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Acute kidney injury (AKI) is an abrupt decline in kidney function that results in an elevation of serum blood urea nitrogen (BUN), creatinine, and other metabolic waste products that are normally excreted by the kidney.
Potentially life-threatening complications of AKI include volume overload, hyperkalemia, acidosis, and uremia.
Volume status should be assessed in all patients with AKI. Fluid should be given to restore intravascular volume in patients who are volume depleted. The amount of administered fluid and the rate of replacement should be targeted to defined endpoints, such as mean arterial pressure. Types of replacement fluid include colloid- and crystalloid-containing solutions. For patients with AKI who require replacement fluid, we generally use a non-potassium-containing crystalloid solution, such as normal saline, rather than colloid-containing solutions.
Diuretics should not be used for prolonged therapy in place of dialysis. Diuretics may be used for a limited period of time to relieve signs and symptoms of volume overload. Loop diuretics may be more effective than thiazides at a glomerular filtration rate (GFR) <30 mL/min per 1.73 m2.
The treatment of hyperkalemia is determined by severity and presence of any associated signs, such as electrocardiographic changes or peripheral neuromuscular abnormalities. The treatment of hyperkalemia includes both medical therapy and dialysis.
Metabolic acidosis is common among patients with AKI. In general, we dialyze patients with AKI who are volume overloaded and have a pH <7.1 mEq/L. Dialysis is preferred to the administration of bicarbonate among such patients because bicarbonate administration results in a large sodium load that may cause or contribute to volume overload.
Among patients with AKI who are not volume overloaded and have no other indication for acute dialysis, bicarbonate may be used in the setting of a non-anion gap acidosis related to diarrhea, or in patients with a severe organic acidosis while awaiting dialysis. We do not use bicarbonate therapy in patients with a less severe organic acidosis (pH ≥7.1).
Hyperphosphatemia and hypocalcemia are commonly observed in patients with AKI. The treatment depends on the degree of hyperphosphatemia and the presence or absence of symptoms from hypocalcemia.
- We treat with dietary phosphate binders all patients with AKI who have moderately to severely elevated serum phosphate concentrations (ie, >6 mg/dL). We do not treat patients with mild hyperphosphatemia (ie, 4.5 to 6 mg/dL) that is due to AKI.
- We generally dialyze patients with severe hyperphosphatemia (defined as >12 mg/dL [3.9 mmol/L]).
- We dialyze patients with less severe hyperphosphatemia (serum phosphorus levels defined as >8 to 10 mg/dL [2.6 to 3.2 mmol/L]) who have symptomatic hypocalcemia.
- Dialysis may also be used in patients who are unable to take oral medication.