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Intern’s Name: Laryssa Grguric Date: 02/12/14
Rotation/Facility: Clinical/NUMC Preceptor’s Signature:

Part I:
A. Patient Information:

Initials: M.B.P. Occupation: Pastor Admission Date: 02/10/14
Gender: M Socioeconomic Status: Middle Marital Status: Married
Age: 56 Residence (Home or LTC): Home Ethnicity: African

B. Diagnosis: ESRD/Stage 5 CKD (Acute on Chronic Kidney Disease)

C. Medical Problem List: Abdominal pain c ! vomiting 3-4x daily, renal insufficiency

D. Medical/Social Hx: A-fib (pacemaker), HTN, Gout, DM Type 2, CKD

E. Physical/Anthropometric Data (if available):

Date: 02/12/14 Height: 68” UBW: 275# %UBW: 100%
Current Wt. 275# IBW: 154 ±10% %IBW: 179% BMI: 43, Class III

Note any findings from physical assessment: Pt. appears to have distention of abdomen.

F. Pertinent Laboratory Data:
( 12.1-
15.6 ) )

( 8.4-
( 2.3-
( 8-23 )

( 0.4-1
( 3.5-
( 70-

2/1 2/10/14 4.08
9.9! 28.9! 3.6
- 136" 5.3" 129! 3.0! 214" - 85!
2/11/14 4.04! 9.9! 27.9! 3.5
- 3.7
145" 5.3" 128! - - 1.8
2/12/14 3.86! 9.6! 27.3! - 9.4
154" 5.6" 126! 3.7
56! 1.8
2/10/14 - - - - 14
2/11/14 31! 246
1174 - 69.1!
2/12/14 - - - -
(Labs continued from last page)

Part II: Medical Problems, Laboratory Tests and Medications

Summary of Medical Text Findings Comparison of Patient to Text
A. Pertinent Medical Problems: include
background of each disease from text and
include medical nutrition therapy (MNT) for
each; include kcal and protein recommended
if noted; highlight information that can
relate to this patient.
A. Pertinent Medical Problems:
include how each disease is
affecting patient; what treatments
patient is receiving; therapeutic
diet PTA and diet order in hospital;
how does the kcal/protein
recommended for each disease
translate for this patient? Do not
complete an assessment.
A. Renal Failure: Acute on Chronic Kidney

1) Acute Kidney Injury (AKI)
Also called Acute Renal Failure (ARF). It is a
rapid accumulation of creatinine and urea in blood
(azotemia) caused by kidney damage from possible
trauma, illness, surgery or intrinsic renal disease
(McMillan, 2011, 2436). AKI can occur c! oliguria
or normal urine flow. Duration lasts from a few
days to several weeks (Wilkens, Juneja &
Shanaman, 2012, 808).

Sx of AKI include anorexia, nausea, vomiting c!
possibility of seizures and coma if left untreated.
Causes of AKI are classified by prerenal, renal or
post renal. Prerenal conditions account for 50-80%
of AKI cases and they are reversible. Renal causes
of AKI involve intrinsic renal disease and
attribute to 10-40% of AKI cases and are generally
caused by ischemia causing tubule damage.
Postrenal instances are caused by obstruction in the

Hx of CKD

Pt. came into ED c! CKD Stage 4. Renal
attending believes AKI has further
progressed CKD to Stage 5.

urinary system. These cases contribute to a small
portion of cases – 5-10% (McMillan, 2011, 2436).

AKI is diagnosed by monitoring serum BUN,
creatinine, CBC, electrolytes including Ca and
phosphate. Serum creatinine can " as much as 2
mg/dL/day. BUN may " by 10-20 mg/dL/day.
However, surgery, trauma, corticosteroid usage,
burns, transfusion reactions, parenteral nutrition or
GI bleeds may affect BUN levels. Urine tests may
also be conducted and examined for Na+ and
creatinine concentration (McMillan, 2011, 2438).

