Acute Kidney Injury: An Overview

Of Pathophysiology and Treatments

Continuing Nursing
Education

Kristina M. Yaklin
here has been an increase in
the prevalence of acute kidney
injury (AKI) over the past 15
years due to the increased percentage of older adults in the population and increased survival rates with
cardiac disease and diabetes mellitus
(Talbot, 2008). Up to 50% of AKI
cases are thought to develop in the
hospital (Armitage & Tomson, 2003).
Approximately 5% of hospital
patients admitted to medical or surgical floors will have their admission
complicated by the development of
AKI (Cheung, Ponnusamy, &
Anderton, 2008; Talbot, 2008).
Research by Barrantes et al. (2009)
found that development of AKI in
hospitalized patients was associated
with a 7-fold increase in likelihood of
death, a 4-fold increase in length of
stay, and a 4-fold increase in the likelihood of transfer to a critical care unit
than those who did not develop AKI
in the hospital. An evaluation of 13
studies comprehensively found that
mortality for patients without AKI
was 6.9% compared with 31.2% in
patients with AKI (Ricci, Cruz, &
Ronco, 2007).
These findings indicate that AKI
leads to increased risk of mortality of
hospitalized patients. Since the prevalence of AKI is increasing, it is very
likely that most healthcare professionals will encounter patients with AKI.
The purpose of this article is to provide education on the pathophysiology of AKI, aid in identifying risk factors, and discuss current research on
treatment options and interventions.

Kristina M. Yaklin, BSN, RN, is a Cross-Trained

Float Registered Nurse, Owosso Memorial Hospital,
and Student in the Doctorate of Nurse Practice,
University of Michigan Flint, Owosso, MI. She
may be contacted via e-mail at kryaklin@umflint.
edu
Statement of Disclosure: The author reported no
actual or potential conflict of interest in relation to
this continuing nursing education article.

Nephrology Nursing Journal

Copyright 2011 American Nephrology Nurses Association

Yaklin, K.M. (2011). Acute kidney injury: An overview of pathophysiology and treatments. Nephrology Nursing Journal, 38(1), 13-19, 30.
Acute kidney injury, or acute kidney failure, is thought to complicate 5% of hospital
admissions (Cheung, Ponnusamy, & Anderton, 2008). Most healthcare providers are
likely to encounter patients experiencing acute kidney injury. Nurses and other healthcare professionals can play a vital role in identifying patients at risk for acute kidney
injury and aid early intervention by identifying decreased kidney function. This article
summarizes the current literature on acute kidney injury, including the definition, pathophysiology, risk factors, diagnostic tests, and current treatments and interventions.

Goal
To provide an overview of acute kidney injury, its pathophysiology, and treatments.

Objectives
1.
2.
3.
4.

Define acute kidney injury (AKI).

Discuss the pathophysiology, including the three categories of AKI.
Identify the risk factors associated with AKI.
Describe treatment options for AKI.

Pathophysiology
AKI is a complex disorder with
varying definitions, most including an
abrupt decline in kidney function
leading to a rise in serum creatinine
and/or blood urea nitrogen levels,
with or without a decrease in urine
output (ADIS International Ltd.,
2009, Barrantes et al., 2009, Cheung
et al., 2008, Talbot, 2008,). AKI can be
classified into three cause categories:
pre-renal, intrinsic, and post-renal.

Pre-Renal Kidney Injury

Pre-renal kidney injury is caused
by hypoperfusion of the kidneys most
commonly caused by volume deple-

tion (burns, hemorrhage, GI losses),

hypotension (sepsis, shock), and renal
artery stenosis (ADIS International
Ltd., 2009, Cheung et al., 2008,
Talbot, 2008). Some vasoactive medications, such as angiotensin-converting enzyme inhibitors, epinephrine,
high-dose dopamine, and angiotensin
receptor antagonists, can also cause
pre-renal kidney injury by producing
intrarenal vasoconstriction leading to
hypoperfusion of the glomeruli
(Cheung et al., 2008; Porth, 2007,
Talbot, 2008).
Kidneys usually receive 20% to
25% of the total cardiac output (Porth,
2007). This blood supply is required to

This offering for 1.3 contact hours is provided by the American Nephrology Nurses
Association (ANNA).
ANNA is accredited as a provider of continuing nursing education (CNE) by the American
Nurses Credentialing Centers Commission on Accreditation.
ANNA is a provider approved by the California Board of Registered Nursing, provider number
CEP 00910.
Accreditation status does not imply endorsement by ANNA or ANCC of any commercial product.
This CNE article meets the Nephrology Nursing Certification Commissions (NNCCs) continuing nursing education requirements for certification and recertification.

