What is an Acute Kidney Injury (AKI)?

Welcome.
The kidneys are two bean-shaped organs about the size of a fist, located on either side of the spine, just below the rib cage. Their essential function is to regulate body fluid levels & remove waste products from the blood in the form of urine.

They filter about 120-150 quarts of blood each day to produce about 1-2 quarts of urine, composed of wastes & extra fluid. The kidneys also keep levels of electrolytes stable, such as sodium, potassium, & phosphate. They make hormones that help regulate BP, make red blood cells, & strengthen the bones.

Acute Kidney Injury (AKI)

Acute kidney injury (AKI) is a condition in which the kidneys suddenly lose their ability to filter waste from the blood. The term AKI has replaced acute renal failure (ARF) to reflect that a decline in kidney function does not necessary lead to organ failure.

Acute kidney injury develops rapidly over a few hours to days, causing creatinine and urea to accumulate in the blood (called azotemia), which leads to fluid and electrolyte disorders. AKI is most common in people who are already hospitalized, especially in the critically ill.
AKI has a poor prognosis, with the mortality rate ranging from 10%-80%, depending on the patient population. Patients with uncomplicated AKI have a mortality rate up to 10%. However, patients with AKI and multi-organ failure have a reported mortality rate over 50%. If dialysis or kidney transplant is required, the mortality rate rises to as high as 80%. The risk for developing AKI increases with the elderly, especially in patients with other diseases such as diabetes, cardiac disease, & hypertension.
Intensive treatment is required, but full recovery is possible if the condition is caught and treated early.

Acute Kidney Injury (AKI)-Kidneys suddenly lose ability to filter waste from the blood.

-Develops rapidly over a few hours to days
-Creatinine and urea in the blood (azotemia)
-leads to fluid & electrolyte disorders
-Most common in hospitalized patients, especially critically ill
-Mortality rate ranges from 10%-80%
-Uncomplicated AKI, mortality rate of 10%
-AKI & multi-organ failure, mortality rate over 50%
-Dialysis or transplant required, mortality rate as high as 80%
-Risk for AKI increases with the elderly,
especially in patients with other diseases such as
diabetes, cardiac disease, & hypertension.
-Intensive treatment required – full recovery possible if condition caught and treated early.

There are 3 main CAUSES of AKI:

1. A sudden dramatic drop in blood flow to the kidneys – For example, sepsis, or overwhelming infection, is one of the most common causes of AKI. Patients with serious infections have reduced BP, which decreases blood flow to the kidneys, as well as other organs. As blood flow slows, some kidney areas have inadequate blood supply (inadequate perfusion), ultimately leading to cell death.
2. Nephrotoxic drugs, such as aminoglycosides and contrast dyes can also cause AKI. These drugs must be given carefully to avoid kidney injury.
3. A sudden blockage that stops urine from flowing out of the kidneys.

Patients with heart failure, liver disease, diabetes, or a history of AKI are at increased risk for developing AKI.

Acute Kidney Injury occurs in three types – prerenal, renal, or postrenal.

Prerenal injury– occurs when there is inadequate perfusion of blood to the kidneys.
-In this case, the problem occurs before the blood enters the kidney – the kidneys are actually not receiving enough blood to filter.
-This is the most common cause of AKI but does not usually lead to permanent kidney damage if treated in the early stages.
-The underlying problem of prerenal AKI is due to:

     Sepsis

     Hypovolemia from severe blood loss, dehydration, burns, etc.

     Heart failure

     Shock (extremely low BP)

     Liver failure

     Drugs that decrease blood flow to the kidneys

Renal (intrinsic) injury– includes diseases affecting the kidney itself.
-In this case, the damage is done in the kidney tissues and structures
-The underlying problem causing this injury to the kidneys is a result of:

    - Decreased blood supply to the kidneys, long enough to damage them

    - Acute tubular necrosis (kidney injury caused by damage to the kidney

      tubule cells - the most common cause of intrinsic AKI)

    - Acute interstitial nephritis (inflammation of the kidneys usually

      from an allergic reaction to a drug)

    - Acute glomerulonephritis (involves inflammation & damage to the glomerular

      membrane, the filtering screen of the kidney)

    - Toxic substances (drugs-specifically aminoglycosides, contrast dyes, & poisons)

Postrenal injury– is generally due to any condition that obstructs the urine flow out of the kidneys, anywhere along the urinary tract.
-The blockage causes pressure to build in all the renal nephrons (the filtering units of the kidney), ultimately causing the nephrons to shut down.
-Postrenal AKI is most often caused by

     -Enlarged prostate gland

     -Bladder stones

     -Kidney stones

     -It can also be caused by a tumor or cancer in the kidney or bladder,

      resulting in an obstruction.

