I. Supportive Care Measures

Optimizing hemodynamics and minimizing further kidney injury are foundational in CIN management. Early vasopressor selection and withdrawal of nephrotoxins preserve renal perfusion and function.

A. Hemodynamic Optimization

1. Goals of Hemodynamic Support

• Target Mean Arterial Pressure (MAP) ≥65 mmHg in most patients; consider individualized MAP 70–80 mmHg in Chronic Kidney Disease (CKD) or chronic hypertension.
• Avoid hypotension to reduce medullary ischemia and tubular injury.

2. Vasopressor Agents

B. Avoidance of Nephrotoxic Agents

Removing or dose-adjusting nephrotoxins lowers additive kidney insult in CIN.

1. Common ICU Nephrotoxins

• Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
• Aminoglycosides
• Amphotericin B
• Repeat or high-volume radiographic contrast

2. Risk Mitigation

• Medication review and deprescribing at ICU admission.
• Therapeutic drug monitoring and renal dose adjustment for essential nephrotoxins.

II. Prevention of Volume Overload and Electrolyte Disturbances

Balance between adequate perfusion and fluid overload is critical. Diuretics and electrolyte repletion require close monitoring.

A. Volume Management

1. Input/Output Monitoring

• Strict intake/output charting, daily weights, physical exam (edema, lung auscultation).
• Fluid balance goals: euvolemia; avoid cumulative positive balance >1–1.5 L in 24 hours if cardiac/renal reserve limited.

2. Diuretic Therapy: Furosemide

B. Electrolyte Management

1. Common Disturbances

• Hyponatremia (can be dilutional or from V₂ effects of vasopressin)
• Hypokalemia (due to diuretic therapy)
• Hypomagnesemia (due to diuretic therapy)

2. Correction Strategies

• Sodium: If hyponatremia is severe or symptomatic, use isotonic saline for volume repletion. Correct chronic hyponatremia slowly, by ≤8 mEq/L per 24 hours, to avoid osmotic demyelination syndrome.
• Potassium: Replete aggressively to maintain serum K⁺ ≥4.0 mEq/L, especially in patients receiving diuretics or those at risk for arrhythmias.
• Magnesium: Supplement to maintain serum Mg²⁺ ≥2.0 mEq/L (or ≥1.7 mg/dL); this helps prevent refractory hypokalemia and reduces arrhythmia risk.

III. Management of Iatrogenic Complications from Prophylactic Therapies

Prophylactic saline or sodium bicarbonate infusions, while intended to prevent CIN, can themselves lead to complications such as volume overload or metabolic alkalosis. Early recognition and intervention are essential.

A. Volume Overload from Aggressive Hydration

• Detection: Monitor for rising daily weight, consistently positive fluid balance, new or worsening peripheral edema, new crackles on lung auscultation, or radiographic evidence of pulmonary congestion.
• Intervention:
  • Restrict intravenous fluids to maintenance rates or aim for a net negative fluid balance.
  • Initiate or escalate loop diuretic therapy as described above.
  • Consider early Renal Replacement Therapy (RRT) if volume overload is refractory to diuretics and associated with significant respiratory compromise or worsening organ dysfunction.

B. Metabolic Alkalosis from Sodium Bicarbonate Infusion

• Pathophysiology: Administration of excess sodium bicarbonate can lead to an increase in serum pH and bicarbonate levels. Severe alkalosis can lower ionized calcium levels (potentially causing neuromuscular irritability or tetany) and shift the oxyhemoglobin dissociation curve to the left (imparing oxygen release to tissues).
• Monitoring: Regularly monitor arterial blood gases (ABGs) for pH and PaCO₂, serum electrolytes (including bicarbonate, chloride, and calcium), and fluid status.
• Management:
  • Decrease the infusion rate or concentration of sodium bicarbonate.
  • Administer isotonic saline (0.9% NaCl) if the patient is not volume overloaded; chloride repletion helps the kidneys excrete bicarbonate.
  • In cases of severe or symptomatic metabolic alkalosis, consider acetazolamide (e.g., 250 mg IV), which inhibits carbonic anhydrase and promotes renal bicarbonate excretion. Use with caution in patients with hepatic impairment.

IV. Multidisciplinary Goals-of-Care for Renal Replacement Therapy

Shared decision-making involving the patient, family, and multidisciplinary team ensures that the initiation and continuation of Renal Replacement Therapy (RRT) align with the patient’s overall prognosis, personal goals, and available resources.

A. Indications for RRT in CIN

Consider RRT for CIN-associated AKI in the presence of life-threatening complications, including but not limited to:

• Refractory Volume Overload: Pulmonary edema or severe systemic congestion unresponsive to maximal diuretic therapy.
• Severe Hyperkalemia: Serum K⁺ >6.5 mEq/L, or lower levels with associated ECG changes or rapid rise.
• Metabolic Acidosis: Severe metabolic acidosis (e.g., pH <7.20 or serum bicarbonate <15 mEq/L) refractory to medical management.
• Uremic Complications: Signs or symptoms of uremia, such as encephalopathy, pericarditis, or pleuritis.

B. RRT Modalities and Selection Criteria

• Continuous Renal Replacement Therapy (CRRT): Generally preferred in hemodynamically unstable patients due to slower, continuous fluid and solute removal, leading to better hemodynamic tolerance.
• Intermittent Hemodialysis (IHD): Provides rapid solute and fluid clearance. Suitable for hemodynamically stable patients who can tolerate rapid fluid shifts. May be logistically simpler in some settings.
• Factors Influencing Choice: Hemodynamic stability, desired rate of solute and fluid removal, anticoagulation needs, ICU staffing and resource availability, and patient-specific factors.

C. Ethical and Palliative Considerations

• Engage patients (if capable) and their families early in discussions about the prognosis of AKI, the potential benefits and burdens of RRT, and how RRT aligns with overall goals of care.
• Review advance directives and existing goals-of-care documentation.
• Incorporate palliative care consultations when the likelihood of renal recovery is low, the overall prognosis is poor, or when symptom management and quality of life are primary concerns.