Course Code: Course Name: Time / Venue:

NCM 108.1 Intensive Practicum February 2, 2016

NCM 107.2 Nursing Leadership & 2:00 PM – 6:00 PM
Management Nursing Skills Laboratory
Faber Hall, 6th Floor
Placement: Topic:
Level 4 Care of clients with Acute Kidney Failure
2nd Semester
Topic Description:

Acute kidney failure/ Acute renal failure is a sudden reduction in kidney function
that results in nitrogenous wastes accumulating in the blood leading to the loss of the
kidneys' ability to remove waste and help balance fluids and electrolytes in your body.
Students Assigned:
1. Mallorca, Kit
2. Real, Sheen Mark
3. Regalado, Janica
4. Roche, Cheney
5. Signey, Leyah
6. Tan, Alyssa
7. Tamolang, Laurice

Learning Outcomes:

Beginning Role on Client Care:

The student nurses will be able to provide safe and quality nursing care to
patients with acute kidney failure and be able to provide holistic care, focusing on the
needs and comfort of the patient.

Beginning Role on Leadership & Management:

To be able to demonstrate leadership and management skills required to provide
optimum holistic quality care through taking responsibility and accountability in leading
and managing themselves and others.

Beginning Role on Research:

To study relevant and up-to-date research based on the findings with regards to
patients who have acute kidney failure , with regards to the care, specific nursing
considerations and new development.
General Objectives:

At the end of 4 hours of interactive discussion on the students will be able to

gain knowledge on providing essential care for patients with acute kidney failure . They
would also be able to learn on the proper handling and the appropriate interventions
and management of certain situations and events that may arise with regards to the
condition.
Specific Objectives:

At the end of the 4 hour interactive discussion and demonstration, the nursing students
will be able to:
 Define acute kidney failure
 Discuss on the risk factors
 Elaborate on the 3 categories of ARF
 Discuss on possible causes of each category
 Identify the signs and symptoms
 State the phases of acute renal failure
 Discuss on the management of said condition
 Know the new developments and findings of the condition.

Bibliography:

 Smeltzer, S., et al. (2010). Brunner & Suddarth’s Textbook of Medical-Surgical

Nursing 12th Edition. Wolters Kluwer | Lippincott Williams & Wilkins
 Webb S, Dobb G (December 2007). "ARF, ATN or AKI? It's now acute kidney
injury". Anaesthesia and Intensive Care 35 (6): 843–4.
 Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P (2004). "Acute renal
failure - definition, outcome measures, animal models, fluid therapy and
information technology needs: the Second International Consensus Conference
of the Acute Dialysis Quality Initiative (ADQI) Group". Crit Care 8 (4): R204–12.
 Intermediate Teaching
Competencies Content Learning References Evaluatio
Activities n
Definition: o Q and A  15 item
 Demonstrate o PowerPoint - Smeltzer, S., et al. quiz
 Acute Renal Failure (2010). Brunner &
knowledge and presentatio
skills in providing Definition: n Suddarth’s Textbook of
safe, quality and o Interactive Medical-Surgical Nursing
 Also called as ACUTE KIDNEY FAILURE 12th Edition. Wolters
holistic nursing Discussion
care. or ACUTE KIDNEY INJURY Kluwer | Lippincott
 Utilize nursing Williams & Wilkins
 Sudden and usually reversible loss of renal -Chan AT, Giovannucci EL,
process in caring of
clients. function which develops over days or Meyerhardt JA et al. Long-
 Establish a term use of aspirin and
weeks accompanied by reduction in urine nonsteroidal anti-
collaborative
relationship volume. inflammatory drugs and
between risk of colorectal cancer.
 Abrupt loss of kidney function that develops JAMA. 2005; 294:914-23.
themselves,
colleagues, CI and within 7 days
- Webb S, Dobb G
other members of
 Can be fatal and may need intensive (December 2007). "ARF,
the health care
ATN or AKI? It's now acute
team to enhance treatment
kidney injury".
nursing and other
 May be REVERSIBLE Anaesthesia and Intensive
health services. Care 35 (6): 843–4.
Risk Factors:
 Being hospitalized, especially for a serious - Bellomo R, Ronco C,
Kellum JA, Mehta RL,
condition that requires intensive care Palevsky P (2004). "Acute
 Advanced age (Over the age of 50, higher renal failure - definition,
outcome measures,
risk) animal models, fluid
 Blockages in the blood vessels in your therapy and information
technology needs: the
 arms or legs (peripheral artery disease) Second International
Consensus Conference of
 Diabetes the Acute Dialysis Quality
 High blood pressure Initiative (ADQI) Group".
Crit Care 8 (4): R204–12..
 Heart failure
 Kidney diseases
 Liver diseases
ARF can be divided into 3 categories:
 PRE-RENAL
 RENAL
 POST RENAL