SIGNS & SYMPTOMS of AKI
-Fluid retention, causing edema in legs, ankles, or feet
-Weight gain
-Decreased urine output (although sometimes, urine output remains normal)
-Chest pain or pressure
-Symptoms of uremia (urea & other nitrogen waste products build up in the blood)

     Weakness & fatigue

     Mental status changes - confusion, agitation, seizures, & coma

     Loss of appetite, nausea, vomiting

     Abnormal bleeding

     Heart problems - irregular heartbeat, pericarditis, chest pain or pressure

     Shortness of breath - from fluid buildup

-To clarify: azotemia & uremia both refer to the buildup of nitrogenous waste products (urea & creatinine) in the blood, but azotemia refers to the patient that does not have symptoms, whereas uremia refers to the patient that does have symptoms.

Azotemia – buildup of nitrogenous waste products (urea & creatinine) in the blood – patient does NOT have symptoms
Uremia – buildup of nitrogenous waste products (urea & creatinine) in the blood – patient DOES have symptoms

Acute kidney injury can be divided into four phases: onset, oliguric, diuretic, & recovery.
The onset is the initial phase of injury to the kidney, in which reversal or prevention of kidney dysfunction is still possible. The events that trigger this phase include blood or fluid loss, burns, & diabetes insipidus. The symptoms are often subtle, and the duration usually lasts from hours to days.
In the oliguric phase the urine output usually decreases to less than 400 ml/day, so the body is unable to excrete metabolic wastes. This leads to electrolyte disturbances, acidosis, & fluid overload (because the kidney is unable to excrete water). The oliguric phase usually lasts from 1 to 3 weeks, but may be longer.
The diuretic phase occurs when the cause of AKI is corrected and urine output increases to >1000 ml/day. There may be possible electrolyte depletion from the excretion of more water. Symptoms include a possible urinary output up to 4-5 L/day, postural hypotension, tachycardia, improved mental alertness, weight loss, & thirst. This phase usually lasts 1-2 weeks.
The recovery phase involves the normalization of fluid & electrolyte balance. Patients have a decrease in edema as well as a decrease in energy levels as the body is recovering, lasting from 3-12 months. Most patients are left with some residual renal dysfunction.

Diagnosis

Diagnostic tests to determine acute kidney injury include:
-Blood tests including BUN, creatinine, electrolytes, & CBC.
-Urine tests including sodium, creatinine concentration, urine protein & microscopic analysis of sediment.
-Urine output monitoring, along with creatinine measurement, is currently being studied much more closely, as a fall in urine output directly reflects GFR (glomerular filtration rate) in the kidney and therefore is a sensitive & early indication of AKI.
-Imaging tests including US, CT or MRI can help identify the cause of AKI, particularly in post-renal failure, obstructive causes, or hydronephrosis.
-When the cause of AKI is unknown, a kidney biopsy can also be done.

When diagnostic tests are done, you will see the following Laboratory results:
-AKI is marked by increases in blood urea nitrogen (BUN) and creatinine levels, as well as a decreased urine output to generally less than 40 ml/hr.
-A daily increase in creatinine indicates AKI, and the higher the level, the more severe the decline in kidney function is likely to be.
-Fluid & electrolyte imbalance occurs in the patient with AKI – the 3 major problems being hyperkalemia (elevated potassium), sodium imbalance, & metabolic acidosis.
-In AKI, many cells in the distal convoluted tubule are not functioning properly, so there is no mechanism to remove potassium from the body. Hyperkalemia develops when the blood serum level of potassium reaches 5.5 mEq/L or higher. Concentrations can quickly increase to 7-10 mEq/L, which is contradictory to normal cardiac function & life. Potassium toxicity is seen as changes on the ECG, laboratory findings, & occasionally neuromuscular symptoms.
–Hyponatremia (low sodium) in AKI usually develops as a result of overhydration, as the acutely ill, oliguric patient receives numerous fluids & drugs in an attempt to treat life-threatening problems. Serum sodium levels are less than 130 mEq/L. Signs of hyponatremia include warm, moist, flushed skin, mental status changes such as confusion, delirium, coma, & convulsions. Dialysis may be required to remove the excess fluid & restore sodium balance.
–Hypocalcemia (low calcium) is common as well as hyperphosphatemia (high phosphorus level).
–Metabolic acidosis is usually moderate, with the blood pH decreasing & the plasma bicarbonate content decreasing. Central nervous system symptoms of drowsiness, stupor & coma may appear.