Prerenal causes of AKI are clinically diagnosed and
easily corrected by correcting underlying cause.
Postrenal causes are determined by measuring
residual urine by use of catheter. If residual urine
volume is > 200 mL an obstruction is suspected.
Renal ultrasonography sensitivity is only 80-85% of
cases. CT can be done to establish obstruction site
to help determine treatment. Renal causes are
determined by clinical findings. Pts often have
edema, proteinuria or signs of arteritis in skin and
retina. Often this type of AKI can be diagnosed
without a history of intrinsic renal disease
(McMillan, 2011, 2439).


Energy and macronutrient needs in AKI are
determined greatly by the underlying cause of the
renal insufficiency (Wilkens et al., 2012, 809).

The amount of protein required can range from 0.5-
0.8 g/kg. Some AKI pts will require hemodialysis
(HD) and therefore their protein needs are higher at
1-2 g/kg. If the pt must undergo continuous renal
replacement therapy (CRRT), protein needs are
even higher due to protein losses during treatment
requiring 1.5-2.5 g/kg protein (Wilkens et al., 2012,

Energy needs also take into account any co-
morbidity that may be present. If possible, indirect
calorimetry can be used to determine needs in an
ICU setting. Otherwise, calorie needs can be

BUN " 136, 145, 154 mg/dL on
consecutive days

estimated at 30-40 kcal/kg of dry or ideal BW. Be
aware of addition of glucose in peritoneal dialysis
(PD) and CRRT that can contribute energy. Pts on
parenteral nutrition (PN) should receive high
amounts of carbohydrate and lipid c! monitored
respiratory status (Wilkens et al., 2012, 809).

Fluid and electrolyte intake should balance with
output. Fever can account for fluid losses via the
skin. When determining fluid needs, IVs, blood
and blood products should be taken into
consideration. Na+ should be restricted to 20-40
mg/day but difficult to obtain due to antibiotics,
blood pressure medication and PN (Wilkens et al.,
2012, 809). K+ balance should be monitored and
intake should be individualized according to serum
K+ levels. HD is used to remove K+ during AKI
(Wilkens et al., 2012, 810).

2) Chronic Kidney Disease

Also called Chronic Renal Failure. Chronic Kidney
Disease (CKD) is a progressive deterioration of
renal function (McMillan, 2011, 2442). CKD
causes permanent damage and eventually leads to
end-stage renal disease (ESRD) also known as
CKD Stage 5. It may result from any cause of renal
dysfunction but the most common is diabetic
nephropathy followed by hypertensive
nephroangiosclerosis (McMillan, 2011, 2442).
Diabetic nephropathy is the leading cause of ESRD
(Escott-Stump, 2012, 861). Metabolic syndrome is
a large and growing cause of renal damage
(McMillan, 2011, 2442). About 23 million people
have CKD c! moderately or severely reduced
glomerular filtration rate (GFR) (Escott-Stump,
2012, 860). Fifty percent of patients with CKD also
have DM (Escott-Stump, 2012, 864).

Sx of CKD include: anorexia, nausea, vomiting,
stomatitis, dysguesia, nocturia, lasstitude, fatigue,
pruritus, decreased mental acuity, muscle twitches,
muscle cramps, water retention, undernutrition, GI
ulceration, GI bleeds, peripheral neuropathies and
seizures (McMillan, 2011, 2442).

Pt. has PMH of DM & HTN

Pt’s chief complaint was abdominal pain
c! nausea & vomiting when admitted.

! renal function interferes c! the kidneys’ ability to
maintain fluid and electrolyte homeostasis. The
ability to concentrate urine occurs early on in the
disease and is followed by ! in ability to excrete P,
acid and K. Soon, the ability to dilute urine is lost
and urinary volume does not differ c! " or ! fluid
intake (McMillan, 2011, 2443). Na+ and water
balance is maintained by " fractional excretion of
Na+ and normal fluid intake due to thirst.
Therefore, hypervolemia does not occur unless
dietary intake of Na+ or water is restrictive or
excessive (McMillan, 2011, 2443). K+ levels "
when kidney failure becomes more advanced. K-
sparing diuretics, ACE inhibitors, beta-blockers,
NSAIDs, cyclosporine, tacrolimus or angiotensin II
receptor blockers may " K in sooner in the
progression of disease (McMillan, 2011, 2443).
Ca+, parathyroid hormone, vitamin D metabolism
and renal osteodystropy can occur resulting in
hypocalcemia, hyperphosphatemia, " or ! bone
turnover. Osteopenia or osteomalacia may also
occur (McMillan, 2011, 2443).

