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Running head: Acute Kidney Injury

Acute Kidney Injury


Bobbie Chahal
California State University, Stanislaus
December 2, 2014

ACUTE KIDNEY INJURY

Acute Kidney Injury


Objectives
The following objectives are utilized to guide a thorough discussion about Acute Kidney
Injury (AKI): etiology, pathogenesis, clinical significance, medical management, nursing
diagnosis and teaching for patients diagnosed or at risk of AKI.
Etiology
AKI is an abrupt decreased renal function that can result in the disturbance of fluid and
electrolyte balance, acid-base homeostasis, calcium and phosphate metabolism, blood pressure
regulation, erythropoiesis (Morton & Fontaine, 2013). The red flags of AKI are decreased
glomerular filtration rate (GFR) (Persson, 2013), increased blood urea nitrogen (BUN) and
increased creatinine. These changes in kidney function are referred to as azotemia (Morton &
Fontaine, 2013).
Pathogenesis
There are three main mechanisms of injury that cause AKI. These three mechanisms are
categorized as pre-renal acute kidney injury, intra-renal acute kidney injury, and post-renal acute
kidney injury (Murphy & Byrne, 2010).
Pre-renal acute kidney injury is any event causing renal hypo-perfusion (Murphy &
Byrne, 2010). Some conditions that can result in renal hypo-perfusion are hypotension,
hypovolemia, and low cardiac output. Hypovolemia can be caused by volume loss through the
gastrointestinal system (vomiting or diarrhea), hemorrhage, renal loss (diuretics or polyuria), and
even through the skin with excess sweating or in fluid loss through burns (Murphy & Byrne,
2010).
Intra-renal acute kidney injury involves any event causing damage to the renal functional
parts such as vascular, glomerular, interstitial, and tubular injury (Murphy & Byrne, 2010).
Glomerular injury can occur as a product of a variety of mostly immune-mediated insults inside
the glomeruli. Glomerular injury is indicated when the patient exhibits proteinuria and

ACUTE KIDNEY INJURY

hematuria. Injury to the tubular region is called Acute Tubular Necrosis (ATN) and can be a
result of nephrotoxicity or ischemia. The ischemia can occur in situations like sepsis or
pancreatitis. The toxicity can originate intrinsically or extrinsically. Intrinsic toxicity can result
from Rhabdomyolysis, tumor lysis, or myeloma. Extrinsic toxicity can result from contrast dye,
drugs, and antibiotics (Murphy & Byrne, 2010).
Lastly, post-renal acute kidney injury results from the interruption of urine flow (Murphy
& Byrne, 2010). The obstruction of the flow can be a result of intrinsic variables or extrinsic
variables. Intrinsic variables can be stones or tumors. Extrinsic variables can be tumors that are
surrounding or infiltrating and large abdominal aortic aneurysms (Murphy & Byrne, 2010).
Clinical Significance
AKI has a prevalence rate of 15% to 18% amongst patients that are in hospitals and as
many as 66% of patients in intensive care units (Morton & Fontaine, 2013). According to
Murphy and Byrne, AKI progression increases mortality of patients with any primary disease. As
cited in Ellis and Jenkins (2014), data in a report from National Confidential Enquiry into Patient
Outcome and Death (2009) concluded that only 50% of AKI care is of good quality.
Risk factors of AKI include an age greater than 75 years, diabetes, chronic kidney
disease, cardiac failure, sepsis, and contrast dye use (Murphy & Byrne, 2010). Most patients with
mild-moderate AKI are asymptomatic and are diagnosed by lab tests (Rahman, Shad, & Smith,
2012). In severe AKI, patients can present with confusion, fatigue, anorexia, nausea and
vomiting, weight gain, and edema (Rahman et al., 2012).
Medical Management
Treatment of AKI begins with fixing the primary cause, balancing fluid and electrolytes,
decreasing infection opportunities, providing adequate nutrition and supplementing the process
of medical management with giving support and education to the patient (Murphy & Byrne,
2010). Medical management of AKI involves maintaining hemodynamic stability, optimizing
cardiac function, keeping Mean Arterial Pressure above 65 mm Hg, avoiding hypovolemia, fluid

