Holy Angel University

College of Nursing

A.Y 2009-2010

A Case Analysis about:

Submitted by:

Group 2B N-304

Dingal, Paolo Junelle S.

Diwa, Jelyn V.
Lacson, Trysha Gail
Tanael, Ulikarl
Tanglao, Ida

Submitted to:

Mr. Michael Louie Celis

Clinical Instructor

August 11, 2010

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 I. INTRODUCTION

Acute kidney failure or Acute Kidney Injury as it is now referred to in the literature is
defined as the abrupt or sudden decline in renal filtration function. This condition is usually
marked by a rise in serum creatinine concentration or azotemia (a rise in blood urea nitrogen
[BUN] concentration). However, immediately after a kidney injury, BUN or creatinine levels
may be normal, and the only sign of a kidney injury may be decreased urine production. AKI
may be classified into three categories: prerenal, intrarenal and postrenal. Prerenal causes of
ARF are those interfere with renal tissue perfusion. Kidney function depends on the adequate
supply of blood to be filtered. Therefore, if the blood supply is not sufficient, it may cause
ischemia which decreases the glomerular filtration rate (GFR) and may lead to Acute Renal
Failure (ARF). Conditions that contribute to decrease blood flow includes; decrease blood
volume which may cause by diarrhea, vomiting, hemorrhage, excessive use of diuretics, burns or
glycosuria. Cardiac diseases may also decrease blood flow as a response to the decrease cardiac
output. Decreased peripheral vascular resistance (PVR) as from spinal anesthesia, septic shock or
anaphylaxis as well plays a role to the decrease blood flow. Other factors consist of vascular
obstruction such as bilateral renal artery occlusion and vasodilation. On the other hand, intrarenal
causes of ARF involve parenchymal changes causes by disease or nephrotoxic substances. Acute
tubular necrosis is the most common cause of intrarenal ARF which comprises of about 75% of
the cases. This necrosis may be cause by decrease renal perfusion or direct damage by
nephrotoxins. Other intrarenal causes of ARF includes glomerulonephritis, microvascular and
macrovascular lesions, thrombosis, vasculitis, scleroderma, trauma, atherosclerosis, tumor
invasion, and cortical necrosis which is caused by prolonged vasospasm of the cortical blood
vessels. Last classification of ARF is the Postrenal ARF which arises from an obstruction in the
urinary tract, may be in any part of the tubules to the urethral meatus. Frequent sources of
impediments include prostatic hypertrophy, calculi, invading tumors, surgical accidents, ureteral
or urethral stenosis and retroperitoneal fibrosis. Spinal cord injury may also contribute as it may
lead to decreases bladder emptying and obstruction in its function.

Acute renal failure is typically diagnosed by observing rises in BUN and plasma
creatinine and decreases in urine flow rates over several days. Unfortunately, creatinine is a
suboptimal indicator of renal function during acute renal failure because plasma creatinine is

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influenced by many non-renal events that regulate creatinine generation, volume of distribution,
and creatinine excretion. Each of these can be dramatically altered in acute renal failure. For
example, patients with ARF are often edematous, which dilutes creatinine and slows recognition
of ARF. Also, creatinine is excreted by glomerular filtration and tubular secretion. As GFR
decreases, the amount of tubular secretion becomes an increasingly important fraction of
creatinine excretion, such that creatinine clearance overestimates GFR by 50 to 100% once the
true GFR is less than 15 ml/min7. The dynamic relationship between creatinine and GFR further
erodes our ability to both detect and quantify renal dysfunction during ARF. Moran and Myers
noted that a sudden fall in GFR to a constant low level causes a slow increase in plasma
creatinine; the rate of rise depends on the new GFR but also on the rate of creatinine generation
and the volume of distribution of creatinine. A new steady state is reached when the creatinine
generation equals creatinine excretion. During recovery from ARF, the reverse occurs. This
dynamic relationship has several consequences. First, it is difficult to estimate GFR from plasma
creatinine during these non-steady state conditions. The continued rise in plasma creatinine does
not indicate that renal function has worsened; rather, it indicates that a steady state has not been
achieved. GFR is a complicated function of the rate of rise of the plasma creatinine, the patient's
baseline GFR, and the presence of edema and altered creatinine production. Second, large
changes in GFR are initially manifested as small changes in creatinine in the first one to two
days after renal injury. Since these changes are near the detection limits of a clinical laboratory,
the diagnosis of ARF may be delayed, especially in the setting of malnutrition or edema. Third,
the degree of renal dysfunction cannot be determined accurately until the new steady state is
reached (creatinine is stabilized), which typically takes one week. Thus, both plasma creatinine
and creatinine clearance are poor markers of renal function in the setting of acute renal failure.
The early diagnosis of ARF would be aided by discovery of a serum marker akin to troponin for
myocardial infarction, or a method that measures renal function more rapidly than a standard
three-hour clearance study (Glofil).

Acute renal failure (ARF) has become increasingly common in patients with critical
illnesses. Up to two-thirds of intensive care unit (ICU) patients develop ARF with the leading
cause being sepsis (Kosinski, 2009). Treatment of ARF has been associated with higher costs
and the following adverse outcomes: increased length of stay, excess mortality of 30-71%, need

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for chronic dialysis in the patients who survive, and the requirement of discharge to short-term or
long-term care facilities (Uchino, Kellum, Bellomo, Doig, Morimatsu, Schetz, Tan, Bouman,
Macedo, Gibney, Tolwani, & Ronco, 2005). Despite the prevalence of the disease and the need
for evidence-based guidelines, over 57 different definitions exist for the critical condition.

