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Introduction
Acute kidney injury (AKI) is a sudden fall in kidney function that lets waste products, fluid and electrolytes build up. It is common in hospitalized patients and is linked to higher mortality and to later chronic kidney disease (Kellum et al., 2021).
Defining and staging AKI
KDIGO defines AKI as any of the following: a rise in serum creatinine of 0.3 mg/dL or more within 48 hours; a rise to 1.5 times baseline or more within the previous seven days; or urine output below 0.5 mL/kg/h for six hours (Kidney Disease: Improving Global Outcomes Acute Kidney Injury Work Group, 2012). Stages 1 to 3 describe increasing severity.
Prerenal AKI
Prerenal AKI results from reduced blood flow to otherwise healthy kidneys, as in dehydration, hemorrhage, heart failure or the hypotension of sepsis. The kidneys respond by conserving sodium and water, so urine becomes scant and concentrated. If perfusion is restored quickly, function usually recovers; if not, ischemia damages the tubules.
Intrinsic AKI
Intrinsic AKI involves damage within the kidney itself. The most common form is acute tubular necrosis (ATN), caused by prolonged ischemia or by nephrotoxins such as aminoglycosides, iodinated contrast and NSAIDs. Injured tubular cells slough into the tubules, form casts that obstruct flow and allow filtrate to leak back into the circulation, so the glomerular filtration rate falls. Glomerulonephritis and acute interstitial nephritis are less common intrinsic causes.
Postrenal AKI
Postrenal AKI follows obstruction to urine flow, for example from an enlarged prostate, kidney stones or a blocked urinary catheter. Back-pressure raises pressure in the tubules and Bowman's capsule, which opposes filtration. Relieving the obstruction early usually restores function.
The course of ATN
ATN typically moves through three phases: initiation; maintenance, in which urine output may fall while creatinine, potassium and fluid accumulate; and recovery, which may include a period of high urine output with a risk of fluid and electrolyte loss.
Nursing implications
- Track intake and output, hourly urine output in high-risk patients, and daily weights.
- Monitor creatinine, potassium and acid-base balance, and report a rising potassium promptly because of the risk of arrhythmias.
- Avoid nephrotoxins where possible, and check that medication doses are adjusted to kidney function.
- In prerenal states, support perfusion as ordered; when obstruction is suspected, check catheter patency and bladder volume.
References
Kellum, J. A., Romagnani, P., Ashuntantang, G., Ronco, C., Zarbock, A., & Anders, H.-J. (2021). Acute kidney injury. Nature Reviews Disease Primers, 7(1), Article 52. https://doi.org/10.1038/s41572-021-00284-z
Kidney Disease: Improving Global Outcomes Acute Kidney Injury Work Group. (2012). KDIGO clinical practice guideline for acute kidney injury. Kidney International Supplements, 2(1), 1–138.