January-February 2011

Vol. 38, No. 1

13

Acute Kidney Injury: An Overview of Pathophysiology and Treatments

remove wastes and manage fluid and

electrolyte balance. If the blood flow
is reduced, the glomerular filtration
rate (GFR) drops, decreasing urine
output and filtration, and reabsorption of substances filtered through the
glomerulus (Porth, 2007). The glomerular capillaries are supplied by
the afferent arteriole; blood then
flows out of the glomerular capillaries
via the efferent arteriole. This location
between two arterioles maintains the
pressure necessary to move fluid
through the glomerular capillaries,
maintaining the GFR. The afferent
and efferent arterioles are innervated
by the sympathetic nervous system
(SNS) and are sensitive to vasoactive
substances. Therefore, kidney blood
flow is affected during times of SNS
stimulation (for example, shock) and
when exposed to vasoactive hormones or drugs (Porth, 2007). When
kidney blood flow reaches approximately 20% of normal, damage can
occur to tubular cells (Porth, 2007).
This is further discussed in the next
section, Intrinsic Kidney Injury.

Intrinsic Kidney Injury

Intrinsic kidney injury involves
structural damage to glomerulus, vessels, or kidney tubules, which can
often be brought on by prolonged
pre-renal causes leading to cell necrosis by ischemia, or by infectious
agents and toxins that result in inflammation or injury (ADIS International
Ltd., 2009; Cheung et al., 2008;
Talbot, 2008). The most common
forms of intrinsic kidney injury are
acute tubular necrosis (ATN), acute
interstitial nephritis (AIN), and contrast-induced nephropathy (CIN).
Acute tubular necrosis (ATN).
ATN is the most common cause of
AKI, particularly in hospitalized
patients (ADIS International Ltd.,
2009; Cheung et al., 2008; Talbot,
2008). ATN typically occurs after an
ischemic or toxic ATN event.
Ischemic ATN is caused by prolonged pre-renal azotemia or by sepsis and toxic ATN is caused by direct
tubular damage by nephrotoxins,
such as aminoglycosides or radio contrast agents (Cheung et al., 2008).

14

Sepsis is the most common cause

of ischemic ATN, occurring in up to
50% of critically ill patients (Cheung
et al., 2008). Sepsis produces ischemia
through systemic vasodilatation leading to intrarenal hypoperfusion.
Sepsis also results in toxins that make
kidney tubular cells more sensitive to
the effects of ischemia (Porth, 2007).
Nephrotoxic agents cause kidney
injury by combinations of kidney
vasoconstriction, direct damage to
tubular cells, or intratubular obstruction (Porth, 2007). The kidneys are
particularly susceptible to nephrotoxic injury due to its rich blood supply,
ability to concentrate toxins, and
metabolic processes within the kidney that can turn substances into
toxic metabolites (Porth, 2007).
No matter what the cause, in
ATN, the necrotic tubular epithelial
cells begin to slough off and lead to
tubular obstruction and back-leak of
filtrate through the damaged epithelium (Cheung et al., 2008). The
obstruction also increases pressure on
the system, decreasing GFR and contributing to afferent arteriole constriction via tubuloglomerular feedback,
which results in decreased glomerular
capillary filtration pressure (Porth,
2007). Tubular injury is frequently
reversible if damage is not severe
enough to cause cortical necrosis
(Porth, 2007).
Clinical progression of ATN typically follows a sequence of three
events: initiation, maintenance, and
recovery. The initiation phase is characterized by an increase in blood urea
nitrogen and serum creatinine levels,
and a decline in urine output (Cheung
et al., 2008). Urine output in ATN can
vary from near normal levels to
anuria (Cheung et al., 2008). The
maintenance phase consists of sustained decrease in kidney function.
This may last 7 to 21 days, and during
this time, kidney support (such as
dialysis) may be required (Cheung et
al., 2008). The recovery phase is
defined by a marked increase in urine
output and decline in serum creatinine and blood urea nitrogen; this is a
time of regeneration of tubular
epithelial cells (Cheung et al., 2008).

