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2025 PACUPrep BCCCP Preparatory Course Acute Kidney Injury (AKI) Pharmacotherapy Optimization and Supportive Care in Acute Kidney Injury

Lesson 15, Topic 4

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Pharmacotherapy Optimization and Supportive Care in Acute Kidney Injury

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Supportive Care Strategies and Complication Monitoring in AKI

Objective

Recommend supportive care and monitoring to manage complications in acute kidney injury (AKI).

Learning Points:

Identify indications for mechanical ventilation and hemodynamic support.
Prevent ICU-related complications: venous thromboembolism, stress-ulcer bleeding, nosocomial infections.
Manage iatrogenic issues: drug-induced nephrotoxicity, electrolyte disturbances.
Engage multidisciplinary teams in shared decision-making around renal replacement therapy (RRT).

I. Supportive Respiratory and Hemodynamic Interventions

In AKI, respiratory and circulatory support must preserve renal perfusion and avoid fluid overload, preventing secondary organ injury.

A. Mechanical Ventilation

Indications:
- Pulmonary edema refractory to diuretics
- ARDS or respiratory failure with hemodynamic instability
Lung-protective strategies:
- Tidal volume 6 mL/kg predicted body weight
- Plateau pressure < 30 cm H₂O
- Conservative fluid balance; target even or negative cumulative net balance
Monitoring:
- Plateau and driving pressures
- MAP and CVP (if available)
- Hourly urine output, daily fluid balance

Key Pearl: Lung Protection in AKI

Maintain low airway pressures and avoid positive fluid balance during mechanical ventilation to minimize renal hypoperfusion and venous congestion, which can exacerbate AKI.

B. Hemodynamic Support

Perfusion targets:
- MAP ≥ 65 mm Hg (individualize for chronic hypertension)
- Use dynamic tests: passive leg raise, stroke-volume variation to assess fluid responsiveness

1. Fluid Resuscitation

First-line: balanced crystalloids (e.g., lactated Ringer’s, Plasma-Lyte)
Avoid starch-based colloids (e.g., HES) due to AKI risk

Fluid Resuscitation Agents in AKI
Agent	Mechanism	Typical Dose	Monitoring	Clinical Pearls
Balanced crystalloids	ECF expansion	500–1,000 mL bolus	Electrolytes, acid-base, UO	Preferred for initial resuscitation
Albumin 5–20%	Oncotic support	25–50 g IV	Volume status, allergy	Consider if hypoalbuminemia; higher cost
Hydroxyethyl starch	Synthetic colloid	Not recommended	Renal function, coagulation	Linked to increased AKI

Key Pearl: Fluid Responsiveness

Use fluid-responsiveness measures (e.g., passive leg raise, stroke volume variation) to guide fluid boluses and avoid iatrogenic fluid overload, which worsens outcomes in AKI.

2. Vasopressors and Inotropes

First-line: norepinephrine to increase SVR and MAP
Adjunct: vasopressin (0.01–0.04 U/min) to spare catecholamines
Avoid dopamine for renal protection—no benefit and higher arrhythmia risk

Vasopressors and Inotropes in AKI
Agent	Mechanism	Dose	Monitoring	Adverse Effects	Pearls
Norepinephrine	α₁, β₁ agonist	0.01–3 μg/kg/min IV	MAP, perfusion markers	Ischemia, arrhythmias	First-line in septic/cardiogenic shock
Vasopressin	V₁ agonist	0.01–0.04 U/min continuous	MAP, Na⁺ levels	Hyponatremia, ischemia	Use in refractory shock
Dopamine	Dose-dependent	2–20 μg/kg/min IV	HR, arrhythmias	Tachyarrhythmias	Not for renal protection

Key Pearl: Vasopressor Titration

Titrate vasopressors to achieve adequate end-organ perfusion (e.g., urine output, lactate clearance, mental status), not just a target MAP, to optimize renal blood flow.

II. Prevention of ICU-related Complications

Prophylaxis against thrombosis, stress ulcers, and infections must be personalized in AKI, considering altered drug clearance and bleeding risk.

A. Venous Thromboembolism Prophylaxis

1. Pharmacologic

Unfractionated Heparin (UFH) 5,000 U SC q8–12h; no renal adjustment generally needed
Low-Molecular-Weight Heparin (LMWH) (e.g., enoxaparin 40 mg SC daily; dose reduce to 30 mg SC daily if CrCl < 30 mL/min)
Monitor anti-Xa levels in severe AKI or obesity if using LMWH

Key Pearl: VTE Prophylaxis in AKI

In severe AKI (CrCl < 30 mL/min) or when renal function is rapidly changing, prefer UFH over LMWH for VTE prophylaxis to avoid LMWH accumulation and increased bleeding risk. Adjust LMWH doses carefully if used.