Approximately 1% of patients admitted to hospitals have AKI at the time of admission,

and the estimated incidence rate of AKI is 2-5% during hospitalization. AKI develops within 30
days postoperatively in approximately 1% of general surgery cases; it develops in up to 67% of
intensive care unit patients. Approximately 95% of consultations with nephrologists are related to
AKI. Feest and colleagues calculated that the appropriate nephrologist referral rate is
approximately 70 cases per million population.

The mortality rate estimates for AKI vary from 25-90%. The in-hospital mortality rate is
40-50%; in intensive care settings, the rate is 70-80%. Increments of 0.3 mg/dL in serum
creatinine have important prognostic significance.

Early recognition of ARF has been instrumental in improving patient outcomes.

Interdisciplinary collaboration is essential for prompt identification of risks and for completing
accurate ongoing assessments. Treatment of ARF includes multiple pharmacological and non-
pharmacological components such as mechanical ventilation, vasoactive intravenous
medications, nutritional support, and dialysis.

On long-term follow up (1-10 years), approximately 12.5% of AKI survivors are dialysis-
dependent (rates range widely, from 1%-64%, depending on the patient population) and 19-31%
of them have chronic kidney disease.

In the country, the direct estimation technique generated a total of 97 small area estimates
of the proportion of having acute renal failure of adults by single visit from 80 provinces and 17
municipalities and cities of the National Capital Region (NCR). The estimates range from 0.0%
to 80.1%. The province/area with the smallest prevalence of acute renal failure is San Juan in the
NCR and the largest estimate is in Guimaras with standard error of 0% and 3.9%, respectively.
On the other hand, the remaining provinces for the Top ten provinces with the highest acute renal
failure prevalence provinces are Camiguin (60.4%), Quirino (54.1%), Sultan Kudarat (51.4%),

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Pasay City (50.7%), Muntinlupa City (50.6%), Las Pinas (49.1%), Davao Oriental (44.8%),
Catanduanes (40.9%) and Kalinga (39.3%).

II. NURSING HEALTH HISTORY

1. Personal History

a. Demographic Profile

Mrs. Kelly Clamp is 77 years old female, second to the five children of Mr. and
Mrs. Babcock. She was born on October 28, 1932 at their house in San Nicholas, Lubao
Pampanga. A Filipino and devoted Roman Catholic and has been married to Mr. Old
Clamp. They were blessed with 11 children but unfortunately her husband died on the
year 1970 due to heart attack. She is currently residing at Purok 1 Del Carmen Lubao
Pampanga with her 4 grandchildren.

b. Socio Economic, Cultural and Environmental Factors

Mrs. Kelly Clamp did not finish her elementary due to financial constraint.
According to her, during her time females are not really expected to be at school but
instead they were trained to do household chores. At present, she is the care taker of her
grandchildren since their parents are working in abroad which give her remittance every
month in return. Since her children are sending her enough money, she does not have any
problem in their daily expenses. They spend 10,000php for their foods, 1000php for
electric bills and 6000php for other daily expenditures such as school allowances. She
usually wakes up at 5 o’clock in the morning to prepare foods for her grandchildren. She
regularly eats her breakfast with her grandchildren at around 6 o’clock. Most of the time,
she only drinks coffee for breakfast. After they gone for school she will clean the house
and do other household chores such as washing and ironing clothes. At 12 noon she will
take her lunch and will sleep for two to three hours. Upon wakening, she will prepare for
the coming of her grandchildren which is usually 4 in the afternoon. At 6 o’clock in the
evening they are having their dinner together and sometimes watch television after
eating. She always makes sure that before 8pm they are all sleeping. During illness, Mrs.

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 Kelly Clamp consults albularyo instead of doctors. She also delivered her 11 children
with the aid of a hilot. According to her their residence is a quiet and peaceful place.
There are no smokers in their house and they have harmonious relationship with their
neighbors.

2. Family Health Illness History

D. 1928 D. 1930

Mr. Mrs. Mr. Mrs.

Super Super Allis Allis
Babcock Babcock

D. 1971 D. 1976

Junior Baby
Babcock Allis

1932
77

Billy Kelly Willy Shelly Belly

HPN (pt) HPN

Legend:

Male Female Deceased

During Interaction, Mrs. Kelly Clamp had mentioned that she was not able to
meet her grandparents but according to her parents, they died due to old age. Her father, Mr.
Junior Babcock died at age of 55 because of unknown reason. She said that one morning they
seen him in the bed unconscious and already dead. Mrs. Babcock, her mother died at the age
of 60 because of heart attack. She has four siblings, two boys and two girls. Two of which
are also hypertensive.

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3. History of Past Illness

Mrs. Kelly Clamp is a hypertensive patient with usual blood pressure of 150/100.
However, she does not take antihypertensive drugs instead she avoids eating fatty to prevent
further increase of her blood pressure. She had measles at the age of 5 and chickenpox when
she was 10. She also experienced fever, headaches and sometimes colds and cough. Mrs.
Kelly Clamp does not consult a doctor during illness instead she resorts to self-medication.
Usual medicines that she is taking include paracetamol and mefenamic acid.

