Updates in Management and Timing of Dialysis in Acute Kidney Injury
Acute kidney injury (AKI) is a common complication in hospitalized patients and is associated with mortality, prolonged hospital length of stay, and increased healthcare costs. This paper reviews several areas of controversy in the identification and management of AKI. Serum creatinine and urine output are used to identify and stage AKI by severity. Although standardized definitions of AKI are used in research settings, these definitions do not account for individual patient factors or clinical context which are necessary components in the assessment of AKI. After treatment of reversible causes of AKI, patients with AKI should receive adequate volume resuscitation with crystalloid solutions. Balanced crystalloid solutions generally prevent severe hyperchloremia and could potentially reduce the risk of AKI, but additional studies are needed to demonstrate a clinical benefit. Intravenous albumin may be beneficial in patients with chronic liver disease either to prevent or attenuate the severity of AKI; otherwise, the use of albumin or other colloids (eg, hydroxyethyl starch) is not recommended. Diuretics should be used to treat volume overload, but they do not facilitate AKI recovery or reduce mortality. Nutrition consultation may be helpful to ensure that patients receive adequate, but not excessive, dietary protein intake, as the latter can lead to azotemia and electrolyte disturbances disproportionate to the patient’s kidney failure. The optimal timing of dialysis initiation in AKI remains controversial, with conflicting results from two randomized controlled trials.
© 2019 Society of Hospital Medicine
Diuretics
As above, volume status is a key component in the management of patients with AKI. In patients with AKI and hypervolemia, loop diuretics are often given prior to the initiation of RRT. Loop diuretics act on the sodium-potassium-chloride cotransporters in the thick ascending limb of the loop of Henle to increase urinary losses of these ions and urine volume. Loop diuretics are dose-dependent, and often, higher doses are needed (eg, furosemide 100 mg intravenous dose) in patients with AKI, since the diuretic effect depends on the proximal tubular secretion of the drug into the urine. The role of diuretics in AKI is controversial and some observational data suggest an increased mortality risk with diuretic use in patients with AKI.37 In critically ill patients with acute lung injury, diuretic use improved survival, which was attributed to better control of volume overload.38 But, a meta-analysis of 11 randomized controlled trials failed to demonstrate that diuretics directly improved survival or recovery of AKI.39 Moreover, randomized controlled trials found that diuretics given to a patient with AKI requiring RRT did not improve recovery of kidney function.40,41 The KDIGO guidelines recommend that diuretics should not be routinely used for AKI except in the management of volume overload.16
Nutritional Targets in Acute Kidney Injury
Critically ill patients have high protein catabolic rates, which put them at increased risk for malnutrition, which in turn is associated with mortality. Patients who receive continuous RRT (CRRT) may lose 5-10 g of protein and 10-15 g of amino acids daily, and these patients may have protein requirements that are twice the usual recommended daily protein intake.16 But excess protein administration can result in high urea generation and azotemia unrelated to the patient’s kidney function. Blood urea nitrogen may also be disproportionately elevated in conditions where tubular reabsorption of urea is increased, such as in volume depletion, diuretic use, corticosteroid use, and gastrointestinal bleeding. Interpretation of blood urea nitrogen results must be made in the appropriate clinical context, with recognition that azotemia alone may not be a good surrogate marker of the patient’s underlying kidney function. We recommend dietary consultation in critically ill patients with AKI to ensure that adequate, but not excessive, protein is administered.
RENAL REPLACEMENT THERAPY IN ACUTE KIDNEY INJURY
In patients with AKI, RRT is initiated for control of volume overload, electrolyte abnormalities, acidemia, or uremic symptoms or complications that are refractory to medical management (Table 3). In a nonoliguric patient, fluid and electrolyte abnormalities can oftentimes be managed medically. Patients with oligoanuria (generally defined as urine output less than 400 mL/day or <20 mL/hour), however, require nephrology evaluation for consideration of RRT. Early nephrology consultation (within 48 hours of AKI diagnosis) may be associated with lower dialysis dependence and mortality in critically ill patients with AKI.42 The decision to initiate dialysis is individualized based on the patient’s comorbid conditions, urine output, and trajectory of kidney function.
Timing of Renal Replacement Therapy
The optimal timing of dialysis initiation in patients with AKI is not known. Theoretically, earlier initiation of dialysis could allow for better volume and electrolyte control and prevent the development of more serious complications of kidney failure such as uremic seizures, encephalopathy, and pericarditis. However, RRT is associated with its own risks and earlier initiation may expose the patient to unnecessary procedures and complications that might delay renal recovery. A meta-analysis of predominantly observational data found that earlier initiation of RRT in AKI was associated with lower 28-day mortality, greater renal recovery, decreased duration of RRT, and decreased ICU length of stay.43 Subsequently, two prospective trials reported conflicting results regarding associations between dialysis timing and outcomes in patients with severe AKI (Table 4).44,45
