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Treatment of Acute Kidney Injury

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Currently, there is no definitive therapy for AKI (Acute Kidney Injury). 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 appropriate 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.Intermittent and continuous options have different advantages (and disadvantages) but, after correcting for severity of illness, have similar outcomes. Consequently, hybrid approaches (eg, sustained lowefficiency 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 monitoring 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 4080 mg) should be administered before starting a continuous infusion (equivalent to furosemide 1020 mg/h).

Strategies are available to overcome diuretic resistance. Administration of agents from different pharmacologic classes, such as diuretics that work at the 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).


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 significant 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.


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