4. History of Present Illness

Based on the statement of Mrs. Kelly Clamp, two days before her hospitalization, she
experienced frequent dizziness and headache. Last July 30, 2010, she was rushed to the
hospital due to severe headache and dizziness. Upon arrival, oxygen inhalation was
administered to her and she was advised to stay at the hospital for observation and
examination. Complete Blood Count, blood chemistry and blood typing was ordered by her
physician. The results showed decrease of her hematocrit and hemoglobin thus she
undergone blood transfusion. Blood chemistry results showed elevation of her blood urea
nitrogen and creatinine level which indicates renal failure. Mrs. Kelly Clamp is still in the
hospital for further treatment with diagnosis of Acute Renal Failure.

III.PHYSICAL ASSESSMENT

a. P.E upon admission: conscious, non-coherent, assisted movements, (+) dyspnea, cold
clammy skin. Vital signs: T= 36.2˚C PR=90bpm RR=20 BP=160/100

On day of admission, CBC showed decreased hematocrit and hemoglobin.

b. Assessment conducted by the student nurses

General Appearance: received pt. lying on bed with ongoing IVF #6 D5LRS @ 500cc level,
regulated @ 32gtts/min, infusing well on the right arm. Seemed to be tired and unable to sit
or stand.

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1. Integumentary
Skin

• Yellowish in color
• Pale palms, soles, nail beds, lips
• Wrinkled texture
• Dry and scaly
• Poor skin turgor, skin recoil beyond 2secs.
• With presence of edema
Hair and Scalp

• Grayish in color and not properly distributed

• Dry
• No lesion, tenderness
• No pediculosis
Nails

• Pale nail beds

• Capillary refill of 2 secs.

2. Head and Neck

Head

• Symmetrical and round

• Located at the center
• Hard and smooth
• No nodules or masses noted
Eyes

• Eyebrows symmetrically aligned and properly distributed

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 • Eyelashes are well distributed and slightly curled outward
• Bulbar conjunctiva clear
• Pink palpebral conjunctiva with no discharge
• Clear sclera
• Moist cornea
• Pupils are equally round and reactive to light accommodation
• Non tender lacrimal apparatus and with no discharge noted
• Both eyes move in smooth, coordinated manners
Ears

• Equal in size and position

• Same color as the face
• No discharge noted
• No lesions
• Non tender auricles
• Pinna recoils after folded
Mouth, Nose and Throat

• Lips are moist, smooth with no lesion

• Pink, smooth, moist with no lesion buccal mucosa
• With 16 teeth
• Tongue located at midline
• Pink hard palate
• Pink tongue with no lesion
• Nose same color as the face
• Nasal septum intact and at the midline
• No tenderness of facial sinuses
Neck

• Smooth
• Full ROM

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 • No palpable lymph nodes
• No tenderness

3. Respiratory
• Chest symmetric
• No tenderness
• No masses or lesion noted

4. Digestive
• Skin is pale
• No scar present
• No tenderness
• Rounded abdomen
• Hyperactive bowel sounds ranging from 5-35 times per minute

5. Peripheral vascular system

Arms

• same color bilaterally

• no edema
• warm to touch
• radial and brachial pulses equal in strength bilaterally
Legs

• bilateral edema present

• Toes, feet and legs are warm bilaterally
• Faint femoral pulses

6. Neurologic

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 Mental status

• Consciousness
o Awake
o Alert
o Responds appropriately
• Grooming/hygiene
o Clean skin and nails
o Appropriate clothing
• Facial expression
o Good eye contact
o Smiles and frowns appropriately.

7. Sensory System
• correctly identifies light touch
• correctly differentiates dull and sharp sensations
• correctly identifies hot and cold temperature throughout the body
• correctly identifies direction, movements and sensations

IV. COURSE IN THE WARD

A. Day to day treatment

 Day 1 ( July 30, 2010)

• O2 inhalation 4L/min

• #1 D5LRS 1L x 8˚ (time started: 8:00 AM)

• Blood typing: A+

• Urinalysis:

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 Result:

Color: Yellow

Character: clear

pH:6.0

Protein: Negative

Sugar: Negative

Sp. Gravity: 1.010

RBC: Negative

Epithelial Cell: Few

• Hematology

Result Normal Value

Hematocrit 0.26 0.37-0.47(37-47%)
Hemoglobin 86g/dL 140-180g/dL
WBC 11.2 5-9x10g/dL
POLYS 0.62 0.40-0.60
LYMPHOS 0.38 0.20-0.40

• Chest X-ray (not done)

• Cross Matching for Blood Transfusion

• Low Salt Low Cholesterol Diet

• Medications ordered: Simvastatin 20mg/tab OD

Serc 8mg/tab q8

 Day 2 (July 31, 2010)

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• #2 D5LRS 1L x 8˚ (time started: 12:00 AM)

• Medication ordered: Beartec 10mg/tab OD

Serc 16mg/tab q8˚

Transferron tab OD x 3orders

 Day 3 (August 1, 2010)

• #3 D5LRS 1L x 32gtts/min (time started: 8:00 AM)

• #4 D5LRS 1L x 32gtts/min (time started: 4:00 PM)

• BP precaution

• Follow up Blood Transfusion

• Continue Monitoring

• Medication ordered: Furosemide 20 mg IV q12

• Day 4 (August 2, 2010)

• #5 D5LRS 1L x 32gtts/min (time started: 12:00 AM)

• BP precaution

• Follow up Blood Transfusion

• Continue Monitoring

• Medication ordered: Furosemide 20 mg IV q12

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 Day 5 (August 3, 2010)

• #1 PNSS 1L x 100cc/hr (time started: 9:00 AM)