2. Mechanical

Intermittent pneumatic compression (IPC) devices when pharmacologic anticoagulation is contraindicated (e.g., active bleeding, severe thrombocytopenia)
Continue mechanical prophylaxis until bleeding risk resolves or the patient is ambulating regularly

B. Stress-related Mucosal Bleeding Prophylaxis

Indications: Mechanical ventilation > 48 hours, coagulopathy (e.g., platelets < 50,000/μL, INR > 1.5), shock, history of GI bleeding within past year, or multiple other risk factors (e.g., sepsis, major surgery, corticosteroid use).

Stress Ulcer Prophylaxis Agents
Agent Class	Example Dose	Renal Dosing	Risks	Pearls
Proton Pump Inhibitor (PPI)	Pantoprazole 40 mg IV/PO daily	No adjustment typically needed	C. difficile infection, pneumonia, fractures (long-term)	Preferred for high-risk patients; more potent acid suppression
Histamine-2 Receptor Antagonist (H2RA)	Famotidine 20 mg IV/PO q12-24h	Adjust if CrCl < 50 mL/min (e.g., 20 mg q24-48h)	CNS effects (confusion, delirium) in elderly or renal impairment, thrombocytopenia (rare)	May have lower risk of C. difficile/pneumonia vs PPIs; less potent

Key Pearl: Judicious SUP

Limit stress ulcer prophylaxis (SUP) to high-risk patients and discontinue when risk factors resolve to minimize potential adverse effects like nosocomial infections (C. difficile, pneumonia).

C. Infection Prevention and Stewardship

CLABSI bundle: Hand hygiene, chlorhexidine skin preparation, maximal barrier precautions during insertion, daily review of line necessity, aseptic technique for access.
VAP bundle: Head-of-bed elevation 30–45°, daily sedation interruption and assessment of readiness to extubate, oral care with chlorhexidine, subglottic suctioning for endotracheal tubes.
Antibiotic stewardship:
- Dose adjust antibiotics based on estimated CrCl and RRT modality (if applicable).
- Utilize therapeutic drug monitoring (TDM) for drugs with narrow therapeutic windows (e.g., vancomycin, aminoglycosides).
- De-escalate antibiotic therapy based on culture results and clinical response.

Key Pearl: Antibiotics in AKI

AKI significantly alters antibiotic pharmacokinetics/pharmacodynamics (PK/PD). Use TDM and consult pharmacy for dose adjustments to balance efficacy and minimize further nephrotoxicity or other adverse effects.

III. Management of Iatrogenic Issues

Prompt recognition and mitigation of drug nephrotoxicity and electrolyte derangements are critical to prevent incremental renal injury.

A. Drug-induced Nephrotoxicity

High-risk agents: Aminoglycosides, NSAIDs, IV contrast media, vancomycin, amphotericin B, certain antivirals.
Prevention strategies:
- IV hydration with isotonic saline (e.g., 1 mL/kg/h for 6-12 hours) pre- and post-contrast exposure for high-risk patients.
- Extended-interval aminoglycoside dosing; target appropriate trough concentrations (e.g., < 1 mg/L for gentamicin/tobramycin).
- Avoid NSAIDs in patients with AKI or those at high risk for AKI.
- Ensure adequate hydration before and during vancomycin or amphotericin B therapy.

Key Pearl: Nephrotoxin Management

Employ therapeutic drug monitoring (TDM) where available, minimize the duration of exposure to nephrotoxic drugs, and consider alternative agents if possible, especially in patients with pre-existing kidney disease or multiple risk factors.

B. Electrolyte Disturbances

1. Hyperkalemia

Assess ECG for changes: peaked T waves, prolonged PR, wide QRS, sine wave pattern.
Stabilize cardiac membrane (if ECG changes or K⁺ > 6.5 mmol/L):
- Calcium gluconate 1–2 g IV over 5–10 min (or calcium chloride 0.5-1g IV via central line).
Shift K⁺ intracellularly:
- Insulin 10 units regular IV + 25 g dextrose (50 mL D50W) IV (onset 15–30 min). Monitor glucose.
- Albuterol 10–20 mg nebulized over 10 min (use with caution in cardiac patients).
- Sodium bicarbonate (if severe metabolic acidosis present, controversial for hyperkalemia alone).
Remove K⁺ from body:
- Loop diuretics (e.g., furosemide) if renal function allows.
- Sodium polystyrene sulfonate 15–30 g PO/PR (slower onset, risk of colonic necrosis).
- Patiromer or sodium zirconium cyclosilicate (slower onset, not for acute emergency, better for chronic management).
- Hemodialysis: most effective and rapid method for severe/refractory hyperkalemia.
Indication for urgent RRT: refractory hyperkalemia (e.g., K⁺ > 6.5 mmol/L despite medical therapy) or severe ECG changes.

