In my previous article, I explained the types, causes and symptoms of Acute Kidney Injury (AKI). Here, I’ll share how physicians treat and manage AKI, as well as what to expect.

First, it’s important to note that patients should get immediate medical care to manage the life-threatening fluid and electrolyte abnormalities that come with AKI. Urgent therapy is required to restore kidney function and prevent further kidney damage.

Complications of AKI include the following:

  • Fluid overload
  • Hyperkalemia (serum potassium level > 5.5 mEq/L)
  • Uremia (pericarditis)
  • Severe metabolic acidosis (PH <7.1)

Patients with these complications often require urgent hemodialysis or continuous renal replacement therapy (CRRT). CRRT is hemodialysis for critically ill patients. This 24-hour-a-day process suits patients who can’t tolerate the rapid electrolyte and fluid shifts of traditional hemodialysis.

AKI complications and treatment in detail

Volume Depletion (Hypovolemia). Patients with clinical history of low blood plasma volume, called hypovolemia, due to fluid loss should be administered intravenous fluid therapy (crystalloid). Studies have shown that prompt reversal of volume depletion may prevent or limit kidney injury. However, such fluid infusion is contraindicated in those with volume overload (heart failure, liver cirrhosis, nephrotic syndrome).

The overall goal of fluid therapy is to increase cardiac output and improve tissue oxygenation in patients who are preload dependent or volume responsive.

Volume Overload (Hypervolemia). Hypervolemia, too much fluid in the blood, occurs due to excessive fluid administration in the setting of impaired ability to excrete sodium and water. This is especially true for patients with sepsis who commonly receive aggressive intravenous fluid resuscitation.

Diuretics may be used to relieve hypervolemia among patients with AKI. However, we generally do not use diuretics for prolonged therapy or to postpone the initiation of hemodialysis or CRRT.

Hyperkalemia. Hyperkalemia, or high potassium, is a life-threatening complication of AKI.

All patients with AKI and hyperkalemia that is refractory to medical therapy should be dialyzed unless hyperkalemia is mild (ie, ≤5.5 mEq/L).

Metabolic acidosis. Metabolic acidosis occurs when the body produces excess quantities of acid or when the kidneys don’t remove enough acid from the body. Excretion of acid and regeneration of bicarbonate is impaired in the setting of a low glomerular filtration rate (GFR), which results in metabolic acidosis.

Metabolic acidosis is more common in critically ill patients. Patients with AKI due to sepsis, trauma, and multi-organ failure often have increased production of lactic acid or ketoacids.

Commonly used treatments for metabolic acidosis include hemodialysis and bicarbonate administration.

Hypocalcemia (low blood calcium) and hypophosphatemia (low serum phosphate levels). Common treatments for hypophosphatemia include oral and parenteral phosphate. Treatment for hypocalcemia in patients with AKI usually requires intravenous calcium gluconate or calcium chloride. Close monitoring for both conditions is required to avoid excessive calcium phosphate intake.

CRRT or intermittent hemodialysis?

To treat AKI, nephrologists primarily use renal replacement therapy (RRT), which includes intermittent hemodialysis, peritoneal hemodialysis, various forms of CRRT, and “hybrid” therapies such as prolonged intermittent renal replacement therapy (PIRRT) or sustained low-efficiency hemodialysis (SLED).

A few clinical trials are taking a look at CRRT and intermittent hemodialysis under different conditions. One recent study aimed to compare the effect of CRRT and intermittent hemodialysis on the mortality and outcome of ICU patients with acute renal failure. Considering patients’ high mortality rate (about 60 to 70%), the authors wanted to find out if the method of RRT made an impact on outcome.

The single-center prospective randomized controlled trial included 252 critically ill patients. At 14 days, survival rates were similar: 39.5% for patients receiving intermittent hemodialysis and 43.9% for the CRRT group.

Outcome in adults with AKI

AKI is associated with a mortality rate of 45 to 70%. An AKI diagnosis increases mortality risk 5.5 to 6.5-fold when compared to similarly ill patients without AKI. AKI negatively affects vital organs, which contributes to the poor mortality rate.

After treatment is initiated, AKI patients experience a maintenance phase that typically lasts between 7 and 21 days. Duration depends on the length and severity of the initial ischemic episode; if recurrent ischemia occurs or exposure to nephrotoxins is ongoing; and, perhaps, whether the patient is oliguric (low urine output) or non-oliguric. Some patients recover within days. Others require renal replacement therapy (RRT) for weeks to months.

Patients who recover from AKI may not return to their baseline kidney function. An irreversible decline in kidney function after recovery is more likely in patients over age 65, those with pre-existing chronic kidney disease (CKD), and those with heart failure. Patients with CKD who develop AKI are more likely to progress to end-stage renal disease (ESRD) compared with patients with CKD who do not experience an episode of AKI.

AKI during hospitalization is associated with high in-hospital and long-term mortality. A variety of factors have been associated with increased mortality, including male sex, race, older age, oliguria, sepsis, respiratory or liver failure and cerebrovascular events.

Patients who develop AKI in the hospital should be evaluated within three months after discharge to test for and treat new onset AKI or worsening of pre-existing CKD.

Get in touch to discuss AKI and different treatment options. If you have a nephrology study that needs to be managed or rescued, schedule a call with one of Biorasi’s clinical experts.