Acute interstitial nephritis (AIN).

AIN accounts for 2% to 3% of AKI,
with most cases of AIN being caused
by exposure to certain nephrotoxic
drugs, such as NSAIDs and antibacterials (Cheung et al., 2008). This is
thought to be an immune reaction
and is not dose dependent (Naughton,
2008). AIN is a result of medications
binding to antigens in the kidney or
acting as antigens deposited in the
interstitium, causing an immune reaction even though the classic symptoms of a hypersensitivity reaction
may be absent (Naughton, 2008).
Contrast-induced nephropathy
(CIN). CIN usually occurs within 12
to 24 hours of a procedure using
radiocontrast agents (ADIS International Ltd., 2009). Risk factors for
developing CIN include underlying
kidney insufficiency, being older than
70 years, volume depletion, repeated
exposures to contrast in a short time
frame, and heart failure and/or diabetes mellitus (Naughton, 2008).
Potential ways to prevent CIN
include using low-osmolar contrast in
the lowest dose possible, avoiding
multiple procedures over a 24 to 48hour time period, hydrating before
and after procedures, or administering prophylactic drugs, such as statins,
sodium bicarbonate, or N-acetylcysteine (ADIS International Ltd., 2009;
Naughton, 2008). Many potentially
preventative measures discussed are
still under investigation and have had
mixed outcomes in studies, particularly the use of prophylactic medications.

Post-Renal Kidney Injury

Post-renal kidney injury is caused
by obstruction either from kidney calculi, strictures, blood clots, benign
prostatic hypertrophy, malignancies,
and pregnancy (ADIS International
Ltd., 2009; Cheung et al., 2008;
Talbot, 2008). Obstructions such as
those mentioned cause kidney injury
by increasing the pressure within the
kidney collecting systems, resulting in
a drop in the GFR, decreased water
and sodium reabsorption, and phosphaturia (Talbot, 2008).

Nephrology Nursing Journal

January-February 2011

Vol. 38, No. 1

Following removal or correction

of obstruction, profuse diuresis can
occur over the next 24 to 48 hours.
Careful monitoring during this period
is required to prevent pre-renal injury
through volume depletion or fluid
overload from too much fluid resuscitation (ADIS International Ltd.,
2009; Cheung et al., 2008; Talbot,
2008).

Table 1
RIFLE Classification System for AKI
Glomerular Filtration Rate Criteria
Increased creatinine x 1.5
or GFR decrease greater
than 25%

Urine output less than 0.5

mL/kg/hour X 6 hours

INJURY

Increased creatinine x 2
or GFR decrease greater
than 50%

Urine output less than 0.5

mL/kg/hour X 12 hours

FAILURE

Increased creatinine x 3
or GFR decrease greater
than 75% or creatinine
greater than
4 mg/100mL

Urine output less than

0.3 mL/kg/hour X 24
hours or Anuria X 12
hours

RISK

Risk Factors and Identification

Of AKI
Common risk factors for developing AKI include age greater than 60
years, diagnosis of sepsis, diabetes
mellitus, heart disease, exposure to
multiple nephrotoxic drugs, volume
depletion, or underlying kidney insufficiency (Cheung et al., 2008;
Naughton, 2008; Talbot, 2008).
There is a higher incidence of
AKI in older adults. Anatomical
changes that occur in the aging kidney include shrinking with loss of
parenchymal volume, cortical atrophy, decreased glomeruli and proximal tubule numbers, thickening of
arteries and arterioles that supply kidneys, and increased glomerulosclerosis (Cheung et al., 2008). Functionally, this means the aging kidney has
a decrease in kidney blood flow and
GFR. The most important functional
factor in aging is the decreased GFR.
Normal GFR is 120 to 130 mL/
min/1.73m2 until about age 30, when
it drops 1 mL/min/year (ADIS
International Ltd., 2009). Despite
having a decreased GFR, it is important to remember older adults may
have a serum creatinine within normal limits due to loss of muscle mass
associated with aging (Cheung et al.,
2008). Another factor in older adults
making them more susceptible to
AKI is their increased vulnerability to
hypovolemia due to impaired ability
to concentrate urine (Cheung et al.,
2008). Older adults are also more
likely to have diabetes mellitus
and/or heart disease, which are contributing factors as well. It is important to remember that with each additional risk factor present, the risk for
AKI goes up (Naughton, 2008).
One of the most commonly used

