Acute Kidney Injury

The literature grounding supports multiple causes, including infections, hypovolaemic shock, sepsis, drugs, invasive procedures, trauma, and chemically induced injury. In the methotrexate literature, acute kidney injury can occur from crystallization of methotrexate in the renal tubular lumen, causing tubular toxicity.

Acute kidney injury reflects diverse pathophysiological mechanisms, but a central feature is acute loss of kidney epithelial cells. In toxic injury such as methotrexate-associated AKI, tubular crystal deposition leads to tubular damage and impaired renal clearance. Regulated cell death pathways are implicated in kidney disease, and ferroptosis is described as an iron-dependent form of cell death involving lipid peroxidation, reduced antioxidant capacity, and oxidative cell death that is linked to kidney injury.

Reported risk factors include older age in hospitalized patients, sepsis, drugs, invasive procedures, infection, trauma, and low-income or middle-income settings where infections and hypovolaemic shock are predominant causes. For methotrexate-associated AKI, risk factors include prior renal dysfunction, volume depletion, acidic urine, and drug interactions.

The supplied grounding supports treatment at the modality and drug-class level only in broad terms. Management includes therapy and drug therapy for the underlying cause and prevention or management of complications, but no specific standard regimen is provided in the grounding.