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Acute Kidney Injury Fact Sheet

Clinical Issues

Overview • Overuse of medications, such as nonsteroidal anti-

inflammatory drugs (NSAIDs, such as ibuprofen,
With over 30 definitions of acute kidney injury (AKI) in pub- naproxen) and angiotension-converting enzyme (ACE)
lished studies, there is no consensus among experts inhibitors.
regarding how AKI is defined (Palevsky et al., 2013).
Palevsky and colleagues (2013) describe AKI as a sudden Intra-Renal or Intrinsic
loss of kidney function occurring over hours to days, result- Direct injury to the kidney or renal parenchyma due to fac-
ing in fluid and electrolyte imbalance, retention of nitroge- tors, such as:
nous waste products in the blood, and acid base irregular- • Cancer.
ity. More specifically, AKI is defined as an increase in serum • Systemic Infection or sepsis.
creatinine of 0.3 m/dL or higher within 48 hours, or an • Interstitial nephritis or allergic reaction to medications.
increase in serum creatinine 1.5 times baseline within the • Scleroderma or other connective tissue disorder.
prior 7 days, or a decrease in urine volume less than 0.5 • Damage to the renal tubules, such as glomerulonephri-
mL/kg/hr for 6 hours (Kidney Disease: Improving Global tis, vasculitis, or thrombotic microangiography.
Outcomes [KDIGO], 2012).
Post-Renal
In the United States, AKI has grown by 14% annually since Obstruction of the urinary tract leading to increase pressure
2001, with approximately 5% to 25% of all hospitalized in the Bowman’s capsule and reduced glomerular filtration
patients diagnosed with AKI (Brown, Rezaee, Marshall, & rate (GFR) caused by:
Matheny, 2016). AKI is associated with high mortality rates. • Enlarged prostate.
The number of AKI hospital-related deaths increased • Cancer of bladder, cervix, or prostate.
almost twofold, from 147,943 deaths in 2001 to 285,768 • Blood clot (thrombus).
deaths in 2011 (Brown et al., 2016). Patients who develop • Kidney stones (renal calculi).
AKI are at risk for adverse outcomes, such as cardiovascu- • Urethral strictures.
lar events, pulmonary complications, and end stage renal
disease (ESRD); however, it is important to note that Risk Factors Associated with AKI
approximately 66% of all AKI episodes develop in the com- • Advanced age.
munity, outside of the hospital setting (Harty, 2014). • Surgical procedures, especially cardiovascular surgery.
Therefore, prevention, early recognition, and management • Sepsis.
are essential to decrease poor health outcomes associated • Major trauma resulting in blood loss and muscle dam-
with AKI. age.
• Multiple organ dysfunction syndrome (MODS) seen in
Causes and Risk Factors critically ill patients.
• Exposure to radiocontrast agents.
The etiologies of AKI are multifactorial and categorized as • Nephrotoxic drugs (NSAIDs, methotrexate, ACE
pre-renal, intra-renal, or post-renal (Lameire, Van Biesen, & inhibitors).
Vanholder, 2005). • Dehydration.

Pre-Renal Signs and Symptoms

Reversible kidney hypoperfusion associated with:
• Hypotension. The clinical presentation of patients with AKI vary depend-
• Volume depletion due to hemorrhage, diarrhea, dehy- ing on the severity and cause of AKI (Rahman, Shad, &
dration, severe burns, or diuretics. Smith, 2012). Many patients with mild or moderate AKI are
• Organ failure, such as pancreatitis and liver disease, asymptomatic (Rahman et al., 2012). According to the
which causes shift of fluid in the abdomen. National Kidney Foundation (2019), patients with more
• Heart failure or heart attack. severe AKI may have the following symptoms:
• Severe allergic reactions. • Jugular venous distention.
 Acute Kidney Injury Fact Sheet
Clinical Issues