ACUTE KIDNEY INJURY

resuscitation, and balancing electrolytes (Rahman et al., 2012). It is also recommended to


discontinue, if possible, or decreasing the dosage of all nephrotoxic medications (Dirkes, 2011),
administering diuretics in case of volume overload, avoiding contrast dye, maintaining nutrition,
and if needed, utilizing mechanical ventilation (Murphy & Byrne, 2010).
If treatment with the previously mentioned management strategies is unsuccessful, the
patient might have to undergo treatment with renal replacement therapy (RTT) (Murphy &
Byrne, 2010). RTT might be indicated when the patient exhibits metabolic acidosis,
hyperkalemia, hypervolemia, or uremia. There are many different kinds of dialysis options
available. Some of the dialysis options are hemodialysis, continuous renal replacement therapy,
sustained low-efficiency dialysis or peritoneal dialysis (Murphy & Byrne, 2010). The choosing
of the kind of dialysis the patient will receive is determined based on many different factors to
meet the unique needs of each patient.
Nursing Diagnosis
Nursing diagnoses for AKI include: (1) Excess fluid volume related to decreased kidney
function, (2) Decreased cardiac output related to fluid volume excess and disturbances in the
renin-angiotensin system, (3) Imbalanced nutrition: less than body requirements related to
anorexia, nausea and vomiting, dietary restrictions, and altered oral mucosa, (4) Activity
intolerance related to shortness of breath, fatigue, anemia, uremia, and dialysis procedure, (5)
Risk for infection related to decreased functioning of the immune system, (6) Risk for
compromised skin integrity related to poor nutritional status, edema, and immobility (Morton &
Fontaine, 2013).
Patient Teaching
As patient advocates, nurses can help inform the patient population about how to
maintain kidney health. Because of the abundance of nephrotoxic drugs, patients must
understand the importance of proper adherence to instructions on easily available medications

ACUTE KIDNEY INJURY

such as aspirin, acetaminophen and ibuprofen (Mayo Clinic Staff, 2012). By knowing that there
is a relationship between increased doses causing increased kidney damage, patients can make
better decisions on their usage of these over the counter medications. Nurses can also make stress
the importance of effective management of diabetes and high blood pressure since these
conditions can increase the risk of kidney damage (Ronco & Chawla, 2013). Lastly, nurses can
focus on patient teaching related to maintaining a healthy lifestyle which includes avoiding
overconsumption of alcohol, exercising daily, and eating a balanced diet (Mayo Clinic Staff,
2012).
Patients can also be taught about oral care and skin care (Murphy & Byrne, 2010). Urea
lysis in saliva can lead to alteration in taste and dry mucosa can increase risk of crust formation
and lesion formation. Nurses must teach the patient about regular oral care with cold water
mouthwash and application of lip lubricants. Patients must be informed about the risk of skin
breakdown due to possible edema development. Skin monitoring is important specifically in the
areas at pressure points. Nurses can take patient interaction opportunities to let patients express
concerns or questions so that the patient has an outlet for difficult emotions and feelings. In
addition, nurses can provide the patient and family with support group information or refer them
to psychological support resources (Murphy & Byrne, 2010).

ACUTE KIDNEY INJURY

References
Dirkes, S. (2011). Acute kidney injury: not just acute renal failure anymore?. Critical Care
Nurse, 31(1), 37-50. doi:10.4037/ccn2011946
Ellis, P., & Jenkins, K. (2014). An overview of NICE guidance: acute kidney injury. British
Journal of Nursing, 23(16), 904-906. doi: 10. 12968/bjon.2014.23.16.904
Mayo Clinic Staff (2012). Acute kidney failure: prevention. Mayo Foundation for Medical
Education and Research. Retrieved from http://www.mayoclinic.org/diseases
conditions/kidney-failure/basics/prevention/con-20024029
Morton, P. G. & Fontaine, D.K. (2013) Critical care nursing: a holistic approach, 10th Ed.
Philadelphia: Wolters Kluwer Health. ISBN 978-1609137496

ACUTE KIDNEY INJURY

Murphy, F., & Byrne, G. (2010). The role of the nurse in the management of acute kidney
injury. British Journal of Nursing, 19(3), 146-152.
National Confidential Enquiry into Patient Outcome and Death (2009). Adding insult to injury.
NCEPOD.
Persson, P.B. (2013). Mechanisms of acute kidney injury. Acta Physiologica, 207(3), 430-431.
doi:10.1111/alpha.12063
Rahman, M., Shad, F., & Smith, M. (2012). Acute kidney injury: a guide to diagnosis and
management. Retrieved from http://www.aafp.org/afp/2012/1001/p631.html
Ronco, C., & Chawla, L. S. (2013). Acute kidney injury: kidney attack must be prevented.
Nature Reviews Nephrology, 9(4), 198-199. doi:10.1038/nmeph.2013.19

Topic Paper Rubric


Criterion

Possible Points

Objectives

Etiology

Pathogenesis

10

Clinical Significance

Management: medical

Nursing Diagnosis

10

Patient Teaching

10

Sources: last 5 years

10

Usefulness of Internet Sites

10

Overall quality of writing


(style, grammar, and

10

Points Earned

ACUTE KIDNEY INJURY

organization of ideas)
Follows APA

20

Total

100

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