Management of Acute Kidney Injury
The management of acute kidney injury requires immediate discontinuation of all nephrotoxic medications, careful volume assessment with isotonic fluid resuscitation for hypovolemia (avoiding fluid overload), and urgent consideration of renal replacement therapy when severe oliguria, life-threatening electrolyte abnormalities, or uremic complications are present. 1, 2
Immediate Assessment and Risk Stratification
Identify AKI severity using the KDIGO staging criteria based on creatinine elevation and urine output—Stage 3 AKI (creatinine ≥3x baseline or oliguria <0.3 mL/kg/hr for ≥24 hours) represents a life-threatening condition requiring urgent intervention. 2
Determine the underlying cause by categorizing as prerenal (hypovolemia, decreased renal perfusion), intrinsic renal (tubular injury, glomerular disease), or postrenal (obstruction). 3, 4
Obtain renal ultrasound immediately to rule out obstructive uropathy, particularly in older men with prostatic hypertrophy or patients with known urologic abnormalities. 2, 4
Drug Management: The Critical First Step
Stop all nephrotoxic medications immediately, including NSAIDs, aminoglycosides, vancomycin, ACE inhibitors, ARBs, and diuretics. 1, 2 This is paramount because each nephrotoxin administration increases AKI odds by 53%, and this risk compounds exponentially with multiple agents. 1
Avoid the "triple whammy" combination of NSAIDs, diuretics, and ACE inhibitors/ARBs, which more than doubles AKI risk—25% of patients receiving three or more nephrotoxins develop AKI. 1, 5
Adjust all medication dosages based on current estimated GFR and reassess frequently as kidney function changes dynamically during AKI and recovery phases. 1, 2
Do not withhold life-saving medications (such as antibiotics for sepsis or contrast for emergent imaging) due to nephrotoxicity concerns—survival takes precedence, and these interventions may actually prevent or ameliorate AKI. 1
Fluid Management: A Delicate Balance
Assess volume status clinically through examination of jugular venous pressure, skin turgor, mucous membranes, peripheral edema, and potentially central venous pressure monitoring. 2, 4
For hypovolemic patients, provide isotonic crystalloid resuscitation (normal saline or lactated Ringer's) rather than colloids—avoid starch-containing fluids entirely in AKI patients. 2, 6 Aggressive early fluid repletion is beneficial in the initial resuscitation phase. 6
Transition to conservative fluid strategy once hemodynamic stabilization is achieved—switch toward neutral then negative fluid balance to prevent fluid overload. 7, 6 Salt and water overload predisposes to organ dysfunction, impaired wound healing, delayed renal recovery, and increased mortality. 7
Monitor for fluid overload by tracking daily weights, peripheral edema, pulmonary congestion on examination, and strict input/output measurements. 2 Fluid overload is associated with increased mortality and reduced kidney recovery rates in observational studies. 7, 6
Avoid overly aggressive fluid administration in non-hypovolemic patients, as this worsens outcomes and may necessitate earlier initiation of renal replacement therapy. 2, 7
Hemodynamic Support
Use vasopressors in conjunction with fluids for patients with vasomotor shock to maintain mean arterial pressure ≥65 mmHg for adequate renal perfusion. 2
Indications for Urgent Renal Replacement Therapy
Initiate RRT urgently for any of the following absolute indications: 2, 4
- Severe oliguria unresponsive to fluid resuscitation
- Life-threatening hyperkalemia refractory to medical management
- Severe metabolic acidosis (pH <7.1)
- Uremic complications (encephalopathy, pericarditis, pleuritis)
- Fluid overload causing respiratory compromise or worsening tissue oxygenation
- Certain toxin ingestions requiring removal
Do not delay RRT when clear indications exist—delayed initiation increases mortality. 2
Monitoring Strategy
Monitor serum electrolytes, BUN, and creatinine every 4-6 hours initially in severe AKI. 2
Track urine output hourly and maintain strict fluid balance documentation. 2
Reassess need for continued RRT daily and monitor for signs of kidney recovery. 2
Perform urinalysis to detect hematuria, proteinuria, or abnormal sediment suggesting intrinsic renal disease. 5, 4
Calculate fractional excretion of sodium (FENa) and fractional excretion of urea (FEUrea)—FENa <1% or FEUrea <28% suggests prerenal causes. 5
Supportive Care
Provide nutritional support with 20-30 kcal/kg/day total energy intake, preferably via enteral route. 2
Administer protein at 0.8-1.0 g/kg/day in noncatabolic AKI patients without dialysis, or 1.0-1.5 g/kg/day in patients requiring RRT. 2
Optimize glycemic control and treat underlying infections aggressively. 5, 3
Drug Stewardship Program Implementation
Include a clinical pharmacist for comprehensive drug stewardship—pharmacist-led programs reduce nephrotoxic exposures and AKI rates in hospital settings. 1, 3
Perform medication regimen review evaluating pharmacokinetic/pharmacodynamic interactions and the dynamic impact of changing kidney function on drug dosing. 1
Undertake dynamic prescription reconciliation at all transitions of care, as kidney function changes rapidly during AKI and recovery phases. 1
Critical Pitfalls to Avoid
Do not continue nephrotoxic medications during the AKI recovery phase—this period represents continued vulnerability to re-injury. 1, 2
Avoid overly rapid correction of severe hyponatremia (>10-12 mEq/L in 24 hours), which can cause osmotic demyelination syndrome. 2
Do not fail to identify and treat the underlying cause—continued exposure to the inciting factor leads to ongoing kidney damage. 2
Avoid hypovolemia from excessive diuresis or ultrafiltration during RRT—accurate fluid status assessment is essential at all stages. 7
Patient Education and Follow-up
Educate patients to avoid NSAIDs and all new medications without consulting their physician, and to use ACE inhibitors, decongestants, antivirals, antibiotics, and herbal products with extreme caution. 1
Counsel on when to seek medical attention for symptoms of worsening kidney function (decreased urine output, confusion, severe fatigue, shortness of breath). 1
Consider nephrology consultation for stage 3 or higher AKI, preexisting stage 4 or higher CKD, unclear etiology, inadequate response to supportive treatment, or need for RRT. 3