Treatment of Acute Kidney Injury (AKI)
Immediately discontinue all nephrotoxic medications—including NSAIDs, aminoglycosides, ACE inhibitors, ARBs, diuretics, and beta-blockers—as this takes priority over all other interventions, then identify and reverse the underlying cause while initiating fluid resuscitation with isotonic crystalloids. 1, 2
Initial Emergency Management
Medication Withdrawal (First Priority)
- Stop all nephrotoxic drugs immediately upon AKI diagnosis, as each additional nephrotoxin increases AKI odds by 53% 1, 2
- Discontinue the "triple whammy" combination (NSAIDs + diuretics + ACE inhibitors/ARBs) which is particularly dangerous 1
- Hold diuretics and beta-blockers when AKI is diagnosed to prevent further kidney injury 2, 3
- Review all medications including over-the-counter drugs that may contribute to kidney injury 2
Fluid Resuscitation
- Use isotonic crystalloids as first-line therapy for volume expansion in hypovolemic patients with prerenal AKI 4, 1, 3
- Avoid hydroxyethyl starches due to increased risk of worsening AKI 1, 3
- Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion 1, 3
- Use dynamic indices (passive leg-raising test, pulse/stroke volume variation) rather than static measurements to guide fluid therapy 1
Hemodynamic Optimization
- Consider vasopressor therapy if fluid resuscitation fails to restore adequate blood pressure 2, 3
- Earlier use of vasoactive medications may be appropriate instead of excessive fluid administration for hypotension 1
Special Population: Cirrhotic Patients with AKI
Initial Management
- Discontinue both diuretics AND beta-blockers (not just diuretics alone) in cirrhotic patients with AKI 1, 2
- Administer IV albumin 1 g/kg bodyweight (maximum 100g) for two consecutive days to differentiate prerenal AKI from other causes 1, 2, 3
Hepatorenal Syndrome-AKI (HRS-AKI)
If serum creatinine remains elevated despite initial albumin and volume management:
Terlipressin (preferred):
- Initiate as bolus dose of 1 mg every 4-6 hours (total 4-6 mg/day) 4
- Increase to maximum 2 mg every 4-6 hours (total 8-12 mg/day) if no 25% reduction in serum creatinine by day 3 4
- Alternative: continuous IV infusion starting at 2 mg/day, increasing gradually every 24-48 hours up to maximum 12 mg/day 4
- Do not use if serum creatinine ≥5 mg/dL or oxygen saturation <90% 4
Norepinephrine (alternative):
- Start at 0.5 mg/hour continuous IV infusion 4
- Increase every 4 hours by 0.5 mg/hour to maximum 3 mg/hour 4
- Goal: increase mean arterial pressure by ≥10 mmHg and/or urine output to >50 mL/hour for at least 4 hours 4
Midodrine + Octreotide (alternative):
Midodrine: start 7.5 mg, titrate to 12.5 mg three times daily 4
Octreotide: start 100 mcg, titrate to 200 mcg subcutaneously three times daily 4
Continue therapy until 24 hours after serum creatinine returns to within ≤0.3 mg/dL of baseline for 2 consecutive days, or for maximum 14 days 4
Monitor closely for ischemic side effects (angina, finger/skin/intestinal ischemia) by starting at lowest dose and titrating gradually 4
Monitoring During Acute Management
- Measure serum creatinine and electrolytes every 12-24 hours during acute management 1
- Monitor urine output, vital signs, and fluid balance closely in the first 48-72 hours 1
- Monitor fluid status closely due to risk of pulmonary edema with excessive albumin use 4
- Use echocardiography or CVP when indicated to assess volume status and prevent fluid overload 1, 2
Renal Replacement Therapy (RRT) Indications
Individualize timing of RRT based on overall clinical condition rather than specific creatinine or BUN thresholds 1, 2
RRT may be used for:
- AKI secondary to acute tubular necrosis 4
- HRS-AKI in potential liver transplant candidates (do not use RRT in HRS-AKI patients who are not transplant candidates) 4
- AKI of uncertain etiology on individual basis 4
- Refractory hyperkalemia, volume overload, intractable acidosis, uremic complications 5, 6
Critical Pitfalls to Avoid
- Never use furosemide in hemodynamically unstable patients with prerenal AKI—it worsens volume depletion and reduces renal perfusion 1, 3
- Do not delay fluid resuscitation in truly hypovolemic patients 3
- Avoid using eGFR equations designed for CKD to assess renal function in AKI—they are inaccurate in this setting 1, 3
- Do not use diuretics to treat AKI except for managing volume overload after adequate renal perfusion is restored 1, 3
- Do not use transjugular intrahepatic portosystemic shunts (TIPS) as specific treatment for HRS-AKI 4