From the Research
Amphotericin B can cause acute kidney injury (AKI) within 2 days of administration, as defined by a ≥0.3 mg/dL increase in serum creatinine, according to the study by 1. The nephrotoxic effect of amphotericin B typically develops rapidly, with detectable changes in kidney function often occurring within the first few days of treatment. The risk of AKI increases with higher cumulative doses, longer duration of therapy, and higher daily doses. Amphotericin B causes nephrotoxicity through multiple mechanisms, including direct damage to renal tubular cells, vasoconstriction of renal blood vessels, and inflammatory responses that further compromise kidney function. Some key factors associated with AKI in patients administered liposomal amphotericin B include prior treatment with certain medications, concomitant administration of catecholamines or immunosuppressants, and higher dosing of liposomal amphotericin B, as reported by 1. Patients receiving amphotericin B should have their kidney function monitored closely, particularly during the initial days of treatment. Preventive strategies include adequate hydration before infusion, slower infusion rates, and using lipid formulations of amphotericin B which have lower nephrotoxicity profiles compared to conventional formulations, as suggested by 2. Early detection of rising creatinine levels or declining glomerular filtration rate can allow for timely intervention to prevent progression to severe kidney injury. Additionally, daily consecutive fluid infusion from the onset of AKI may be associated with recovery from stage 1 AKI in patients administered liposomal amphotericin B, with daily fluid volume positively correlating with the incidence of AKI recovery, as found by 3. It is essential to weigh the benefits and risks of using amphotericin B, especially in critically ill patients with invasive fungal infections, as discussed by 4. Overall, the minimum duration for amphotericin B to cause AKI is 2 days, as supported by the study by 1.