• Edema (peripheral, periorbital). increases, allowing plateau of the BUN and creatinine,
• Dyspnea. then a gradual decline. Although significant improvement
• Nausea and vomiting. in kidney function is observed in the first 1 to 2 weeks of
• Fatigue. this phase, it may take up to 12 months for kidney func-
• Confusion. tion to stabilize. Some patients do not recover and
• Chest pain or pressure. progress to ESRD. The outcome of AKI is contingent
• Back pain. upon the patient’s overall health, the severity of kidney
• Decreased urine output (oliguria). damage, and the presence of complications and comor-
• Seizure or coma in severe cases. bid conditions. With aggressive treatment, most patients
achieve normal kidney function without complications.
There are four phases of AKI. Depending on the phase of
AKI, other clinical manifestations of AKI often present in crit- Diagnosis and Evaluation
ically ill patients, including metabolic acidosis, hyperkalemia,
hypophosphatemia, uremia, and azotemia. Although the The diagnosis of AKI is multifactorial, with an emphasis on
severity of symptoms and the complexity of renal dysfunc- identifying the underlying cause. History and physical
tion vary, the clinical course and manifestations of AKI gen- examination are important components in the diagnosis of
erally progress over the following four phases (Dirkes, 2015; AKI, including assessment of volume status (Rhaman et al.,
Lewis, Dirksen, Heikemper, Bucher, & Harding, 2014): 2012). When conducting the physical examination, assess-
• Onset Phase: Initial insult to kidney due to factors such ment of intravascular volume status and skin rash, which
as blood loss, dehydration, burns, diabetes insipidos, or indicates systemic illness, is essential (Rahman et al., 2012).
infection, resulting in a decrease in renal blood flow and Initial laboratory studies to assist in identifying the cause of
tissue oxygenation 25% of normal and urine output less AKI include complete blood count, urinalysis, and kidney
than 0.5 mL/kg/hr. This phase last hours to days. function studies, such as measurement of serum creatinine,
• Oliguric Phase: The most common initial clinical mani- BUN, and fractional excretion of sodium (Rahman et al.,
festation of AKI is oliguria, defined as a reduction in urine 2012). According to Workeneh, Agraharkar, and Gupta
output less than 400 mL/day. Oliguria is manifested with- (2017), the following laboratory and diagnostic studies are
in 1 to 7 days of kidney injury. This phase typically lasts often performed to diagnose and determine the cause of
10 to 14 days but can last months in some cases. The AKI:
longer the oliguric phase, the poorer the prognosis for • BUN and Creatinine: Elevation of creatinine and BUN
the recovery of kidney function. However, approximately are hallmark indicators of kidney injury. The BUN-to-cre-
50% of patients will not experience oliguria, making diag- atinine ratio can exceed 20:1 in conditions that promote
nosis difficult. In the oliguric phase, signs of fluid volume reabsorption of urea, such as large volume loss, which
overload, such as edema, distended neck veins, hyper- suggests pre-renal AKI.
tension, pulmonary edema, and heart failure, may occur. • Complete Blood Count: Used to detect infection,
In addition to signs of volume overload, metabolic acido- chronic anemia, blood loss, or thrombotic microan-
sis, hyperkalemia, hyperphosphatemia, and uremic giopathy.
symptoms may also be present. • Urinalysis: Muddy, brown, granular casts; oxalate crys-
• Diuretic Phase: In this phase, daily urine output is tals; and tubular casts in urine sediment may indicate
approximately 1 to 3 liters but can reach as high as 5 acute tubular necrosis (ATN). Urine that is reddish-brown
liters or more. The kidneys recover their ability to excrete in color indicates myoglobinuria or hemoglobinuria.
waste but cannot concentrate the urine. Hypovolemia Further, renal tubular injury will result in proteinuria.
and hypotension may occur due to massive volume Urinary red blood cells (RBCs) occur due to bleeding
loss. Due to the loss of large volumes of fluid and elec- along the collecting system. RBC casts or dysmorphic
trolytes, patients should be monitored for hyponatremia, RBCs in the urine are the result of glomerular inflamma-
hypokalemia, and dehydration. This phase may last 1 to tion or glomerulonephritis. The presence of white blood
3 weeks. During the end of this phase, fluid and elec- cells (WBCs) or WBC casts suggests pyelonephritis or
trolytes, acid-base balance, and waste product values interstitial nephritis.
(blood urea nitrogen [BUN] and creatinine) start to nor- • Peripheral Smear: The presence of schistocytes sug-
malize. gests hemolytic uremic syndrome and thrombotic
• Recovery Phase: This phase begins when the GFR thrombocytopenic purpura.