1. Pre Renal ARF

Pre-renal causes of ARF include:
 Heart Failure.
 Blood/Fluid loss as in major
surgery,trauma,dehydration
sec. to severe diarrhea and vomiting.
 Renal artery stenosis/Occlusion.
 Diseases Affecting the arterioles.
 What Happens in Pre renal ARF
 In circumstances which dec the perfusion
pressure(Heart
 failure,Shock,Hypovolemia),Kidneys
maintain their perfusion by constriction of
renal vasculature and selective constriction
of efferent arterioles
 Drugs like NASIDs and ACE inhibitors
affect these compensatory mechanisms.
 Prolonged hypo perfusion and drug toxicity
halt these compensatory mechanisms
leading to acute decline in GFR.

2. Intrinsic ARF
Intrinsic causes of Acute renal failure include:
 Acute tubular necrosis:
May occur as a result of Ischemia,sepsis or
Nephrotoxic drugs.
 Glomerular diseases:
Primary or Secondary glomerulonephritis
 Vascular diseases:
E.g. Vasculitis or malignant hypertension
 What Happens in Pre renal ARF
 Ischemia,Nephrotoxic agents(drugs and
bacteria) or a
 combination of these two can cause
damage to the
tubular cells leading to their necrosis.
Tubular cells shed
and block the tubular lumen along with
interstitial edema.
 Tubular cells regenerate from the
basement membrane
resulting in recovery of renal function if the
patient is
supported in the recovery phase.
 Nephrotoxic drugs leading to ATN include
I. Aminoglycosides
II. Cisplatin
III. Amphotericin B

3. Post renal ARF

Post renal ARF occurs secondary to any
obstruction in the urinary tract which include:

 Renal stones
 Tumors
  Benign prostatic hyperplasia

SIGNS AND SYMPTOMS

Signs and symptoms of acute kidney failure
includes:
 Decreased urine output, although
occasionally urine output remains normal
 Fluid retention, causing swelling in your
legs, ankles or feet
 Drowsiness
 Shortness of breath
 Fatigue
 Confusion
 Nausea
 Seizures or coma in severe cases
 Chest pain or pressure
 Sometimes acute kidney failure causes no
signs or symptoms
Phases of Acute Renal Failure
Acute Renal Failure is divided into 4 phases
 Initiation Phase:
Asymptomatic
 Oliguric phase:
Lasts 7-14 days. Urine output
<400ml/day.
 Diuretic Phase:
Urine output can reach up to
2500ml/day. Adequate fluid replace
required for good recovery
 Recovery Phase:
GFR returns to normal. Renal
parameters decline towards the normal
range

Management
1.Treat the underlying cause:
 Pre renal failure:
Restore the blood volume by transfusing Blood,
Plasma or isotonic
saline carefully monitoring CVP and PWP
 Renal Cause of ARF:
I. ATN responds to restoration of renal
perfusion
II. Immunosuppressive therapy for
glomerulonephritis
 Post renal cause:
Prompt relive of obstruction restores the renal
functions.
2.Fluid and Electrolyte Balance:
 Strict monitoring of Intake and output
 Daily fluid intake should be equal to
output+500ml
 Additional replacement required in case of
abnormal losses like Diarrhea and
Vomiting.
3.Hyperkalemia:
Potassium concentration >6mmole/L can cause
serious
arrthymias.Immediate intervention required
4.Metabolic Acidosis:
Restoration of blood volume will correct
acidosis. Treat with sodium
bicarbonate(50ml of 8.4%) in severe cases.
5.Proteins and energy Intake:
 Protein restriction to less than 40g/day.
 Major source of energy should be fats and
carbohydrates
 Enteral and parenteral nutrition may be
required in patients with hyper catabolic
states(e.g. burns and sepsis)
6.Infection Control:
Prompt diagnosis and treatment with antibiotics
required
7.Avoidance of nephrotoxic drugs:
NSAIDS and ACE inhibitors may prolong ARF
and should be avoided.
8.Renal replacement therapy:
May be required as supportive management
Lifestyle Modifications:
  Choose lower potassium foods. High-
potassium foods include bananas, oranges,
potatoes, spinach and tomatoes. Examples
of low-potassium foods include apples,
cabbage, green beans, grapes and
strawberries.
 Avoid products with added salt. Lower
the amount of sodium you eat each day by
avoiding products with added salt, including
many convenience foods, such as frozen
dinners, canned soups and fast foods.
Other foods with added salt include salty
snack foods, canned vegetables, and
processed meats and cheeses.
 Limit phosphorus. Phosphorus is a
mineral found in foods, such as milk,
cheese, dried beans, nuts and peanut
butter. Too much phosphorus in your blood
can weaken your bones and cause skin
itchiness

Updates:
Summary of "Contrast-Induced Acute Kidney
Injury: An Update."

