SECTION 14   |   Renal Disorders

GENERAL APPROACH TO TREATMENT

• Currently, there is no definitive therapy for AKI. Supportive care is the mainstay of
AKI management regardless of etiology.
Nonpharmacologic Therapies
• Supportive care goals include maintenance of adequate cardiac output and blood
pressure to optimize tissue perfusion while restoring renal function to pre-AKI
baseline.
• Discontinue medications associated with diminished renal blood flow. Initiate appro-
priate fluid and electrolyte management. Avoid use of nephrotoxins.
• In severe AKI, renal replacement therapy (RRT), such as hemodialysis and peritoneal
dialysis, maintains fluid and electrolyte balance while removing waste products. See
Table 73–4 for indications for RRT in AKI. Intermittent and continuous options
have different advantages (and disadvantages) but, after correcting for severity of
illness, have similar outcomes. Consequently, hybrid approaches (eg, sustained low-
efficiency dialysis and extended daily dialysis) are being developed to provide the
advantages of both.
• Intermittent hemodialysis (IHD) is the most frequently used RRT and has the
advantage of widespread availability and the convenience of lasting only 3 to 4 hours.
Disadvantages include difficult venous dialysis access in hypotensive patients and
hypotension due to rapid removal of large amounts of fluid.
• Several continuous RRT (CRRT) variants have been developed including continuous
hemofiltration, continuous hemodialysis, or a combination. CRRT gradually removes
solute, resulting in better tolerability by critically ill patients. Disadvantages include
limited availability of equipment, need for intensive nursing care, and the need to
individualize IV replacement, dialysate fluids, and drug therapy adjustments.
Pharmacologic Therapies
• Mannitol 20% is typically started at a dose of 12.5 to 25 g IV over 3 to 5 minutes.
Disadvantages include IV administration, hyperosmolality risk, and need for moni-
toring urine output and serum electrolytes and osmolality because mannitol can
contribute to AKI.
• Loop diuretics effectively reduce fluid overload but can worsen AKI. Equipotent
doses of loop diuretics (furosemide, bumetanide, torsemide, and ethacrynic
acid) have similar efficacy. Ethacrynic acid is reserved for sulfa-allergic patients.
Continuous infusions of loop diuretics appear to overcome diuretic resistance and
to have fewer adverse effects than intermittent boluses. An initial IV loading dose
(equivalent to furosemide 40–80 mg) should be administered before starting a con-
tinuous infusion (equivalent to furosemide 10–20 mg/h).
• Strategies are available to overcome diuretic resistance (Table 73–5). Administration
of agents from different pharmacologic classes, such as diuretics that work at the

TABLE 73–4 Common Indications for Renal Replacement Therapy

Indication for Renal
Replacement Therapy Clinical Setting
A: Acid–base abnormalities Metabolic acidosis resulting from the accumulation
of organic and inorganic acids
E: Electrolyte imbalance Hyperkalemia, hypermagnesemia
I: Intoxications Salicylates, lithium, methanol, ethylene glycol,
theophylline, phenobarbital
O: Overload of fluid Postoperative fluid gain/overload
U: Uremia Accumulation of uremic toxins

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 Acute Kidney Injury   |   CHAPTER 73

TABLE 73–5 Common Causes of Diuretic Resistance in Patients With Acute Kidney Injury
Causes of Diuretic Resistance Potential Therapeutic Solutions
Excessive sodium intake (sources may Remove sodium from nutritional sources and
be dietary, IV fluids, and drugs) medications
Inadequate diuretic dose or Increase dose, use continuous infusion or
inappropriate regimen combination therapy
Reduced oral bioavailability (usually Use parenteral therapy; switch to oral torsemide
furosemide) or bumetanide
Nephrotic syndrome (loop diuretic Increase dose, switch diuretics, use combination
protein binding in tubule lumen) therapy
Reduced renal blood flow
  Drugs (NSAIDs, ACEIs, vasodilators) Discontinue these drugs if possible
  Hypotension Intravascular volume expansion and/or
vasopressors
  Intravascular depletion Intravascular volume expansion
Increased sodium resorption
  Nephron adaptation to chronic Combination diuretic therapy, sodium restriction
diuretic therapy
  NSAID use Discontinue NSAID
  Heart failure Treat the heart failure, increase diuretic dose, switch
to better-absorbed loop diuretic
  Cirrhosis High-volume paracentesis
Acute tubular necrosis Higher dose of diuretic, diuretic combination
therapy; add low-dose dopamine