Nephrology Nursing Journal

Urine Output Criteria

LOSS

Persistent loss of kidney function greater

than 4 weeks

ESRD

End stage kidney disease/failure

Source: Adapted from Ricci et al., 2008.

systems to identify and classify AKI

or kidney dysfunction is the Risk,
Injury, Failure, Loss, End Stage
(RIFLE) classification. Ricci and coauthors (2007) conducted an analysis
of research using RIFLE criteria and
found it is a useful predictor of relative risk of mortality in hospitalized
patients. The RIFLE classification
system for AKI is shown in Table 1
(Ricci et al., 2008).
Laboratory and diagnostic tests
that aid in the diagnosis of AKI and in
the determination of the possible
cause are shown in Table 2. Along
with the diagnostics, it is important to
test and monitor for complications of
AKI that may be life-threatening,
such as hyperkalemia, pulmonary
edema, and metabolic acidosis.
Hyperkalemia with serum potassium
of greater than 6.5 mmol/L is an
emergency due to the risk of cardiac
arrhythmias. Patients should be
assessed for pulmonary edema by
watching for signs of respiratory distress, ascultating the lungs for crackles
or other abnormalities through chest
X-ray, and monitoring blood gases or
oxygen saturation regularly. Meta-

January-February 2011

Vol. 38, No. 1

bolic acidosis is also a life-threatening

emergency; when blood pH is less
than 7.2, systemic vasodilation is produced, and the risk of hyperkalemia
and cardiac arrhythmias is increased.
If any of the above occur and are
unresponsive to medical treatment,
the patient should be referred for
urgent dialysis (Cheung et al., 2008;
Talbot, 2008).

Current Treatment
Nurses can play a vital role in
identifying patients who are at risk for
AKI and intervening early, possibly
preventing life-threatening complications. It is also important for nurses to
be aware of the currently suggested
treatments and implications for their
practice. This knowledge can be used
for nurses to advocate on behalf of
patients, provide the best care, and be
mindful of current research.

Managing Hemodynamics and

Fluid Status
Monitoring fluid balance in the
patient with AKI is extremely important. This includes the monitoring of

15

Acute Kidney Injury: An Overview of Pathophysiology and Treatments

Table 2
Laboratory and Diagnostic Tests that Aid in the Diagnosis of AKI and in the
Determination of the Possible Cause
Laboratory Test or Diagnostic

Normal Value

Abnormal Value

Possible Indication

Blood Tests
Serum creatinine

Adult women: 0.6 to

1.1 mg/dL
Adult men: 0.9 to
1.3 mg/dL

Greater than 1.3 mg/dL Impaired kidney function, chronic nephritis, or

obstruction of urinary tract. Dependent upon
muscle mass of individual. Gives indication of
GFR related to excretion of creatinine by
kidneys.

Blood urea nitrogen (BUN)

Adults: 6 to 20 mg/dL
Elderly (over 60
years): 8 to
23mg/dL

Greater than 23 mg/dL

Panic value greater
than 100 mg/dL

Can indicate impaired kidney function caused

by CHF, hypovolemia, shock. May also
indicate glomerulonephritis or pyelonephritis
or urinary tract obstruction.

BUN/creatinine ratio

10:1 to 20:1

Greater than 20:1

Less than 10:1

Increased with elevated creatinine may

indicate obstruction of urinary tract or prerenal azotemia. Decreased ratio with elevated
creatinine may indicate rhabdomyolysis.
Decreased ratio with decreased BUN may
indicate acute tubular necrosis.

Cystatin C

Adults: Less than 0.70

mg/mL
Elderly: Less than
0.85 mg/mL

Elevated above stated

levels

Not affected by age, lean body mass,

infection, or inflammation. Is a more sensitive
indicator of kidney function, particularly in the
elderly.

Urine Tests
Dipstick

Blood: Negative
Protein: Negative

Hematuria
Protein:+3 to +4
on strip

Blood may indicate glomerulonephritis or

rhabdomyolosis. Protein may indicate intrinsic
kidney disease or rhabdomyolosis.

Osmolality

24-hour specimen:
300 to 900
mOsm/kg of water
Random specimen: 50
to 1200 mOsm/kg
of water
Urine-to-serum ratio:
1:1 to 3:1

Above or below stated

values

Increased in pre-renal azotemia, hypovolemia.

