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Abstract: FR-PO054

AKI in COVID-19 Infection: Role of Hypercatabolic Status

Session Information

Category: Coronavirus (COVID-19)

  • 000 Coronavirus (COVID-19)

Authors

  • Muhammad, Qasim, The George Washington University, Washington, District of Columbia, United States
  • Li, Ping, Veterans Health Administration, Washington, District of Columbia, United States
Introduction

Acute Kidney Injury (AKI) is a very common complication of patients with SARS-COV-2 virus (COVID-19) infection. COVID-19 infected patients have longer hospital length of stays and higher mortality rate. There are multiple postulated mechanisms for AKI in the setting of COVID-19. Some researchers reported that the COVID-19 virus directly binds to the ACE-2 receptors in proximal tubules and leads to tubular dysfunction. In rare cases, a hypercatabolic state can be seen that carries a significantly higher mortality rate with ensuing hyperuricemia and hyperphosphatemia.

Case Description

We describe a patient presenting with severe AKI with hypercatabolic state in the setting of COVID-19 infection. 40 year old male with a history of hypertension and CHF (EF 35%) presented with fatigue, diarrhea, nausea and vomiting for 10 days after COVID-19 infection. He was found to have severe AKI with blood urea nitrogen of 254 and creatinine of 21 mg/dl which was associated with hyperkalemia, gap acidosis, severe hyperuricemia (23 mg/dl) and hyperphosphatemia (17 mg/dl) . Despite aggressive volume resuscitation in the ICU, the patient remained oliguric with no improvement in kidney function for two days. He was subsequently initiated on hemodialysis. After getting 2 sessions of dialysis without ultrafiltration, renal recovery was noted eventually normalizing within 10 days. Extensive work up indicated the patient had no tumor lysis syndrome and rhabdomyolysis on this admission.

Discussion

There are multifactorial mechanisms for AKI in patients with COVID-19 infection including direct viral invasion of the kidney proximal tubules. Our case demonstrated that a hypercatabolic state may contribute to AKI in these patients. The proposed mechanisms involve elevated serum uric acid levels causing small renal arterial constriction, glomerular auto-dysregulation and tubular crystallization due to supersaturation causing to kidney tubular injury. Thus, clearance of uric acid and phosphorus with dialysis may promote more rapid kidney function recovery.