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 Acute Kidney Injury Fact Sheet
Clinical Issues

Table 1.
Staging of AKI

Stage Serum Creatinine Urine Output

1 1.5 to 1.9 times baseline < 0.5 mL/kg/h for 6 to 12 hours
OR
≥ 0.3 mg/dL (≥ 26.5 mmol/l) increase

2 2.0 to 2.9 times baseline < 0.5 mL/kg/h for ≥ 12 hours

3 3.0 times baseline < 0.3 mL/kg/h for X 24 hours

OR OR
Increase in serum creatinine to ≥ 4.0 mg/dL (≥ 353.6 mmol/L) Anuria for X 12 hours
OR
Initiation of renal replacement therapy
OR
In patients <18 years, decrease in eGFR to < 35 mL/min/1.73 m2

Source: KDIGO, 2012.

• Fraction of Urinary Sodium (FENa): Measures the identified AKI when serum creatinine levels remained within
percent of sodium excreted in the urine and is used to the normal range (Bongiovanni et al., 2015).
determine pre-renal vs. ATN as the cause of AKI. This
test is useful only in the presence of oliguria. In pre-renal KDIGO (2012) makes the following recommenda-
conditions, FENa is usually less than 1%. In ATN, the tions for patients at risk for AKI:
FENa is typically greater than 1%. • Patients should be tested with measurements of serum
• Renal Ultrasound: Used to evaluate potential obstruc- creatinine and urine output to detect AKI.
tion of the renal collection system and existing renal dis- • The frequency and duration of monitoring is individual-
ease. Hydronephrosis may be present, and small kid- ized according to patient risk and clinical course.
neys indicate chronic kidney disease (CKD). Doppler • Evaluate patients with AKI promptly to determine the
ultrasound assists in the diagnosis of renovascular or cause, with special attention to reversible causes.
thromboembolic disease. Elevated restrictive indices • Monitor patients with AKI with measurements of serum
may suggest hepatorenal syndrome. creatinine (SCr) and urine output to stage the severity.
• Nuclear Scanning: Allows assessment of renal tubular • Manage patients with AKI according to the stage and
function and blood flow. cause.
• Aortorenal Angiography: Helpful in diagnosing renal According to KDIGO (2012), AKI is staged by criteria dis-
vascular disorders, such as atherosclerosis with aortore- played in Table 1.
nal occlusion, certain cases of necrotizing vasculitis,
renal artery stenosis, and renal atheroembolic disease. Management and Treatment
• Renal Biopsy: Useful in determining intra-renal causes
of AKI. Also indicated if renal function has not returned to Optimal management of AKI requires close collaboration
baseline for a prolonged period and prognosis is needed among the interprofessional team. Most patients with AKI
for long-term management. will be hospitalized, unless the condition is mild with a clear-
ly reversible cause (Rahman et al., 2012). The goal of man-
In addition to routine diagnostic studies, biomarkers are agement is to ensure adequate renal perfusion by maintain-
emerging as significant tools for the identification of AKI. ing and achieving hemodynamic stability, avoiding hypo-
One example is cyastatin C. In a study conducted by volemia, and preventing further kidney damage (Rahman et
Bongiovanni and colleagues (2015) of 198 emergency al., 2012). KDIGO (2012) clinical practice guidelines suggest
department patients, serum cyastatin C alone or in combi- the management of AKI should be based on the stage and
nation with serum creatinine and GFR was a strong predic- cause of AKI, and include the following recommendations:
tor of AKI risk. One advantage of cyastatin C was that it • In patients at risk for or with AKI who are not in hemor-