Decrease in AKI. Urine to serum osmolality is
increased in azotemia, decreased in acute
tubular necrosis.

Urine sodium and electrolytes

Adult: 40 to 220
mEq/24 hours

Above or below stated

level

Low excretion may indicate pre-renal failure.

High excretion with low osmolality may
indicate acute tubular necrosis.

Diagnostic Tests
Kidney ultrasound

Normal size, shape,

and structure

Kidney doppler

Equal blood flow to

Deviation from stated
both kidneys,
normal
excretion of 50% of
radiopharmaceutical
agent within 10
minutes.
Normal tissue
Deviation from normal
composition

Biopsy

Cysts, masses,
obstruction of
ureters, calculi, or
hydronephrosis

Can show intrarenal or postrenal obstructions

potential causes of intrinsic or post-renal
kidney injury.
Deviation may indicate obstruction,
hypertension, or other acute or chronic kidney
injury, such as renovascular disease.

May indicate glomerulonephritis, vasculitis, or

malignancy.

Note: AKI = acute kidney injury.

Sources: Compiled from Cheung et al., 2008; Fischbach, 2004; Talbot, 2008.

16

Nephrology Nursing Journal

January-February 2011

Vol. 38, No. 1

strict intake and output from all

sources, such as IV and oral intake,
urine output, and wound or nasogastric drainage (Sumnall, 2007). It is
beneficial to have a Foley catheter
inserted in patients with AKI so that
urine output can be closely monitored. Patients should also be assessed
for dependent or peripheral edema,
third spacing of fluids, and for signs of
pulmonary edema. Since patients
with AKI can be intravascularly
hypovolemic, it is important to determine accurate fluid status to prevent
overload; this monitoring is done
through keeping intake and output, or
through more invasive means, such as
central venous pressure monitoring
(Cheung et al., 2008; Talbot, 2008).
The loss of plasma proteins that
occurs in AKI can alter the oncotic
pressure (a form of osmotic pressure
within the vasculature/capillaries that
pulls fluid into the capillaries because
the plasma proteins cannot cross the
capillary wall). This causes fluid to
leak out of the capillaries into the tissues leading to edema of the lungs
and periphery, while the vasculature
becomes hypovolemic (Sumnall,
2007). The goal of therapy is to optimize hemodynamics. If fluid resuscitation fails to maintain cardiac output
or correct hypotension, inotropic support may be required (Cheung et al.,
2008). Fluid overload may be managed by diuretics, particularly loop
diuretics that inhibit the sodiumpotassium-chloride pump in the loop
of Henle. Diuretics are thought to
reduce the oxygen demands of the
cells and reduce susceptibility to
ischemia; however, there are scarce
data supporting the benefit of their
use (Talbot, 2008). Sumnall (2007)
suggests that continuous infusions of
small amounts of diuretics may be
more beneficial than bolus doses. In
some cases, dialysis may be required
to treat fluid overload.

Nutritional Considerations
When planning for nutritional
needs of the patient experiencing
AKI, it is important to consider both
the severity of AKI and other co-morbidities the patient may have and how

Nephrology Nursing Journal

Table 3
Summary of Suggestions of Nutritional Needs for Patients with AKI
Severity of AKI
Mild AKI

Daily Nutritional Suggestions

30 to 35 kcal/kg of desirable weight
0.8 to 1.0 gm protein/kg of desirable weight
May consider oral supplement if nutritional status is poor or
oral intake is inadequate

Moderate AKI

25 to 35 kcal/kg of edema free weight, limit to 25 kcal/kg if

on ventilator
0.8 to 1.2 gm protein/kg if not on dialysis, minimum of 1.2
gm protein/kg if on dialysis
If enteral nutrition use renal formula to avoid excess vitamins
A and C
May consider renal vitamin

Severe AKI

20 to 25 kcal/kg of edema free weight

2.0 to 2.5 gm protein/kg
Early introduction of enteral feedings suggested for ventilated patients to maintain gut integrity
Parental nutrition should be maximally concentrated to avoid
further fluid overload

Note: AKI = acute kidney injury.

