Acute kidney injury
Acute kidney injury is a sudden rise in serum creatinine or fall in urine output from prerenal, intrinsic, or postrenal causes, defined and staged by KDIGO criteria. Management targets the underlying cause, corrects volume and electrolyte derangements, and escalates to renal replacement therapy for refractory hyperkalemia, acidosis, volume overload, or uremia.
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What this article covers
- Overview
Sudden decline in kidney function: acute kidney injury (AKI) is a rapid decrease in glomerular filtration, commonly with decreased urine output, fluid retention, metabolic acidosis, hyperkalemia, and hyperphosphatemia.
- Epidemiology
Common in hospitalized patients: AKI complicates about 20% of all hospital admissions, of which roughly 10% require dialysis support.
- Risk factors
Sepsis and hypotension: the leading precipitants of ischemic ATN through prolonged renal hypoperfusion.
- Pathophysiology
Prerenal AKI is a hemodynamic response to underperfusion: volume depletion, decreased effective arterial circulation, renal vasoconstriction, or drugs impairing autoregulation (NSAIDs block afferent…
- Clinical features
Often asymptomatic: mild to moderate AKI is frequently detected only on laboratory studies; patients can remain asymptomatic until extreme loss of kidney function occurs.
- Differential diagnosis
Chronic kidney disease: documented elevated creatinine for ≥3 months and small echogenic kidneys on ultrasound rule this in over AKI.
- Diagnosis
The diagnosis is established by the KDIGO criteria, met by either the serum creatinine (SCr) or the urine output criterion, and staged by the same framework: stage 1: SCr 1.5-1.9x baseline within 7…
- Management
First, stop every nephrotoxin and vasoactive drug that is not essential, including NSAIDs, ACE inhibitors/ARBs, aminoglycosides, and diuretics, and adjust the doses of all renally cleared medications…
- Complications
Increased mortality: AKI severity correlates directly with in-hospital and long-term mortality, exceeding 50% in critically ill patients with multiorgan failure who require dialysis.
- Prognosis
Recovery depends on cause and severity: prerenal and postrenal AKI relieved within 1-2 weeks generally recover well; established ATN takes days to weeks, and nonoliguric ATN has a better prognosis than oliguric ATN.
- Prevention
Avoid or minimize nephrotoxins in at-risk patients: discontinue NSAIDs, and hold ACE inhibitors/ARBs and diuretics during acute illness or volume depletion ("sick day" rules), particularly when eGFR is <60 mL/min/1.73 m2.
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