ACEIs, angiotensin-converting enzyme inhibitors; IV, intravenous; NSAIDs, nonsteroidal anti-

inflammatory drugs.

distal convoluted tubule (thiazides) or the collecting duct (amiloride, triamterene,

and spironolactone), may be synergistic when combined with loop diuretics.
Metolazone is commonly used because, unlike other thiazides, it produces effective
diuresis at GFR less than 20 mL/min (0.33 mL/s).

ELECTROLYTE MANAGEMENT AND NUTRITION INTERVENTIONS

• Serum electrolytes should be monitored daily. Hyperkalemia is the most common
and serious electrolyte abnormality in AKI. Hypernatremia and fluid retention
commonly occur, requiring calculation of daily sodium intake, including sodium
contained in commonly administered antibiotic and antifungal agents.
• Phosphorus and magnesium should be monitored, especially in patients with signifi-
cant tissue destruction due to increased amounts of released phosphorus; neither is
efficiently removed by dialysis.
• Nutritional management of critically ill patients with AKI is complex due to multiple
mechanisms for metabolic derangements. Nutritional requirements are altered by
stress, inflammation, and injury that lead to hypermetabolic and hypercatabolic
states.

DRUG-DOSING CONSIDERATIONS
• Drug therapy optimization in AKI is a challenge. Confounding variables include
residual drug clearance, fluid accumulation, and use of RRTs.

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SECTION 14   |   Renal Disorders

TABLE 73–6 Key Monitoring Parameters for Patients With Established Acute Kidney Injury
Parameter Frequency
Fluid ins/outs Every shift
Patient weight Daily
Hemodynamics (blood pressure, heart rate, Every shift
mean arterial pressure, etc)
Blood chemistries
  Sodium, potassium, chloride, bicarbonate, Daily
calcium, phosphate, magnesium
  Blood urea nitrogen/serum creatinine Daily
Drugs and their dosing regimens Daily
Nutritional regimen Daily
Blood glucose Daily (minimum)
Serum concentration data for drugs After regimen changes and after renal
replacement therapy has been instituted
Times of administered doses Daily
Doses relative to administration of renal Daily
replacement therapy
Urinalysis
  Calculate measured creatinine clearance Every time measured urine collection
performed
  Calculate fractional excretion of sodium Every time measured urine collection
performed
Plans for renal replacement Daily

• Volume of distribution for water-soluble drugs is significantly increased due to

edema. Use of dosing guidelines for CKD does not reflect the clearance and volume
of distribution in critically ill patients with AKI.
• Patients with AKI may have a higher residual nonrenal clearance than those with
CKD with similar creatinine clearances; this complicates drug therapy individualiza-
tion, especially with RRTs.
• The mode of CRRT determines rate of drug removal, further complicating indi-
vidualization of drug therapy. Rates of ultrafiltration, blood flow, and dialysate flow
influence drug clearance during CRRT.

EVALUATION OF THERAPEUTIC OUTCOMES

• Vigilant monitoring of patient status is essential (Table 73–6).
• Therapeutic drug monitoring should be monitored frequently because of changing
volume status, changing renal function, and RRTs in patients with AKI.

See Chapter 28, Acute Kidney Injury, authored by William Dager and Jenana Halilovic,
for a more detailed discussion of this topic.

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