Source: Compiled from Cotton, 2007.

that may affect his or her nutritional

needs. The purpose of nutritional
management is to avoid further stress
on the body to control intake of specific nutrients to avoid further damage to the kidneys and promote healing (Cotton, 2007). A summary of
suggestions of nutritional needs for
patients with AKI is shown in Table 3.

Pharmocologics
The use of pharmacological
agents in AKI is a complex process
that may require renal dosing and
careful selection of medications.
Several drugs have been researched
and are still being debated as to the
benefit of their use in patients with
AKI. Those that will be discussed
here are dopamine, atrial natiuretic
peptide, fenoldopam, and pentoxifylline. Diuretics were discussed previously.
Prior to discussing any medications, it is important to once again
stress the avoidance or stopping of
nephrotoxic medications in the
patient with AKI. Naughton (2008)
provides a more comprehensive
guide of nephrotoxic medications
than what is within the scope of this
article. Commonly used nephrotoxic

January-February 2011

Vol. 38, No. 1

medications include aminoglycoside

antibiotics, non-steroidal anti-inflammatory drugs, and antiretroviral medications (Cheung et al., 2008, Naughton,
2008).
Kidney doses of dopamine (0.5 to 3
mcg/kg/min) have been used previously in hopes of limiting kidney
injury. At this dose, dopamine dilates
both afferent and efferent arterioles
and increases kidney blood flow; however, little gain in GFR is experienced
(Cheung et al., 2008). Recent research
has shown no benefit to the use of
dopamine in AKI, with some research
showing further harm in older
patients; therefore, currently available
evidence does not support the routine
use of dopamine in treating AKI
(Cheung et al., 2008, Talbot, 2008).
Atrial natiuretic peptide (ANP)
vasodialates the afferent arteriole and
constricts the efferent arteriole
increasing GFR (Cheung et al., 2008).
The use of this medication is still
being researched and is largely investigational. One meta-analysis found
that in low doses, ANP reduced the
need for dialysis and decreased overall hospital length of stay. However,
in high doses, ANP was associated
with more hypotension and cardiac

17

Acute Kidney Injury: An Overview of Pathophysiology and Treatments

arrhythmias; there was no difference

in mortality between the two groups
(Nigwekar, Navaneethan, Parikh, &
Hix, 2009). Perhaps in the future,
more research may support low-dose
ANP for prevention and faster recovery time for those at risk for or who
have AKI.
Another potentially preventative
drug is fenoldopam, which can
reduce vascular resistance in the kidney and increase kidney blood flow.
Several studies, though small in size,
have shown potential prevention of
AKI in patients undergoing cardiovascular procedures who receive
fenoldopam (Cheung et al., 2008).
Finally, pentoxifylline, a tumor
necrosis factor-a production, has
shown results in animal studies in the
prevention of further kidney tubular
damage from ischemia or reperfusion
injury. This has not been widely studied in humans but shows potential for
future research (Cheung et al., 2008).

Stem Cell Treatment

Current research is looking into
the use of stem cells for regeneration
of tubular epithelial cells. It is thought
that the kidney has some stem cells
within itself contributing to its ability
to regenerate after injury; however, a
certain number of cells need to
remain functional for regeneration to
take place (Cheung et al., 2008;
Yokoo, Kawamura, & Kobayashi,
2008). Experimental studies have
been conducted that show promising
results with both hemopoetic and
mesenchymal stem cells differentiating into kidney tubular cells; however, more research is needed to support the use in humans (Cheung et al.,
2008; Yokoo et al., 2008).

Renal Replacement Therapy

Some guidelines for the initiation
of renal replacement therapy (RRT)
include hyperkalemia that is unresponsive to medical treatment or
presents with EKG changes, metabolic acidosis with pH less than 7.2, or
presentation of uremic encephalopathy or pericarditis (Cheung et al.,
2008). There is conflicting research
regarding when dialysis should be ini-