Moderate acidosis and anemia are often evident.
Anemia in CKD is normochromic-normocytic: Hct
20-30% and is caused by ! erythropoietin. CKD
pts may also be deficient in Fe, folate, and vitamin
(McMillan, 2011, 2443).

CKD is suspected when creatinine " but initial
steps include determining if renal insufficiency is
acute, chronic or acute superimposed on chronic.
Testing includes urinalysis, electrolytes, BUN,
creatinine, phosphate, Ca+ and CBC (McMillan,
2011, 2443).

Staging of CKD:
Stage 1: GFR " 90 mL/min/1.73 m
(normal) plus
albuminuria or known structural or hereditary renal
Stage 2: GFR 60-89 mL/min/1.73 m
Stage 3: GFR 30-59 mL/min/1.73 m
Stage 4: GFR 15-29 mL/min/1.73 m

Stage 5: GFR < 15 mL/min/1.73 m
2011, 2443).

Pt Rx’d Lasix

Hct 28.9%, 27.9%, 27.3%

Folate 12.2 WNL, Vit B12 1174 WNL.
Fe 31!

Pt’s diagnosis by Attending Renal MD.

GFR 14 mL/min/1.73 m

GFR indicates pt. is in ESRD; team details
he will begin hemodialysis (HD) as an

Progression of the disease is determined by degree
of proteinuria (McMillan, 2011, 2443). The kidney
plays a role in regulation of blood pressure (BP)
through the renin-angiotensin system (Escott-
Stump, 2012, 860). HTN and other underlying
disorders are associated with more rapid
progression (McMillan, 2011, 2443). Weight loss
and anorexia are associated with mortality (Escott-
Stump, 2012, 860).


The primary goal in MNT for CKD is to manage sx
such as edema, hypoalbuminemia and
hyperlipidemia, decrease the risk of progression to
renal failure and maintain nutritional stores
(Wilkens et al., 2012, 810).

A renal patient needs a detailed nutrition
assessment including Subjective Global Assessment
(SGA) to monitor physical changes such as weight
changes and changes in muscle mass, diet history
and gastrointestinal symptoms. Fluid shifts related
to edema may cause difficulty in tracking weight
losses (Escott-Stump, 2012, 860).

Early nutritional intervention can help to reduce
Na+ intake, control BP, manage DM and reduce
excessive protein intake that can help slow
progression of the disease (Escott-Stump, 2012,
861) and postpone initiation of HD (Escott-Stump,
2012, 869).

Following a HTN diet, such as the DASH diet, low
in sodium c! regular exercise can help to reduce BP
to goal of <130 mm Hg systolic and <80 mm Hg
diastolic. Blood glucose should be under control;
aim for HbA1c " 7%. DM pts may have to initiate
carbohydrate counting. All pts would benefit from
and increase whole grains, fruits and vegetables
while limiting processed foods (Escott-Stump,
2012, 869).

It is imperative to maintain or improve nutritional
status when possible. Aim to keep serum albumin
at 4.0 g/dL. A 10:1 ratio of BUN:creatinine is

CKD may be exacerbated by Type 2 DM,

Pt’s alb 3.6, 3.5 g/dL
~27:1 ratio BUN:creat
desirable. Urinary creatinine doubles when renal
function is <50% (Escott-Stump, 2012, 868).
Energy requirements for nondialyzed patients >60
years of age with GFR <25 mL/min need 35
kcal/kg/day. Those <60 years of age need 30-35
kcal/kg/day. Intake from carbohydrates should be
50-60% (Escott-Stump, 2012, 869). If DM or
heart disease is present, limit fat to 30% of
calories with >10% of total calories from
saturated fats (Escott-Stump, 2012, 869).

