Acute Kidney Injury

Acute kidney injury (AKI) is an abrupt decline in kidney function over hours to days. The kidneys may produce less urine, lose the ability to regulate potassium and acid-base balance, retain sodium and water, and clear medications more slowly. A patient can therefore become unstable before the serum creatinine has had time to rise substantially. The usual classification asks where the initiating problem is: - Pre-renal AKI: inadequate renal perfusion, with initially intact renal tissue. - Intrinsic or intra-renal AKI: injury within the tubules, glomeruli, interstitium, or renal vasculature. - Post-renal AKI: impaired urinary outflow from obstruction. These categories organize the differential diagnosis; they are not KDIGO stages. Consider a patient who has had several days of vomiting, is taking lisinopril and ibuprofen, and now has a falling urine output. The immediate concern is not simply “a high creatinine.” The combination of volume loss, an afferent-arteriole constricting drug, and an efferent-arteriole relaxing drug can sharply reduce filtration. The nurse’s first task is to identify the reversible perfusion problem and prevent the decline from becoming tubular injury.