• Consent for Blood Transfusion

• Carry out Blood Transfusion: PRBC 500cc

• Decrease Beartec to 1/2 tab OD

• Paracetamol 500mg/tab q4˚

 Day 6 (August 4, 2010)

• Hematology:

Results Normal Values

Hematocrit 0.27 0.37-0.47
Hemoglobin 90g/dL 140-180g/dL

• Blood Chemistry:

Results Normal Values

BUN 10.6mmol/L 2.5-6.4mmol/L
Creatinine 185mmol/L 53-106mmol/dL

• Medication Ordered: venteril tab TID PO

 Day 7 (August 5, 2010)

• #6 D5LRS 1L x 32gtts/min (time started 6:32 AM)

• Allopurinol 100mg/tab PO OD

• Serc 16mg/tab q8˚

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 • Ketosteril 1tab TID

• Transferron 1 tab ODx30 days

• Simvastatin 20mg/tab OD

• Furosemide 20mg IV q12˚

• Beartec ½ tab OD

B. Summary of Laboratory and Diagnostic Procedures

1. Hematology

2. Blood Chemistry

3. Urinalysis

C. Summary of Medications

1. Allopurinol

2. Serc

3. Ketosteril

4. Transferron

5. Simvastatin

6. Furosemide

7. Beartecto

8. Venteril

9. Paracetamol

NURSING RESPONSIBILITIES

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  IVF: D5LRS and PNSS

BEFORE:
 Check doctor’s order
 Explain the procedure to the pt.
 Inform pt. that the procedure required vein puncturing thus may cause discomfort or pain
 Prepare the correct IVF
DURING:
 Apply sterile to sterile technique
 Regulate IVF
AFTER:
 Check the puncture site for signs of bleeding, edema or thrombophlebitis
 Always make sure that the IVF is patent and regulated properly
 Chart the procedure done.

 BLOOD TRANSFUSION

BEFORE:

 Compare the request to the doctor’s order to check that you request the correct blood
component

 Review blood value that trigger the procedure

 Verify patient’s identity. Ask the patient’s to state full name before proceeding to the
procedure

 Check patient’s temperature, pulse, respiratory rate, blood pressure and auscultate lungs
for any abnormalities

 Check again the blood component. Make sure that the blood you will hang is the correct
blood component ordered

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  Double-check the label for accuracy and make sure the unit blood type is compatible with
the patient’s type

 Check the expiration date and time on the compatibility report to be sure the
compatibility testing has not expired

 Do not start the transfusion unless all the comparisons are exactly match

DURING:

 Start the transfusion slowly at a rate of 5ml/minute for the first 15 minutes. If vital signs
are stable after 15 minutes of transfusion, adjust the rate as ordered.

 Remain at the patient’s side for the first 15 minutes of the transfusion. Monitor for
increase of temperature or chills, hypotension, dyspnea, headache or skin rashes.

AFTER:

 Document the starting time of the transfusion, the type of blood component and unit
number.

 HEMATOLOGY:

BEFORE:

 Check doctor’s order

 Explain the procedure to the patient.

 Inform patient that the procedure requires vein puncturing which may cause discomfort.

DURING:

 Apply sterile technique

 Make sure that the blood sample will not be taken at the arm with intravenous line.

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  Collect 5-7 ml of blood sample in a examination tube.

AFTER:

 Apply pressure to the puncture site.

 Check the site for bleeding or swelling.

 Send the sample to the laboratory immediately.

 Document the procedure done.

 CROSS MATCHING

BEFORE:

 Verify doctor’s order.

 Check patient’s history for recent blood administration.

 Explain the procedure to the patient.

DURING:

 Apply sterile technique

 Collect blood sample in a 10 ml red top tube, ABO

 Apply pressure to the venipuncture site.

AFTER:

 Monitor puncture site for bleeding. If hematoma develops, apply warm compress.

 Handle the sample carefully to prevent hemolysis.

 Label the sample with the patient’s name, hospital or blood bank number, the date and
the phlebotomist initials.

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  Send the sample to the laboratory immediately.

 URINALYSIS

BEFORE:

 Check doctor’s order.

 Explain the procedure to the patient.
 Instruct the patient to obtain clean sample by collecting the midstream urine.

AFTER:

 Label the specimen

 Bring the specimen at the laboratory immediately.

• Document the procedure done.

V. CLIENT-CENTERED PATHOOPHYSIOLOGY

Hypertension Age of 77 y/o

↑ Heart pump ↓ Kidney Cells Integrity

↓ Filtration Ability
↑ Arterial Pressure

↑ Kidney arterioles tone

Arterioles Damage/Injury

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 ↓ Blood Flow

Ischemia

Glomerular Injury Vasoconstriction

↓ Glomerular Permeability

↓ GFR

↑BUN ↓ Urine Production ↑serum

creatinine

↓ Renal Excretion

Edema Fluid Retention

Dizzines
s
Hypertension
Headach
e

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 VI. EVIDENCED-BASED FOCUS

Acute renal failure in an AIDS patient on tenofovir: a case report

Published: 31 March 2008

Journal of Medical Case Reports 2008, 2:94 doi:10.1186/1752-1947-2-94

Received: 11 June 2007

Accepted: 31 March 2008

Abstract

Tenofovir is a potent nucleotide analogue reverse-transcriptase inhibitor used with other

antiretroviral agents for the treatment of human immunodeficiency virus (HIV) infection.

Despite the absence of renal toxicity observed in the major clinical trials of tenofovir, several
case reports of acute renal failure (ARF) and proximal tubule dysfunction have been described.