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 Acute Kidney Injury Fact Sheet
Clinical Issues

rhagic shock, use isotonic crystalloids (0.9% normal intravascular volume by assessing for an increase in
saline) rather than colloids (albumin or hetastarch) in the blood pressure (BP) and central venous pressure (CVP).
initial management of intravascular volume expansion. • Strict measurement and documentation of intake and
• In patients with vasomotor shock at risk for or with AKI, output (I & O) every shift.
use vasopressors along with fluids. • Implement infection control measures. Use aseptic
• In high-risk patients with septic shock or in the perioper- technique and protect the patient from others with
ative setting, use protocol-based management of hemo- infectious diseases.
dynamic and oxygenation parameters to prevent devel- • Review medications for nephrotoxins.
opment or worsening of AKI. • Monitor volume status including I & O, BP, heart rate,
• In patients who are critically ill, initiate insulin therapy tar- body weight, jugular venous distention, and peripheral
geting plasma glucose 110 to 149 mg/dL (6.1 to 8.3 and pulmonary edema.
mmol/L). • Weigh patients with the same scale at the same time
• Do not use diuretics to prevent or treat AKI, except in the each day.
management of volume overload. • Perform skin care and take measures to prevent pres-
• Achieve a total energy intake of 20 to 30 kcal/kg/d in sure ulcers.
patients with any stage of AKI. • To prevent stomatitis that develops when ammonia in
• Low dose dopamine should not be used to prevent or saliva irritates the mucous membranes, perform mouth
treat AKI. care daily.
• Prior to administration of contrast medium, assess the • Review laboratory results daily for electrolyte and acid
risk of contrast-induced AKI (CI-AKI) by screening for base imbalance.
pre-existing kidney impairment. • Monitor continuous electrocardiogram (ECG) to detect
• In patients at risk for CI-AKI, intravenous volume (IV) cardiac arrhythmias.
expanders are recommended with either isotonic sodi- • Assess the heart for an S3 gallop, murmurs, or a peri-
um chloride or sodium bicarbonate solutions. cardial friction rub.
• Consider oral acetylcysteine along with IV isotonic crys- • Auscultate the lungs for crackles, rhonchi, or dimin-
talloids in patients at increased risk for CI-AKI. ished breath sounds.
• Renal replacement therapy (RRT) should be initiated • Observe dialysis access site for inflammation and exu-
emergently when life-threatening changes in fluid, elec- date.
trolyte, and acid-base imbalance exists.
• Do not rely solely on BUN and creatinine thresholds Prevention
when making the decision to start RRT; rather, consider
the broader clinical context, presence of conditions that The National Institute of Healthcare Excellence (NICE)
can be modified with RRT, and trends of laboratory tests. (2013) developed the following guidelines for the prevention
• When initiating RRT, use an uncuffed, non-tunneled of AKI in patients at risk:
hemodialysis catheter rather than a tunneled dialysis • Implement tracking and/or trigger systems (early warn-
catheter in patients with AKI. ing scores) to identify adults at risk of AKI due to clinical
• Obtain a chest X-ray promptly after placement and deterioration or at risk for clinical deterioration.
before the first use of a subclavian or internal jugular • In patients with risk factors for AKI scheduled to receive
vein hemodialysis catheter. iodinated contrast media, offer IV volume expansion
• For patients who are hemodynamically unstable, use (0.9% normal saline or sodium bicarbonate) prior to the
continuous renal replacement therapy (CRRT) rather procedure.
than standard RRT. • Consider temporarily stopping ACE inhibitors or
• Use bicarbonate, rather than lactate, as a dialysate and angiotensin receptor blockers (ARBs) in adults with
replacement fluid buffer for RRT in patients with AKI. CKD and an estimated GFR (eGFR) less than 40
• Deliver a Kt/V of 3.9 per week when using intermittent mL/min/1.73m2 prior to receiving iodinated contrast
or extended RRT for AKI. medium and adults experiencing vomiting, diarrhea, or
• Nursing care and management (Thornburg & Gray- sepsis until their symptoms improve or stabilize.
Vickrey, 2016). When administering fluid bolus(es), • Consult pharmacist regarding optimizing medications
monitor cardiovascular response to the increased and drug dosing in patients at risk for AKI.