Key Pearl: Hyperkalemia Management Priority

In severe hyperkalemia with ECG changes, always protect the heart first with intravenous calcium to stabilize the cardiac membrane before initiating therapies to shift or remove potassium.

2. Other Electrolytes

Hypocalcemia: Treat if symptomatic (tetany, seizures, QT prolongation) or ionized calcium is critically low. Calcium gluconate 1–2 g IV over 10-20 min.
Hypomagnesemia: Often coexists with hypokalemia and hypocalcemia. Treat if symptomatic or Mg < 1.2 mg/dL. Magnesium sulfate 1–2 g IV over 1 hour (slower if renal impairment).
Hyperphosphatemia: Common in AKI. Manage with dietary phosphate restriction, phosphate binders (e.g., sevelamer, calcium acetate) with meals. Dialysis is effective for severe cases.
Hypophosphatemia: Can occur, especially with RRT or refeeding. Replete orally or IV if severe (<1 mg/dL) or symptomatic.

Key Pearl: Calcium and Phosphate

Avoid routine calcium replacement in asymptomatic hypocalcemia if hyperphosphatemia is also present, due to the risk of calcium-phosphate precipitation in soft tissues. Address phosphate levels first or concurrently.

IV. Multidisciplinary Goals of Care in AKI

Shared decision-making and coordinated supportive plans ensure that invasive therapies like RRT align with patient goals and optimize resource use.

A. Shared Decision-Making around RRT

Absolute indications for RRT: Refractory hyperkalemia, severe metabolic acidosis (e.g., pH < 7.1), symptomatic uremia (e.g., pericarditis, encephalopathy), refractory fluid overload causing respiratory compromise, certain poisonings.
Weaning criteria from RRT: Evidence of intrinsic kidney function recovery (e.g., sustained urine output > 0.5 mL/kg/h or >400-500 mL/day without diuretics), resolution of metabolic derangements and fluid balance control.
Actions:
- Early multidisciplinary discussion involving nephrology, critical care, primary team, pharmacy, nursing, and importantly, the patient and family.
- Clearly document goals of care, prognosis, and the anticipated benefits and burdens of RRT, including potential duration.

Key Pearl: RRT Goals

Documenting and regularly revisiting goals of care for RRT helps prevent unwanted prolonged therapy and ensures that interventions remain aligned with the patient’s overall condition and wishes, avoiding nonbeneficial care.

B. Coordination of Supportive Plans

Nursing: Meticulous fluid balance monitoring, vascular access care, patient mobility, early recognition of complications.
Respiratory therapy: Ventilator management to minimize lung and kidney injury, airway clearance, coordination for RRT if patient is ventilated.
Nutrition: Assessment of caloric and protein needs (often increased in AKI/critical illness), electrolyte monitoring in nutritional formulations, adjustments for RRT losses.
Pharmacy: Renal dose adjustments for all medications, TDM, screening for nephrotoxins, advising on drug removal by RRT.
Tools for consistency: Structured interdisciplinary rounds, standardized order sets, care pathways, and checklists can improve communication and ensure consistent application of best practices.

Key Pearl: Team Communication

Regular multidisciplinary rounds with clearly defined roles and open communication are crucial for integrated care, reducing errors, and enhancing patient-centered outcomes in complex AKI management.

References

KDIGO. Clinical Practice Guideline for AKI and AKD Update. Kidney Int Suppl. 2023;13(2):1–20.
Bellomo R, Kellum JA, Ronco C, et al. Acute kidney injury in sepsis. Intensive Care Med. 2017;43(5):816–828.
Bagshaw SM, Bellomo R. Mechanical ventilation and acute kidney injury: cause or effect? Crit Care Med. 2007;35(6):1709–1710.
Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. Acute renal failure—Definition, fluid therapy and information needs: ADQI consensus. Crit Care. 2004;8(4):R204–R212.
Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369(18):1726–1734.
Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: ACCP guidelines. Chest. 2004;126(3 Suppl):338S–400S.
Perazella MA. Drug-induced nephrotoxicity: an update. Expert Opin Drug Saf. 2018;17(11):1105–1117.
Kovesdy CP, Kalantar-Zadeh K. Electrolyte disorders in acute kidney injury. Semin Nephrol. 2017;37(4):283–292.
Gameiro J, Fonseca JA, Jorge S, Lopes JA. AKI definition and diagnosis: a narrative review. J Clin Med. 2018;7(10):307.

2025 PACUPrep BCCCP Preparatory Course

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