Contrast-induced acute kidney injury (CI-AKI) is

defined as an abrupt deterioration in renal function
associated with the administration of iodinated
contrast media. This type of acute kidney injury is
frequently encountered as a complication of
percutaneous coronary intervention (PCI) and is
associated with adverse short- and long-term
outcomes including mainly mortality,
cardiovascular morbidity and prolongation of
hospitalization. The incidence of CI-AKI after PCI
ranges from 2 to 20 % according to baseline
kidney function. It may also range according to the
clinical setting, being higher after emergency PCI.
The primary manifestation is a small decline in
kidney function, occurring 1 to 3 days after the
procedure. Kidney function usually returns to
preexisting levels within 7 days. Incidence of
acute renal failure requiring dialysis following PCI
is rare (<1 %). The present article aims to review
up-to-date published data concerning diagnosis,
definition, epidemiology and prognosis of this
novel in-hospital epidemic.
Update on Biomarkers of Acute Kidney Injury

Acute kidney injury (AKI) represents a common

disorder in hospitalized patients, and its incidence
is rising at an alarming rate. Despite significant
improvements in critical care and renal
replacement therapies (RRT), the outcome of
critically ill patients with AKI necessitating RRT
remains unacceptably dismal. In current clinical
practice, the diagnosis and severity classification
of AKI is based on a rise in serum creatinine
levels, which may occur 2–3 days after the
initiating renal insult and delay potentially effective
therapies that are limited to the early stage.
The emergence of numerous renal tubular
damage-specific biomarkers offers an opportunity
to diagnose AKI at an early timepoint, to facilitate
differential diagnosis of structural and functional
AKI, and to predict the outcome of established
AKI. The purposes of this review are to
summarize and to discuss the performance of
these novel AKI biomarkers in various clinical
settings.
The most promising AKI biomarkers include
plasma and urinary neutrophil gelatinase-
associated lipocalin (NGAL), urinary interleukin
(IL)-18, urinary liver-type fatty acid binding protein
(L-FABP), urinary cystatin C, and urinary kidney
injury molecule (KIM)-1. However, enthusiasm
about their usefulness in the emergency
department seems unwarranted at present. There
is little doubt that urinary biomarkers of nephron
damage may enable prospective diagnostic and
prognostic stratification in the emergency
department. However, comparison of the areas
under the receiver-operating characteristic curves
of these biomarkers with clinical and/or routine
biochemical outcome parameters reveals that
none of these biomarkers has a clear advantage
beyond the traditional approach in clinical decision
making in patients with AKI. The performance of
various biomarkers for predicting AKI in patients
with sepsis or with acute-on-chronic kidney
disease is poor. The inability of biomarkers to
improve classification of ‘unclassifiable’ (structural
or functional) AKI, in which accurate differential
diagnosis of pre-renal versus intrinsic renal AKI
has the most value, illustrates another problem.
Future research is necessary to clarify whether
serial measurements of a specific biomarker or
the use of a panel of biomarkers may be more
useful in critically ill patients at risk of AKI.
Whether or not the use of AKI biomarkers
revolutionizes critical care medicine by early
diagnosis of severe AKI and individualizes the
management of AKI patients remains to be
shown. Currently, the place of biomarkers in this
decision-making process is still uncertain.
Indiscriminate use of various biomarkers may
distract clinicians from adequate clinical
evaluation, may result in worse instead of better
patient outcomes, and may waste money. Future
large randomized studies are necessary to
demonstrate the association between biomarker
levels and clinical outcomes, such as dialysis,
clinical events, or death. It needs to be shown
whether assignment to earlier treatment for AKI on
the basis of generally accepted biomarker cut-off
levels results in a reduction in mortality and an
improvement in recovery of renal function.

Toxin in seafood causes kidney damage in

mice at levels considered safe for
consumption
A chemical that can accumulate in seafood and is
known to cause brain damage is also toxic to the
kidneys, but at much lower concentrations. The
findings, which come from a study appearing in an
upcoming issue of the Journal of the American
Society of Nephrology (JASN), suggest that
officials may need to reconsider what levels of the
toxin are safe for human consumption.

Researchers generate kidney tubular cells

from stem cells
Investigators have discovered a cocktail of
chemicals which, when added to stem cells in a
precise order, turns on genes found in kidney cells
in the same order that they turn on during
embryonic kidney development. The kidney cells
continued to behave like kidney cells when
transplanted into adult or embryonic mouse
kidneys.