18

tiated and what modality or intensity

should be utilized (Cheung et al.,
2008; Talbot, 2008). Two common
modalities of RRT are continuous
renal replacement therapy (CRRT)
and intermittent hemodialysis (IHD).
CRRT is a 24-hour-a-day, 7-day-aweek process that slowly removes
excess fluid and solutes, and corrects
electrolyte imbalances associated
with AKI (Talbot, 2008). CRRT can
be administered at different intensities. Bellomo and colleagues (2009)
conducted a study evaluating different intensities of CRRT and found
that higher intensity CRRT did not
reduce mortality or rate of dependence on dialysis, and the higher intensity group had more adverse outcomes. Some advantages to CRRT
compared with IHD include increased hemodynamic stability and fluid
control, greater effectiveness in managing acid/base and electrolyte balance, improved nutritional support
and removal of toxins, and the ability
to remove inflammatory mediators
(Talbot, 2008).
IHD is a process of removing soluble substances and water across a
semi-permeable membrane outside
the body through the process of diffusion and trans-membrane pressure
(Talbot, 2008). IHD requires a dual
venous access device and is done for
three to five hours, three to seven
times a week. Caution is needed with
IHD to prevent hypotension during
and after dialysis that may lead to further kidney damage (Talbot, 2008).
Benefits of IHD compared with
CRRT include decreased risk of systemic bleeding, more time for diagnostic testing, better control of hyperkalemia, more cost-effective, and
shorter ICU stays (Talbot, 2008).
In summary, there are many factors and much debate about the use of

RRT in AKI. It is suggested that a

specialist be consulted to manage
AKI patients who may require RRT
(Cheung et al., 2008).

Conclusion
AKI is a complex disorder that
affects many body systems and carries a high mortality rate. Research by
Hsu and colleagues (2007) found that
community-based incidence of AKI is
increasing. It is likely that rates of
AKI will continue to increase with
time. As healthcare professionals, it
will become more important to
understand the pathophysiology,
treatments, and risk factors for AKI.
By the brief understanding of these
factors discussed in this article, one
might be able to identify, intervene
earlier, and possibly prevent serious
complications from AKI in a patient
who is at risk.
References
ADIS International, Ltd. (2009). Treatment of acute renal failure (ARF) in
elderly patients requires early recognition and initiation of supportive
treatment. Drugs & Therapy Perspectives, 25(4), 14-17.
Armitage, A.J., & Tomson, C. (2003).
Acute renal failure. Medicine, 31(6),
43-48.
Barrantes, F., Feng, Y., Ivanov, O.,
Yalamanchili, H.B., Patel, J., Buenafe,
X., ... Manthous, C. (2009). Acute
kidney injury predicts outcome of
non-critically ill patients. Mayo Clinic
Proceedings, 84(5), 410-416.
Bellomo, R., Cass, A., Cole, L., Finfer, S.,
Gallagher, M., Lo, S., ... Su, S.(2009).
Intensity of continuous renal-replacement therapy in critically ill patients.
The New England Journal of Medicine,
361(17), 1627-1638.
continued on page 30

Nephrology Nursing Journal Editorial Board Statements of Disclosure

In accordance with ANCC-COA governing rules Nephrology Nursing Journal Editorial Board statements of disclosure are published with each CNE offering. The statements of disclosure for this offering are published below.
Paula Dutka, MSN, RN, CNN, disclosed that she is a consultant and research coordinator, is on the speakers
bureau, and has sat on the advisory board for Genentech.
Patricia B. McCarley, MSN, RN, NP, disclosed that she is on the Consultant Presenter Bureau for Amgen,
Genzyme, and OrthoBiotech. She is also on the Advisory Board for Amgen, Genzyme, and Roche and is the
recipient of unrestricted educational grants from OrthoBiotech and Roche.