Case presentation: We report a patient who developed ARF and Fanconi syndrome during
treatment with tenofovir. Despite severe metabolic acidosis associated with a creatinine of 9.8
mg/dL (866 μmol/L), this patient's condition improved on discontinuation of tenofovir treatment
without requiring renal replacement therapy.

Conclusion: Vigilant screening of kidney function is required regularly after initiation of

tenofovir due to possible appearance of renal failure.

Introduction

Tenofovir is a nucleotide reverse-transcriptase inhibitor which was approved for use by the Food
and Drug Administrationin 2001 for the treatment of HIV. It belongs to the same class as
adefovir and cidofovir which have well documented renal toxicities including proximal renal
tubule cell dysfunction and acute renal failure (ARF) [1,2]. The described mechanism of tubular
toxicity for the latter two drugs is cellular accumulation through increased entry from the hOAT

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(organic anion transporters located on the basolateral side of the tubule) and decreased efflux
into tubular lumen mediated by the MRP 2 (Multidrug- Resistance-Protein) [3]. Similar effects
were not expected with tenofovir due to decreased interaction with human organic transporter 1
and minimal mitochondrial toxicity in vitro [2,3]. Twenty seven cases of tenofovir related
tubular dysfunction and Fanconi syndrome have been described in the medical literature. We
describe another case of a patient in whom ARF and Fanconi syndrome developed during
treatment with tenofovir.

Case presentation

A 53-year-old woman with AIDS of 6 years duration developed progressive weakness, dyspnea
on exertion and constipation. Her symptoms also included decreased appetite, weight loss and
episodes of lightheadness. She had a history of drug and alcohol addiction, seizure disorder,
stroke, pancreatitis and chronic low back pain and she was known to have been Hepatitis B and
C positive since 2002. Antiretroviral therapy, consisting of abacavir, lamivudine and zidovudine,
had been started in March 2002, when she was found to have Pneumocystis jirovecii pneumonia.
She had not developed any other opportun-istic infections. Eighteen months later, in October
2003, her HAART regimen was switched to tenofovir (300 mg/ day), sustiva (600 mg/day) and
Epivir (300mg/day). At that time, her creatinine was 0.8 mg/dL (71 μmol/L). A recheck in
December 2005 revealed a creatinine of 0.9 mg/dL (80 μmol/L) corresponding to Egfr 75
ml/min. She had been on this regimen without any change in the dose of tenofovir until she
presented to hospital. Her other medications included aspirin 81 mg/day, folic acid and
hydroxyzine. She had also been started on trimethoprime-sulfamethoxazole but discontinued this
herself in April 2006. On admission, clinical examination revealed signs of mild dehydration.
Laboratory tests disclosed the following concentrations: sodium, 134 mEq/L; potassium, 3.4
mEql/L; chloride, 115 mEq/L; bicarbonate, 8 mEq/L; BUN, 57 mg/dL (20 mmol/L); creatinine,
9.8 mg/dL (866 mmol/L); phosphorous, 5.7mg/dL (1.8 mmol/L); CPK, 119 U/L; uric acid, 4.9
mg/dL; lactate, 0.63 mmol/L and albumin 3.8 g/dL (38 g/L). Arterial blood gas showed academia
(pH: 7.15) with appropriate respiratory response (pCO2 21 mmHg). In a urine sample, sodium
was 44 mEq/L with a FeNa of 4%, potassium 39 mEq/L, chloride 43 mEq/L and creatinine 82
mg/dL (7249 mmol/L). Urinalysis showed marked glucosuria (294 mg/dL) with normoglycemia
and proteinuria (124 mg/dL) and an absence of active urinary sediment. Urine pH was 6.0. The

22
rates of fractional excretion of phosphorus and uric acid were 58% and 37% respectively. The
findings of renal ultrasound were normal, as were the findings for all serologic tests. Her CD4+
lymphocyte count was 241 and her viral load 460 HIV RNA copies/ml. Tenofovir therapy was
discontinued and her HIV regimen was adjusted to abacavir, sustiva and epivir. Intravenous
bicarbonate therapy was initiated with simultaneous potassium supplementation. Within the next
few days, there was slow improvement in serum creatinine and bicarbonate levels but
hypokalemia (minimum 2.5 mEq/L) recurred, requiring discontinuation of bicarbonate. Five
days after her admission to our hospital, the patient discharged herself against medical advice. At
that time she still had hypokalemia (2.7 mEql/L), low bicarbonate level (16 mEq/L) and a
creatinine of 6.1 mg/dl (539 mmol/L). At follow-up at 7 months, her kidney function had
returned to normal.

Discussion

In short-term clinical trials, tenofovir did not exhibit more frequent nephrotoxicity compared to
placebo [4]. Recently, however several case reports documenting nephrotoxicity have been
described in the literature [5-8]. A number of different manifestations of kidney disease have
been reported with tenofovir, including ARF, rhabdomyolysis, Fanconi syndrome and diabetes
insipidus[6]. Many patients diagnosed with AIDS develop acute or chronic diarrheal syndromes
with associated non-anion gap metabolic acidosis from bicarbonate loss in the stool. However,
our patient did not report any episodes of diarrhea and the positive urine anion gap was not
consistent with that possibility. Exposure to trimethoprime-sulfamethoxazole can induce acute
interstitial nephritis. High-dose trimethoprime-sulfamethoxazole has been associated with
unexplained RTA in a series of patients. The discontinuation of trimethoprime sulfamethoxazole
three months prior to presentation makes both of these scenarios in our case unlikely. Type B
lactic acidosis resulting from mitochondrial dysfunction is well described for nucleoside reverse
transcriptase inhibitors. No hyperlactemia was found in this patient. Other potential causes of
severe metabolic acidosis were not identified. Our patient had typical findings of Fanconi
syndrome (hyperchloremic metabolic acidocis, hypokalemia, glucosuria) but she was
hyperphosphatemic. Hyperphosphatemia was attributed to decreased GFR whereas the
possibility of pseudohyperphosphatemia secondary to multiple myeloma was ruled out with
negative SPEP (serum protein electrophoresis). The constellation of ARF and Fanconi syndrome

