COVID-19 and Acute Kidney Injury (AKI)

(See also Acute Kidney Injury and COVID-19.)

The presence of AKI increases risk of mortality in patients with COVID-19 (1). In a systematic review and meta-analysis, the incidence of AKI was 17%, although it varied from 0.5 to 80% among individual studies depending on geographic location and number of critically ill patients. In this meta-analysis, the overall mortality was 11% and AKI increased the risk of death; utilization of renal replacement therapy was 5% overall (2).

While the data are new and evolving, the following have been described as independent risk factors for AKI with COVID-19 (3) thus far:

• Age

• Race (higher among Black people)

• Diabetes

• Obesity

• Hypertension

• Cardiovascular disease

• Low baseline kidney function

• Mechanical ventilation

• Shock requiring vasopressors

Early studies suggest that the pathophysiology of AKI may be due to ischemia during sepsis, systemic inflammatory response to the virus, and potentially direct viral toxicity to the kidneys. Kidney histopathology most commonly shows acute tubular necrosis (ATN) and, less commonly, collapsing focal segmental glomerulosclerosis (FSGS; [4]) or renal infarction.

Presentation of AKI in patients with COVID-19 is similar to that of other infectious etiologies, including elevated creatinine, oliguria or anuria, and in some cases proteinuria (including nephrotic range) and hematuria (1). Treatment is focused on supportive care, including intravascular volume optimization (balanced against the risk of pulmonary edema in patients with respiratory distress), monitoring of electrolytes, and possibly dialysis. Due to the increased risk of dialysis circuit thrombosis, patients requiring hemodialysis are treated with anticoagulation unless contraindicated by bleeding risk. Infection control is of the utmost importance.