In CKD stages 1-3, limit protein to 0.8-1.0 g
protein/kg IBW. Choose high-quality proteins. In
CKD stage 4 reduce protein with GFR <25
mL/min reduce protein to 0.6 g protein/kg
IBW/day (Escott-Stump, 2012, 869).

Patients c! DM, HTN or edema should limit their
Na+ intake to 2.3 g/day (Escott-Stump, 2012,
869). When monitoring phosphorus and K+,
guidelines are based on CKD stage. Phosphorus:
Stages 1-2 limit 1.7 g/day. Stages 3-4 limit to 0.8-
1.0 g/day. Phosphate binders are recommended
along with limited intake of dairy: 1-2 servings/day
(Wilkens et al., 2012, 812). K+: Stages 1-2 keep to
>4 g/day. Stages 3-4: 2.4 g/day (Escott-Stump,
2012, 869). Intake and K-depleting medication
such as diuretics can affect K+ level (Wilkens et al.,
2012, 812). Fluid intake should be restricted to
output +500-1000mL (Escott-Stump, 2012, 869).

Patients c! CKD are routinely recommended to take
a vitamin to replace water-soluble vitamins lost.
There are renal formulations available (Wilkens et
al., 2012, 812).

Not everyone requires a strict HD diet and
therefore, diet therapy should be personalized to the
patient based on his or her needs (Escott-Stump,
2012, 860). In diabetic patients, glycemic control
can no longer reverse progression of CKD and
instead more importance relies on control of BP and
protein restriction when appropriate (Escott-Stump,
2012, 861).

B. Atrial Fibrillation

MNT Goals for Pt based on current status

Not currently on any vitamin/mineral

Atrial fibrillation (AF or A-fib) is defined as a
rapid, irregular artrial rhythm caused by a failure of
the atria to contract resulting in inconsistent
electrical stimuli. Ventricular rate is also affected
but becomes tachycardic. Sx of A-fib are
palpitations, weakness, dyspnea and presyncope
(Merck, 2011, 2165). AF is often asymptomatic but
pts may experience palpitations, chest discomfort or
sx of heart failure (Mitchell, 2011, 2166).

AF affects 2.3 million in the US with a higher
prevalence in men. Whites are most likely to be
affected. Almost 10% of people >80 years old have
A-fib (Mitchell, 2011, 2166). It is most often
caused by HTN, cardiomyopathy, valvular
disorders, hyperthyroidism and binge ETOH
drinking. Risk of stroke " in those with rheumatic
valvular disorder, hyperthyroidism HTN, DM, left
ventricular systolic dysfunction or previous
thromboembolic events (Mitchell, 2011, 2166).

AF can cause atrial thrombi, which can lead to
embolic stroke. AF is diagnosed by ECG and is
treated with anticoagulation medication or other
drugs that work to correct sinus rhythm.
Sometimes, surgery is required to install a
pacemaker that works to correct sinus rhythm
(Mitchell, 2011, 2165).

b. MNT for Cardiovascular Disease

Therapeutic Lifestyle Changes (TLC) is helpful for
preventing Coronary Heart Disease (CHD) and
reducing cardiovascular disease (CVD). These
guidelines in conjunction with the Dietary
Approaches to Stop Hypertension Diet (DASH),
which increases fruits, vegetables, whole grains,
lean meats and non-fat dairy products (while
decreasing processed foods) are helpful in
prevention and treatment (Raymond & Couch,
2012, 753).

Dietary Pattern for TLC:
Total fat should be restricted to 25-35% of total
calories. Saturated fat should contribute >7% of

calories and trans fatty acids should be kept as close
to zero as possible. Therefore, only lean meats,
poultry and fish should be included in the diet.
Protein in this dietary pattern attributes to 15% of
total calories. Polyunsaturated fats (PUFAs) and
monounsaturated fats (MUFAs) can help to lower
triglycerides and LDL while raising HDL should
contribute 10% and 20% of calories respectively.
Carbohydrates, mostly fiber rich whole grain,
should contribute to 50-60% of the diet. Guidelines
recommend 2 g of fiber daily. Cholesterol is
restricted to 200 mg/daily. Desirable body weight
should be obtained and further weight loss should
be prevented. The guidelines also recommend
moderate physical activity daily (Raymond &
Couch, 2012, 753).