23
and the close temporal relationship between discontinuation of tenofovir and improvement of
renal function suggest that tenofovir-induced nephrotoxicity was the most likely diagnosis. The
creatinine of 9.8 mg/dL (866 mmol/L) and bicarbonate of 8 mEq/L are the highest and lowest
respectively reported in the literature among the non-hemodialysis requiring cases of ARF
secondary to tenofovir. The first case of hemodialysis requiring ARF secondary to tenofovir was
of a 40 year-old HIV man who presented with oliguria, acidemia (pH 7.10, HCO3 6 mEql/L),
lactate 7 mmol/L and creatinine of 20 mg/dL (1768 mmol/L)[7]. However, this patient was also
receiving metformin, which could be implicated particularly in the setting of high lactate levels.
The second case of hemodialysis in ARF induced by tenofovir was a 65 year-oldman with
diabetes and AIDS who was admitted with creatinine, 7.1 mg/dL (628 mmol/L, GFR 6.8
ml/min), blood urea nitrogen, 68 mg/dL (24 mmol/L) and bicarbonate, 10 mEq/L [7]. This
patient received two hemodialysis treatments for azotemia. Expecting recovery of kidney
function after discontinuation of tenofovir treatment, we did not dialyse our patient, as she was
asymptomatic. In a recent review, Zimmermann et al. analyzed the findings for the 27 patients
described in the literature with tenofovir-associated ARF since December 2002 [8]. The mean
age was 45.5 years, with a ratio of men to women 3.5:1. The mean duration of tenofovir
treatment was 11 months (range, 1–29 months). Our patient was taking tenofovir for 32 months,
which is to our knowledge the latest presentation of tenofovir- induced ARF. There are no
known predictors of which patients will develop ARF associated with tenofovir. There was no
correlation of CD4 cell count and plasma HIV load with the development of ARF [8]. However,
low baseline GFR may contribute to tenofovir's toxicity via increase in the serum concentration
[8]. Similarly, no predictors for occurrence of Fanconi syndrome exist. A recent study identified
genetic variants of hOAT1 and investigated potential effects on the functional properties of this
transporter. Kinetic analysis indicated that the transport affinity for the nucleoside phosphonate
analogues adefovir, cidofovir and tenofovir seemed to be decreased in the R50H-hOAT1 variant
compared with the wild type. This study raises the genetic variation in hOAT1 as potential
explanation of "different handling" of these drugs with the associated clinical implications [9].
Tenofovir is primarily excreted by the kidneys. Elimination is accomplished by glomerular
filtration as well as by active tubular secretion. There are several medications that compete for
renal tubular secretion, including acyclovir, cidofovir, valcyclovir, ganciclovir and
valganciclovir. Coadministration may lead to increased serum levels of tenofovir. Additionally,

24
tenofovir causes CYP1A2 inhibition, and drug levels may be increased when given with other
antiretroviral medication. Administration of ritonavir alone or with lopinavir has been shown to
increase the maximum serum concentrations of tenofovir by 30%, while didanosine and
atazanavir also have been described to have potential interactions with tenofovir [10]. Notably,
our patient was not receiving tenofovir concurrently with any of the above listed medications.
Until recently, no long-term renal impairment was expected as a consequence of tenofovir-
related nephrotoxicity. However the incomplete recovery of kidney function in 5 out of 27
reported cases after a mean duration of follow- up of 7.5 months raises serious concerns for
occurrence of chronic kidney disease after discontinuation of tenofovir [8]. A follow-up of serum
creatinine, urinalysis and electrolytes should be performed in patients taking tenofovir. Early
diagnosis is important so that this medication can be discontinued in a timely manner and life-
threatening electrolyte imbalances can be avoided. Hemodialysis will not be necessary in the
majority of cases, given the rapid resolution of ARF with the discontinuation of tenofovir.
Physicians should continue to be vigilant in screening patients well after initiation of tenofovir
due to possible late appearance of renal failure. In cases of ARF occurrence, persistence of
kidney damage should be considered as a possibility so that early optimization of coexistent risk
factors can be attempted.

Conclusion

We describe the case of a patient in whom ARF and Fanconi syndrome developed during
treatment with tenofovir. Vigilant screening of kidney function is required regularly after
initiation of tenofovir due to possible late appearance of renal failure.

