Management of acute kidney injury

OVERVIEW ― Acute kidney injury is defined as an abrupt (within 48 hours) reduction in kidney function based on an elevation in serum creatinine level, a reduction in urine output, the need for renal replacement therapy (dialysis), or a combination of these factors. It is classified in three stages. The term acute kidney injury should replace terms such as acute renal failure and acute renal insufficiency, which previously have been used to describe the same clinical condition. Diagnosis of AKI was discussed separately ― see topic on Diagnosis of acute kidney injury (AKI).

MANAGEMENT OF AKI

TREATMENT ― Patients with acute kidney injury generally should be hospitalized unless the condition is mild and clearly resulting from an easily reversible cause. The key to management is assuring adequate renal perfusion by achieving and maintaining hemodynamic stability and avoiding hypovolemia. In some patients, clinical assessment of intravascular volume status and avoidance of volume overload may be difficult, in which case measurement of central venous pressures in an intensive care setting may be helpful. 

HYPOVOLEMIA OR INTRAVASCULAR VOLUME DEPLETION ― start fluid resuscitation with normal saline. Normal saline is preferred over hyperoncotic solutions (e.g., dextrans, hydroxyethyl starch, albumin). Use a wide bore cannula to allow adequate fluid resuscitation and give Give a 500 mL bolus of intravenous fluid over 15 minutes. A smaller bolus (e.g., 250 mL) may be more appropriate if the patient has a history of cardiac failure. If persistent hypotension, vasopressors may be required to achieve the goal of mean arterial pressure greater than 65 mm Hg. Noradrenaline (norepinephrine) 0.4 to 0.8 mg/hour intravenous infusion initially, adjust dose according to response. Vasopressin may be added to norepinephrine by dose 0.01 units/minute intravenous infusion initially, adjust dose according to response, maximum 0.03 units/minute. Renal-dose dopamine is associated with poorer outcomes in patients with acute kidney injury; it is no longer recommended. 

ELECTROLYTE IMBALANCES ― attention to electrolyte imbalances (e.g., hyperkalemia, hyperphosphatemia, hypermagnesemia, hyponatremia, hypernatremia, metabolic acidosis) is important.  

          Hyperkalemia. Severe hyperkalemia is defined as potassium levels of 6.5 mEq per L (6.5 mmol per L) or greater, or less than 6.5 mEq per L with electrocardiographic changes typical of hyperkalemia (e.g., tall, peaked T waves). Hyperkalemia can be treated by regular insulin (Actrapid) 5 to 10 units and dextrose 25% or 50% given intravenously can shift potassium out of circulation and into the cells. Calcium gluconate (10 mL [one ampoule] of 10% solution infused intravenously over five minutes) is also used to stabilize the membrane and reduce the risk of arrhythmias when there are electrocardiographic changes showing hyperkalemia. In patients without electrocardiographic evidence of hyperkalemia, calcium gluconate is not necessary, but sodium polystyrene sulfonate (Kayexalate) can be given to lower potassium levels gradually, and loop diuretics can be used in patients who are responsive to diuretics. Dietary intake of potassium should be restricted. 

MEDICATIONS IN AKI

DIURETICS ― The main indication for use of diuretics is management of volume overload. Intravenous loop diuretics, as a bolus or continuous infusion, can be helpful for this purpose. However, it is important to note that diuretics do not improve morbidity, mortality, or renal outcomes, and should not be used to prevent or treat acute kidney injury in the absence of volume overload.

          All medications that may potentially affect renal function by direct toxicity or by hemodynamic mechanisms should be discontinued, if possible. For example, metformin (Glucophage) should not be given to patients with diabetes mellitus who develop acute kidney injury. The dosages of essential medications should be adjusted for the lower level of kidney function. Avoidance of iodinated contrast media and gadolinium is important and, if imaging is needed, noncontrast studies are recommended. For further information see topic on Contrast-induced nephropathy prevention strategy.

PREVENTION

Table (1). Preventive Strategies for Patients at High Risk of Acute Kidney Injury
Risk factors	Preventive strategies
Cancer chemotherapy with risk of tumor lysis syndrome	Hydration and allopurinol (Zyloprim) administration a few days before chemotherapy initiation in patients at high risk of tumor lysis syndrome to prevent uric acid nephropathy
Exposure to nephrotoxic medications	Avoid nephrotoxic medications if possible
	Measure and follow drug levels if available
	Use appropriate dosing, intervals, and duration of therapy
Exposure to radiographic contrast agents	Avoid use of intravenous contrast media when risks outweigh benefits
	If use of contrast media is essential, use iso-osmolar or low-osmolar contrast agent with lowest volume possible
	Optimize volume status before administration of contrast media; use of isotonic normal saline or sodium bicarbonate may be considered in high-risk patients who are not at risk of volume overload
	Use of N-acetylcysteine may be considered
Hemodynamic instability	Optimal fluid resuscitation; although there is no consensus, a mean arterial pressure goal of > 65 mm Hg is widely used; isotonic solutions (e.g., normal saline) are preferred over hyperoncotic solutions (e.g., albumin)
	Vasopressors are recommended for persistent hypotension (mean arterial pressure < 65 mm Hg) despite fluid resuscitation; choice of vasoactive agent should be tailored to patients’ needs
	Dopamine is not recommended
Hepatic failure	Avoid hypotension and gastrointestinal bleeding
	Early recognition and treatment of spontaneous bacterial peritonitis; use albumin, 1.5 g per kg at diagnosis and 1 g per kg at 48 hours
	Early recognition and management of ascites
	Albumin infusion during large volume paracentesis
	Avoid nephrotoxic medications
Rhabdomyolysis	Maintain adequate hydration
	Alkalinization of the urine with intravenous sodium bicarbonate in select patients (normal calcium, bicarbonate less than 30 mEq per L [30 mmol per L], and arterial pH less than 7.5)
Undergoing surgery	Adequate volume resuscitation/prevention of hypotension, sepsis, optimizing cardiac function Consider holding renin-angiotensin system antagonists preoperatively

REFERENCES

• Mahboob Rahman, Shad, F. and Smith, M.C. (2012). Acute Kidney Injury: A Guide to Diagnosis and Management. American Family Physician, [online] 86(7), pp.631–639. Available at: https://www.aafp.org/afp/2012/1001/p631.html