Acute Kidney Injury

Acute kidney injury (AKI) is an abrupt decline in glomerular filtration caused by reduced renal perfusion, renal ischaemia, or direct nephrotoxic injury. The resulting fall in filtration impairs excretion of potassium, acid, fluid, and uraemic waste. The cause may be outside the kidney, within the kidney, or downstream from it. Reduced circulating volume, sepsis, or haemorrhage can deprive the kidneys of perfusion. Ischaemia and nephrotoxins can injure renal tissue directly. Urinary obstruction can raise pressure behind the nephron and reduce effective filtration. These mechanisms can coexist; a patient with sepsis may be both vasodilated and exposed to nephrotoxic medications. Urine output is often the first useful bedside signal, but AKI is not always oliguric. A patient can have a meaningful creatinine rise while continuing to produce urine. Conversely, a single low-volume void does not establish AKI. The pattern over time matters. The nurse’s task is therefore not simply to “watch the creatinine.” It is to connect urine output, perfusion, volume status, medication exposure, laboratory trends, and the patient’s overall trajectory.