25
 VII. NURSING CARE PLANS

Nutritional imbalance: less than body requirements

Cues Nursing Scientific Planning Interventions Rationale Evaluation

Diagnosis explanation
S: “Ala kung Imbalance A common After 2 hours of > Determine > This are After 2 hours of
ganang mangan” nutrition less diagnosis for nursing client’s ability to factors that may nursing
than body clients with interventions chew, swallow affect ingestion intervention, the
O:
requirements acute renal patient will be and taste food. and/or digestion patient was able
-Hyperactive
related to failure. An ARF able to verbalize of nutrients to enumerate
bowel sound
anorexia and patient may have understanding of > Note > To determine importance of
-Muscle
altered metabolic a bitter taste due why she should availability/ use ability to acquire adequate food
weakness
state secondary to the decrease eat adequate of financial and store various intake to regain
-Seemed to be
to renal failure excretion of urea food so as to resources and types of food. energy and to
tired/ lack of
which is regain energy support system. meet metabolic
energy
> To appeal to
converted into and to meet > Discuss eating needs.
-Dry buccal
client’s
ammonia that metabolic needs. habits, including
cavity
likes/dislikes
causes the food preferences,
-Decreased
muscle mass unpleasant taste intolerances/
of the patient. In aversion.
> To establish
this case, patient > Asses body
baseline
appetite will fats and muscle
parameters.
decrease thus mass via triceps
patient’s intake skin fold and

26
of nutrients is mid-arm muscle
less than what circumference or
the body other
requires to meet anthropometric
its metabolic measurements
needs. Due to > Provide diet
decreased modifications > To enhance
metabolism of such as several food satisfaction
nutrients patient small meals and and stimulate
may suffer from snacks daily. appetite.
fatigue as well. > Use flavoring
agents on foods, > This may help
like lemon and to enhance
herbs because intake.
salt is restricted.
> Provide a
pleasant > This may aid
environment at in increasing
meal time and patient’s appetite
prepare the food
in an attractive
manner.

27
 > Administer
prescribed > To improve
medications the nutritional
value of foods
taken by the
patient

28
Anxiety

Cues Nursing Scientific Planning Interventions Rationale Evaluation

Diagnosis Explanation
S: “Eku Anxiety related Anxiety is After 2 hours of > Determine > This After 2 hours of
mipapatudtud to unknown characterized as nursing current medications can nursing
uling isipan ku outcome of a vague uneasy interventions prescribed heighten interventions,
ing kundisyun disease process feeling of patient will be medications and feelings/sense of the patient was
ku ngeni” discomfort or able to verbalize recent drug anxiety able to verbalize
dread feelings of history of feelings of
O: accompanied by anxiety, would prescribed or anxiety, identify
-Teary eyes an autonomic appear to be OTC medication. ways to deal
-Seemed to be response. A relaxed and > Identify >To know with anxiety and
preoccupied feeling of would be able to client’s appropriate appeared
diminished apprehension identify ways to perception of the intervention relaxed.
concentration caused by deal with and treat represented
with the topic anticipating express anxiety. by the situation.
danger. > Monitor vital > To identify
signs physical responses
associated with
both medical and
emotional
conditions

29
 > Observe
patient’s > Points the
client’s level of
behavior like
anxiety
restlessness,
irritable, wakeful,
and reports
insomnia.
> Note reports of > May be
insomnia or behavioral
excessive indicators of use
sleeping, of withdrawal to
limited/avoidance deal with
interactions with problems
others.
> Review results > This may point
of diagnostic to physiological
tests. source of anxiety
> Establish a > To avoid the
therapeutic contagious
relationship, effect/transmission
conveying of anxiety.
empathy and

30
 unconditional
positive regard.
> Provide > Helps client to
accurate identify what is
information reality based
about the
situation.
> Encourage > This may serve
client to develop to reduce level of
an exercise/ anxiety by
activity program. relieving tension.

31
Excessive fluid volume

Cues Nursing Scientific Planning Interventions Rationale Evaluation

diagnosis explanation
S: Ø Excess fluid Presence of ARF After 2 hours of > Note > This may serve After 2 hours of
nursing
volume related decreases the nursing amount/rate of as baseline data
O: interventions,
to inability of the ability of the interventions fluid intake from patient was able
-Bilateral edema
to maintain
kidneys to kidneys to patient will be all sources
on the lower balance fluid
produce urine excrete waste able to maintain > Instruct the > To prevent intake and output
extremities
and identify
secondary to products. Urine balanced fluid patient to further
-oliguria importance of
ARF production is intake and decrease intake worsening of decreasing fluid
intake.
decreased which output and of fluids. edema
causes fluid would also >Explain the >Increase
retention thus identify relevance of patient’s
resulting into importance of fluid restriction awareness and
excess interstitial fluid restriction. participation
fluid. > Monitor input >To evaluate
and output prognosis of
problem
>Inform patient >Increase
to Low Salt Diet sodium intake
may aggravate
edema

32
Altered Renal Tissue Perfusion

Cues Nursing Scientific Planning Interventions Rationale Evaluation

diagnosis explanation
S: Ø Altered renal Decrease blood After 4 hours of >Monitor vital >To have After 4 hours of
tissue perfusion supply will nursing signs baseline data nursing
O: r/t glomerular cause the intervention, the >Ascertain >to compare interventions,
Increase BUN malfunction glomerulus to patient will be voiding pattern with current patient was able
and serum secondary to malfunction able to manifest situation to comply to
creatinine level renal failure which may lead willingness of >Assess mental >Increase BUN treatment
AEB elevation to decrease treatment status and and creatinine program and
of BUN and permeability program and review levels alter lifestyle
serum creatinine thus decreasing lifestyle changes laboratory mental status. modification.
level its ability to compliance for results such as
filter waste regulating blood BUN and
products such as chemistry level creatinine.
BUN and and preventing >Monitor BP >↓GFR may
creatinine. complications. increase BP
Unfiltered waste >Observe >To evaluate
will remain to presence of degree of kidney
the blood which edema impairment
may cause >Monitor urine > To assess renal
further injury to output perfusion and