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 Acute Kidney Injury Fact Sheet
Clinical Issues

Other strategies to prevent AKI, according to Rahman and Ishani, A., Xue, J.L. Himmelfarb, J., Eggers, P.W., Kimmel, P.L.,
colleagues (2012), include: Molitoris, B.A., & Collins. A.J. (2009). Acute kidney injury
increases risk of ESRD among elderly. Journal of the
• Avoid nephrotoxic medications if possible.
American Society of Nephrology, 20(1), 223-228.
• Measure and follow drug levels, if available, and use doi:10.1681/ASN.2007080837
appropriate dosing, intervals, and duration of therapy. Kidney Disease: Improving Global Outcomes (KDIGO). (2012).
• Optimize fluid resuscitation in patients hemodynamical- KDIGO clinical practice guidelines for acute kidney injury.
ly unstable to achieve a mean arterial pressure (MAP) of Journal of the International Society of Nephrology, 2(1),
1-141. Retrieved from http://www.kdigo.org/clinical_
greater than 65 using isotonic solutions (e.g., 0.9% nor-
practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf
mal saline). Lameire, N., Van Biesen, W., & Vanholder. R. (2005). Acute renal
• For persistent hypotension not responsive to fluid failure. The Lancet, 365(9457), 417-430.
resuscitation, start vasopressors with the goal of a Lewis, S.L., Dirksen, S.R., Heitkemper, M.M., Bucher. L., &
mean arterial pressure (MAP) of 65 or greater. Harding, M.M. (2014). Medical surgical nursing: Assess-
ment and management of clinical problems (9th ed.). St.
• Maintain adequate hydration.
Louis MO: Elsevier Mosby.
• For patients having surgery, adequate volume and pre- National Institute of Healthcare Excellence (NICE). (2013). Acute
vention of hypotension is important. Optimize cardiac kidney injury: Prevention, detection and management.
function and consider holding renin-angiotensin system Retrieved from https://www.nice.org.uk/guidance/cg169/
antagonists preoperatively. chapter/1-Recommendations#preventing-acute-kidney-
injury
National Kidney Foundation (NKF). (2019). Acute kidney injury.
References New York, NY: Author. Retrieved from https://www.
kidney.org/atoz/content/acutekidneyinjury
Bongiovanni, C., Magrini, L., Salerno, G. Gori, C.S., Cardelli, P., Palevsky, P.M., Liu, K.D., Brophy, P.D., Chawla, L.S., Parikh,
Hur, M., … Di Somma, S. (2015). Serum cystatin C for the C.R., … Weisbord, S.D. (2013). KDOQI US commentary on
diagnosis of acute kidney injury in patients admitted in the the 2012 KDIGO clinical practice guideline for acute kidney
emergency department. Retrieved from https://www. injury. American Journal of Kidney Diseases, 61(5),649-672.
semanticscholar.org/paper/Serum-Cystatin-C-for-the- Retrieved from https://www.kidney.org/sites/default/files/
Diagnosis-of-Acute-Kidney-Bongiovanni-Magrini/dd27 PIIS027263861300471X.pdf
bef8cefd29744f2556e0f57fde686b71dd5f Rahman, M., Shad, F., & Smith, M.C. (2012). Acute kidney injury:
Brown, J.R., Rezaee, M.E., Marshall, E.J., & Matheny M.E. A guide to diagnosis and management. American Family
(2016). Hospital mortality in the United States following Physician, 86(7), 631-639. Retrieved from https://www.
acute kidney injury. Biomed Research International, aafp.org/afp/2012/1001/p631.html
4278579, 1-6. doi:10.1155/2016/4278579 Thornburg, B., & Gray-Vickrey, P. (2016). Acute kidney injury:
Dirkes, S. (2015). Acute kidney injury: Causes, phases, and early Limiting the damage. Nursing2016, 46(6), 24-34.
detection. American Nurse Today, 10(7), 20-25. Retrieved doi:10.1097/01.NURSE.0000482865.61546.b4
from https://www.americannursetoday.com/acute-kidney- Workeneh, B.T., Agraharkar, M., & Gupta, R. (2017). Acute kid-
injury/ ney injury. Retrieved from https://emedicine.medscape.
Harty, J. (2014). Prevention and management of acute kidney com/article/243492-overview
injury. Ulster Medical Journal, 83(3), 149-157.

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