Nephrology Nursing Journal

January-February 2011

Vol. 38, No. 1

Acute Kidney Injury

continued from page 18
Cheung, C.M., Ponnusamy, A., &
Anderton, J.G. (2008). Management
of acute renal failure in the elderly
patient: A clinicians guide. Drugs &
Aging, 25(6), 455-476.
Cotton, A.B. (2007). Medical nutrition therapy in acute kidney injury. Nephrology
Nursing Journal, 34(4), 444-446.
Fischbach, F. (2004). A manual of laboratory
and diagnostic tests (7th ed.). Philadelphia: Lippincott, Williams &
Wilkins.
Hsu, C., McCulloch, C.E., Fan, D.,
Ordonez, J.D., Chertow, G.M., & Go,
A.S. (2007). Community-based incidence of acute renal failure. Kidney
International, 72, 208-212.
Naughton, C.A. (2008). Drug-induced
nephrotoxicity. American Family Physician, 78(6), 743-750.
Nigwekar, S.U., Navaneethan, S.D.,
Parikh, C.R., & Hix, J.K.(2009) Atrial
natriuretic peptide for preventing and
treating acute kidney injury. Cochrane
Database of Systematic Reviews, 4,
CD006028. DOI:10.1002/14651858.
CD006028.pub2.
Porth, C.M. (2007). Renal failure. In C.M.
Porth (Ed.), Essentials of pathophysiology:
Concepts of altered health (2nd ed., pp.
521-536). Philadelphia: Lippincott,
Williams & Wilkins.
Ricci, Z., Cruz, D., & Ronco, C. (2008).
The RIFLE criteria and mortality in
acute kidney injury: A systematic
review. Kidney International, 73, 538546.
Sumnall, R. (2007). Fluid management and
diuretic therapy in acute renal failure.
Nursing in Critical Care, 12(1), 27-33.
Talbot, S. (2008). Acute renal failure. In P.
Jevon, B. Ewens, & M. Humphreys
(Eds.), Nursing medical emergency
patients (pp. 199-229). United Kingdom: John Wiley & Sons.
Yokoo, T., Kawamura, T., & Kobayashi, E.
(2008). Stem cells for kidney repair:
Useful tool for acute renal failure?
Kidney International, 74, 847-849.

30

Nephrology Nursing Journal

January-February 2011

Vol. 38, No. 1

ANNJ1101

ANSWER/EVALUATION FORM

Acute Kidney Injury: An Overview of Pathophysiology and Treatments

Kristina M. Yaklin, BSN, RN
1.3 Contact Hours
Expires: February 28, 2013
ANNA Member Price: $15
Regular Price: $25

Complete the Following:

Name: ____________________________________________________________
Address: __________________________________________________________
__________________________________________________________________

Posttest Instructions
Complete the evaluation.
Send this page to the ANNA National
Office; East Holly Avenue Box 56;
Pitman, NJ 08071-0056; or fax this
form to (856) 589-7463.
Enclose a check or money order
payable to ANNA. Fees listed in
payment section.
A certificate for the contact hours will
be awarded by ANNA.
Please allow 2-3 weeks for processing.
You may submit multiple answer forms
in one mailing; however, because of
various processing procedures for
each answer form, you may not receive
all of your certificates returned in one
mailing.

Telephone: ______________________ Email: _____________________________

CNN: ___ Yes ___ No

CDN: ___ Yes ___ No

CCHT: ___ Yes ___ No

Payment:
ANNA Member: ____ Yes ____ No
Check Enclosed

Member #___________________________

American Express

Visa

MasterCard

Total Amount Submitted: _________________

Credit Card Number: _______________________________ Exp. Date: _______
Name as it Appears on the Card: ______________________________________

Online submissions through a partnership with HDCN.com are accepted on this posttest at
$20 for ANNA members and $30 regular price. CNE certificates will be available immediately
upon successful completion of the posttest.
Note: If you wish to keep the journal intact, you may photocopy the answer sheet or access this posttest at
www.annanurse.org/journal
1. What would be different in your practice if you applied what you have learned
from this activity?
____________________________________________________________
____________________________________________________________
____________________________________________________________
____________________________________________________________
____________________________________________________________

To provide an overview of acute kidney

injury, its pathophysiology, and treatments.
Please note that this continuing nursing education activity does not
contain multiple-choice questions. This posttest substitutes the multiple-choice questions with an open-ended question. Simply answer
the open-ended question(s) directly above the evaluation portion of
the Answer/Evaluation Form and return the form, with payment, to
the National Office as usual.

Strongly
disagree

Evaluation
2. By completing this offering, I was able to meet the stated objectives
a. Define acute kidney injury (AKI).
b. Discuss the pathophysiology, including the three categories of AKI.
c. Identify the risk factors associated with AKI.
d. Describe treatment options for AKI.
3. The content was current and relevant.
4. This was an effective method to learn this content.
5. Time required to complete reading assignment: _________ minutes.

1
1
1
1
1
1

2
2
2
2
2
2

Strongly
agree
3
3
3
3
3
3

4
4
4
4
4
4

5
5
5
5
5
5

I verify that I have completed this activity ________________________________________________________________________________

(Signature)

Nephrology Nursing Journal

January-February 2011

Vol. 38, No. 1

19

Copyright of Nephrology Nursing Journal is the property of American Nephrology Nurses' Association and its
content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's
express written permission. However, users may print, download, or email articles for individual use.