Author: Ibrahim Mahmoud, et al.
Cureus, May 30, 2026
Acute kidney injury in critically ill patients should no longer be viewed as a single event defined only by an increase in serum creatinine. This narrative review describes AKI as a dynamic and heterogeneous syndrome involving kidney stress, structural injury, declining function, possible renal replacement therapy, and incomplete recovery.
Key points
• AKI affects approximately 30% to 60% of critically ill adults and is associated with increased mortality, prolonged mechanical ventilation, longer ICU stays, chronic kidney disease, cardiovascular complications, readmission, and impaired quality of life.
• Serum creatinine remains essential but may rise late and can underestimate kidney injury in patients with fluid overload, reduced muscle mass, liver dysfunction, or changing creatinine production.
• Urine output may provide an earlier warning, but oliguria does not always indicate inadequate intravascular volume. It may result from venous congestion, low cardiac output, obstruction, abdominal hypertension, neurohormonal responses, or tubular injury.
• Clinicians should not automatically administer fluid whenever urine output decreases. The patient’s cardiac output, mean arterial pressure, central venous pressure, right ventricular function, intra-abdominal pressure, fluid balance, and likelihood of venous congestion should first be assessed.
• Venous congestion is increasingly recognized as an important cause of AKI. Elevated central venous pressure, right ventricular dysfunction, pulmonary hypertension, mechanical ventilation, and fluid overload can impair renal drainage and reduce filtration.
• Point-of-care ultrasound and venous Doppler assessment, including the venous excess ultrasound score, may help identify congestion. However, evidence that VExUS-guided treatment improves clinical outcomes remains primarily observational.
• Balanced crystalloids are generally preferred over chloride-rich saline in many critically ill patients, although their kidney-protective benefit is modest and varies according to the clinical situation.
• Kidney biomarkers such as NGAL, KIM-1, TIMP-2, IGFBP7, cystatin C, and proenkephalin may identify stress, structural injury, or functional decline before creatinine rises. Biomarkers should be ordered only when the result will trigger a defined management response.
• Biomarker-triggered prevention bundles may be particularly helpful in high-risk postoperative patients. Appropriate responses include closer monitoring, medication review, nephrotoxin avoidance, hemodynamic optimization, and prevention of excessive fluid or chloride administration.
• Medication stewardship is essential. Every ICU patient with evolving AKI should undergo a systematic review for nephrotoxic drugs, medications requiring renal dose adjustment, agents requiring therapeutic monitoring, and drugs that can be discontinued.
• No medication reliably reverses established ICU-associated AKI. Treatment remains focused on source control, hemodynamic optimization, relieving obstruction, treating congestion, correcting abdominal hypertension, avoiding nephrotoxins, adjusting medication doses, and managing electrolyte and acid-base complications.
Renal replacement therapy
Renal replacement therapy should not be initiated solely because the serum creatinine reaches a particular level. Urgent indications include refractory hyperkalemia, severe metabolic acidosis that does not respond to medical treatment, pulmonary edema or hypoxemia from fluid overload, uremic complications, and selected toxic ingestions.
Large multicenter trials have not demonstrated a consistent survival advantage from routinely starting RRT early in patients without urgent indications. Careful observation with predefined escalation criteria can prevent unnecessary treatment while avoiding dangerous delays.
Intermittent hemodialysis is generally appropriate for hemodynamically stable patients who require rapid correction of potassium, acidosis, toxins, or solute accumulation. Continuous renal replacement therapy is often preferred for patients with vasopressor-dependent shock, severe fluid overload, acute brain injury, liver failure, major osmolar concerns, or a need for precise fluid removal.
For most patients receiving continuous therapy, a delivered effluent dose of approximately 20 to 25 mL/kg/hour is appropriate. Higher-intensity therapy has not consistently improved survival.
Recovery and follow-up
Recovery from AKI is not simply present or absent. Patients may experience complete recovery, partial recovery, persistent acute kidney disease, recurrent AKI, reduced renal reserve, albuminuria, hypertension, or progression to chronic kidney disease.
Kidney abnormalities lasting from 7 through 90 days are classified as acute kidney disease. ICU discharge documentation should include the highest AKI stage, suspected cause or phenotype, nephrotoxic exposures, renal replacement therapy history, unresolved kidney abnormalities, medication changes, and a follow-up plan.
Patients with stage 3 AKI, dialysis exposure, incomplete recovery, preexisting chronic kidney disease, significant albuminuria, recurrent AKI, or an uncertain diagnosis should receive early nephrology follow-up.
Clinical implications
The most important bedside distinction is determining whether a patient needs improved forward perfusion or relief of venous congestion. A patient may respond to a fluid bolus with a temporary increase in stroke volume while still experiencing worsening pulmonary edema, abdominal pressure, renal venous congestion, or kidney injury.
Fluids should therefore be treated like medications: they require a defined indication, dose, reassessment interval, monitoring for adverse effects, and a stopping point.
Bottom line
Modern ICU kidney care requires more than monitoring creatinine. Clinicians should integrate urine-output trends, hemodynamics, venous congestion, biomarkers when actionable, fluid tolerance, nephrotoxic exposure, renal replacement therapy objectives, and long-term recovery planning.
The central message is straightforward: do not reflexively treat oliguria with fluid, do not start dialysis based on creatinine alone, and do not assume that improved creatinine means the patient’s kidney risk has resolved.
Thank you to Cureus for allowing us to summarize this important review.