Comprehensive Care

Treatment of AKI is supportive. The primary goal is to regain normal function of the kidney, which usually involves adjusting medications, providing appropriate nutrition, and correcting volume status, hyperkalemia, and acidosis.
-Life-threatening complications, such as pulmonary edema & hyperkalemia must be treated immediately in a critical care unit. The ICU allows for constant monitoring of BP, ECG, pulmonary, & mental status. Patients may also require mechanical ventilation and hemodynamic monitoring to monitor intravascular fluid volume.
-Treatable causes are treated as soon as possible – if obstruction is the cause, a catheter, endoscopy, or surgery may be needed to relieve the obstruction.
-Nephrotoxic drugs are stopped and drugs excreted by the kidneys are adjusted.
-If AKI is caused by a lack of fluids, then IV fluids are given. If AKI has caused fluid excess & edema, then daily water intake is restricted.
-Na+ and K+ intake is minimized.
-Kayexalate may be given to lower the level of potassium in the blood – it substitutes sodium for potassium in the GI tract (remember K+, or potassium, exiting).
-If conservative management is not effective, then dialysis is required.

Hemodialysis (often referred to as dialysis) is the process by which blood is removed from the body and waste products are filtered out through a semipermeable membrane, then the blood is returned to the body. In effect, it works as an artificial kidney, when the kidney is not functioning properly. In AKI, dialysis may just be needed temporarily, until the kidneys recover their function, usually over several days to weeks.

Hemodialysis is needed when:

-Severe electrolyte abnormalities cannot be controlled, such as hyperkalemia

-Fluid overload with pulmonary edema persists despite drug treatment

-Metabolic acidosis is unresponsive to treatment

-Symptoms of uremia occur

A healthy diet is important for patients with AKI.
A low-protein diet of 0.5-0.6 g/kg/day is recommended initially while the GFR is reduced. If dialysis is initiated, protein may be increased to 1.0-1.5 g/kg/day to compensate for protein losses during dialysis.
Since protein is restricted, calorie needs may need to be met by increasing carbohydrates and fat in the diet. Calories generally need to be increased to 35-50 cal/kg to provide positive nitrogen balance under stressful conditions.
Salt (sodium) is restricted depending on serum sodium levels, urinary excretion, edema, & dialysis needs. Fluid requirements are based on replacing losses (of urine, vomit, diarrhea) plus 500 mL per day. If the patient has hyponatremia (sodium too low), free water is usually restricted.
Potassium may be restricted to 1,000 mg/day during the oliguric phase, depending on the patient’s degree of hypermetabolism due to stress, infection, or fever.
Restricting foods high in phosphorus, such as dairy products, liver, legumes, nuts, & most soft drinks, will lower the phosphate concentration in the blood.

Nursing Guidelines when caring for the patient with AKI:
Maintain fluid & electrolyte balance

     -Maintain fluid restrictions

     -Monitor IV fluids carefully

     -Keep accurate records of intake & output

     -Weigh patient daily

     -Monitor vital signs frequently

     -Monitor serum electrolytes

Maintain nutrition
-Provide a diet low in protein & potassium and high in carbohydrates & fat
(however, if serum potassium is low, increase potassium intake).
-Take measures to relieve nausea.
-Be aware that many patients with AKI are too ill to tolerate oral feedings.

Prevent injury

     -Protect patient from injury & bleeding

Prevent infection

     Avoid sources of infection

     Assess for S/S of infection

     Maintain asepsis for indwelling lines or catheters

     Turn patients every 2 hours and as needed

     Provide careful skin care & pulmonary hygiene

Facilitate coping

     Provide emotional support for the patient and family

     Promote patient independence

Teach the patient with Acute Kidney Injury about:
-Identifying factors that contribute to AKI, such as hypertension & nephrotoxic drugs
-Prescribed medications, including name of drug, dosage, reason for taking, desired effects & adverse effects
-Prescribed dietary guidelines
-The risk of hypokalemia (low potassium) & symptoms – muscle weakness, anorexia, N/V, lethargy
-S/S of returning kidney injury – decreased urinary output without decreased fluid intake, signs of fluid retention, weight gain
-S/S of infection & methods to avoid infection
-Importance of follow-up care

Review

Acute kidney injury (AKI) is a condition in which the kidneys suddenly lose their ability to filter waste from the blood.
There are 3 main causes of AKI… A sudden dramatic drop in blood flow to the kidneys; nephrotoxic drugs; or a sudden blockage.
AKI occurs in 3 types…
-Prerenal – occurs when there is inadequate perfusion of blood to the kidneys.
-Renal (intrinsic) injury includes diseases affecting the kidney itself.
-Postrenal injury – generally due to any condition that obstructs the urine flow out of the kidneys, anywhere along the urinary tract.

2 common signs of AKI include edema & urine retention.

Acute kidney injury can be divided into four phases –

  Onset

   Oliguric

    Diuretic

     Recovery

Lab results will show:

	Increased BUN & Creatinine, Increased Potassium & Phosphorus,

	Decreased sodium & calcium; and Metabolic acidosis

Treatment is supportive & depends on the cause of the AKI, sometimes requiring hemodialysis. Provide the patient with a diet low in protein & potassium, and high in carbohydrates & fat.