33
the patient. function
>Provide diet >Restriction of
restriction such protein helps
as Low Protein limit BUN;
Low Salt diet, decrease in salt
while providing intake may
adequate calories prevent fluid
excess while
calories meet
body needs.
>Administer >To
medications as treat/manage the
ordered patient’s
condition

34
Fatigue

Cues Nursing Scientific Planning Interventions Rationale Evaluation

diagnosis explanation
S: Ø Fatigue related A decrease in After 4 hours of >Establish rapport >to facilitate After 4 hours of
nursing
to decreased Hgb count nursing client and
intervention,
O: hemoglobin would be a intervention, the student nurse goal was met as
evidenced by:
-generalized count factor in having patient will interaction
*clients
body weakness fatigue because demonstrate an >Discuss with the >education may verbalization of
feeling of less
-pale RBC plays an improve ability patient the need provide
fatigue and
-dizzy important role in to participate in for activity. Plan motivation to weakness
*patient
-Hgb count of our cells and desired activities schedule with the increase activity
participates in
90g/dL muscle to and he will patient and level through some activities
as much as she
function verbalize an identify the patient may feel
could
normally. increase energy activities that leads too weak *patient is
Patient with level. to fatigue. initially awake
ARF may suffer
to anemia
because our >Monitor vital >indicates
kidney is one of signs physiological
the producers of level of
erythropoietin tolerance
that is one >Encourage the >to gain energy

35
component for patient to eat
RBC production >Administer >for the body to
and RBC are the medications such have enough
one who carries as ferrous sulfate RBC to supply
oxygen and as prescribed the muscles and
nutrients to other cells enough
cells and nutrients to
muscles for function
them to function. properly
A decrease in >Encourage/advise >to increase the
erythropoietin the patient to patients activity
production will perform ROM level in a step-
tend to produce exercise by-step manner
a small amount >Encourage the >restoration of
of RBC that patient to rest energy
would lead to a >Promote overall >to correct the
decreased supply health measures need of supply
of oxygen to such as proper of RBC and to
different cells nutrition, adequate reduce fatigue
and muscles in fluid intake and by gaining
the body. appropriate energy
Therefore, vitamin/iron

36
leading to poor supplement.
muscle tone and >Maintain >to improve
a problem with strenuous activity activity
muscle restrictions. tolerance, avoid
contractility that activities that
could make the requires too
client feel that much energy
he is weak.

37
Impaired Urinary Elimination

Cues Nursing Scientific Planning Interventions Rationale Evaluation

diagnosis explanation
S: Ø Impaired urinary Decrease in After 4 hours of >Monitor vital >To have Goal was met as
elimination GFR, reduces client and signs baseline data evidenced by the
O:
-oliguria related to kidney’s ability student nurse >Review >To determine clients
-irritability decreases urine to excrete excess interaction the laboratory tests for causative factors verbalization of
-decreased urine production fluids and waste client will be renal changes understanding of
output secondary to products. Fluid able to verbalize >Determine >To evaluate condition
renal failure retention and understanding of patient’s pattern of degree of
remained waste condition elimination interference
products further >Palpate Bladder >To assess for
contributes to possible urinary
kidney damage retention
which may >Investigate pain, >To determine
result to noting location extent of
decrease interference
production of >Determine >To determine
urine causing patient’s usual level of
impairement in daily fluid intake dehydration
elimination. >Encourage to >Open
verbalize fear or expressions

38
 concern allows patient to
deal with
feelings and
begin problem
solving
>Emphasize the >To prevent
need to adhere worsening of
with prescribed disease
diets condition
>Emphasize the >to prevent
importance of infection and
having good promote
hygiene and wellness
adherence to
treatment program

39
Knowledge Deficit

Cues Nursing Scientific Planning Interventions Rationale Evaluation

diagnosis explanation
S: “Eku balu Knowledge Acute Renal After 4 hours of >Review disease >To provide After 4 hours of
nukarin ku ikwa Deficit r/t lack Failure is not an nursing process/prognosis knowledge base nursing
ini, enaku man of information ordinary disease interventions, and future from which the interventions,
mapamangan thus community the patient will expectations. patient can make the patient was
malat ampong people does not be able to informed able to
mataba” have sufficient verbalize choices verbalized
information understanding of >Fluid and >Sodium may understanding of
O: regarding the disease process, Sodium restriction further increase disease
-seemed to be disease. potential if indicated. water retention condition,
confused complications, and BP possible
-narrowed focus and therapeutic >Discuss diet >salt and fats complication
-frequently ask needs and modification such may contribute and treatment
about disease participate in as Low salt, Low to hypertension program
condition treatment fat and high while protein compliance.
program. protein may aid in
wound healing
of the kidney
>Discuss drug >To prevent
therapy including hypertension

40
 anti-hypertensive and further
drugs and diuretics damage to
kidney’s arteries
and to prevent
excess fluid
accumulation.
>Instruct self- >ARF patient
monitoring of BP, are usually
including taking hypertensive
rest before BP
taking and proper
positioning
>Establish routine >Helps in
exercise within maintaining
patient’s ability muscle tone and
and intersperse joints flexibility
rest periods within and reduces risk
activities associated with
immobility
while preventing
fatigue.
>Discuss the signs >suggestive of

41
 and symptoms poor control of
including hypertension
headache, blurring
of vision and
dizziness.

42