratory system, but renal involvement is increasingly recognized.
Prerenal acute kidney injury (AKI) is a common and potentially reversible complication driven by hypovolemia, hypoxia, systemic inflammation, and hemodynamic instability.
Case Presentation: A 60-year-old male presented with fever, dry cough, dyspnea, oliguria, and generalized weakness.
Laboratory findings revealed elevated blood urea nitrogen and serum creatinine, a high BUN/creatinine ratio, low urine sodium (18 mmol/L), high urine osmolality (650 mOsm/kg), and a low fractional excretion of sodium (0.
67%), consistent with prerenal AKI.
Chest imaging suggested viral pneumonia, and RT-PCR confirmed COVID-19 infection.
Renal ultrasonography showed normal kidney structure with reduced renal perfusion.
The patient was diagnosed with stage II prerenal AKI secondary to COVID-19.
Management included oxygen therapy, prompt fluid resuscitation with lactated Ringer’s solution, anticoagulation, and supportive care.
Renal function and urine output improved within 48 hours without the need for renal replacement therapy.
Conclusion: COVID-19 can precipitate prerenal AKI through hypovolemia, hypoxia, and inflammation-mediated hemodynamic disturbances.
Early diagnosis using urinary biomarkers and prompt fluid resuscitation can lead to complete renal recovery.
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