AKI

Acute kidney injury (AKI) is a rapid decline in kidney function, leading to the accumulation of waste products, disturbances in fluids and electrolytes, and potential problems with acid-base balance. It develops over hours to days and is common in hospitalized and critically ill patients. AKI differs from chronic kidney disease in its sudden onset and potential for partial or complete recovery.

AKI is usually categorized by site of injury: prerenal AKI results from reduced kidney perfusion; intrinsic (or intrarenal) AKI involves damage to kidney tissue, most often from ischemia or nephrotoxins; and postrenal AKI arises from obstruction of urine flow. Risk factors include advanced age, preexisting CKD, diabetes, hypertension, heart failure, sepsis, dehydration, major surgery, and exposure to nephrotoxins such as NSAIDs, aminoglycosides, and contrast agents.

Diagnosis relies on rapid changes in renal function. KDIGO criteria define AKI as an increase in serum creatinine by at least 0.3 mg/dL within 48 hours, an increase to 1.5 times baseline within 7 days, or urine output under 0.5 mL/kg/h for 6 hours. AKI is staged from 1 to 3 based on the degree of creatinine rise and urine output. Management focuses on identifying and treating the underlying cause, maintaining adequate blood flow to the kidneys, avoiding nephrotoxic drugs, and adjusting medications. In severe cases, renal replacement therapy (dialysis or continuous therapies) supports patients with refractory metabolic disturbances or fluid overload. Prognosis varies; many patients recover renal function, but AKI is associated with higher short-term mortality and an increased risk of developing chronic kidney disease or end-stage kidney disease after an episode.