HTN is defined as sustained SBP and DBP
greater than 140 and 90 mm Hg (Escott-Stump,
2012, 367). Pre-HTN is defined as SBP between
120-139 mm Hg or DBP b/w 80-89 mm Hg. Stage
1 HTN (140 to 159/90 to 99 mm hg) is the most
prevalent level seen in adults – this population is
most likely to have MI or CVA (Raymond &
Couch, 2012, 758). HTN risk increases with age
and therefore is prevalent in the elderly. HTN
doubles risk for heart attack, stroke, HF (Escott-
Stump, 2012, 367). Essential HTN (HTN with
unknown cause) is prevalent in 90-95% of pt
(Raymond & Couch, 2012, 758).

HTN is asymptomatic until complications develop
(Bakris, 2011, 2067). Sx of HTN include frequent
headaches, impaired vision, sob, nosebleeds, chest
pain, dizziness, failing memory, snoring, sleep
apnea and GI distress (Escott-Stump, 2012, 367).

Sleep apnea, drug-related causes, CKD, Cushing’s
syndrome, steroid therapy, pheochromocytoma,
reno vascular disease can cause high BP (Escott-
Stump, 2012, 368). Lifestyle choices such as poor
diet, smoking, physical inactivity, stress, obesity
can contribute to HTN. Secondary HTN is a result
of another disease, usually endocrine in nature
Pt’s diet PTA " in fat

Pt’s BP 146/90 mm Hg.

Diet hx reveals diet " in fat, large portion
BMI = 43: class III obesity

(Raymond & Couch, 2012, 758).

If left untreated, HTN can lead to stroke, HF, renal
failure, MI, accelerated bone loss, increase risk of
fracture and LT memory problems (Escott-Stump,
2012, 367).

c. MNT for HTN

For dietary tx of HTN, the DASH diet is
recommended. DASH is rich in fiber, includes 5-
10 servings of fruit and vegetables a day and non-
fat dairy products. In comparison to BP lowering
medication, DASH significantly reduced BP
(Escott-Stump, 2012, 368). DASH can reduce SBP
8-44 mg Hg. Sodium should be limited to 2300
mg/day. If target BP is not reached, sodium can be
further decreased to 1600 mg/day. Reduction of
sodium can reduce SBP 2-8 mm Hg (Raymond &
Couch, 2012, 762).

Fish oil rich in omega-3, antioxidants such as
vitamin C, folic acid, vitamin K, soy protein and a
Mediterranean style diet may also have a positive
effect in HTN tx (Escott-Stump, 2012, 368).
Including physical activity of 30 min/day on most
days can reduce SBP by 4-9 mm Hg Reducing
ETOH to 2 drinks/day for men and 1 drink/day for
women can reduce SBP 2-4 mm Hg (Raymond &
Couch, 2012, 762).

By following DASH and including an exercise
regime, weight management can be achieved and
possibly reduce SBP by 5-20 mm Hg (Raymond &
Couch, 2012, 762).

D. Gout

Gout is a collection of monosodium urate crystals
into tissue (McCarty, 2011, 350). The etiology
behind gout is unknown (McCarty, 2011, 354), but
gout can be induced by diuretics (Bakris, 2011,
2071). Accumulation, called tophi (Winkler &
Malone, 2012, 917) usually occurs in and around
joints and can cause recurrent acute or chronic
arthritis. Diagnosis is determined by clinical
criteria and presence of crystals in synovial fluid

Currently consuming " Na+

Pt. is Rx’d Lasix.

(McCarty, 2011, 349). Tests performed include
synovial fluid analysis, serum urate level and x-rays
(McCarty, 2011, 351). Gout occurs more often in
men during middle age. If a pt under 30 develops
gout, it is often more severe (McCarty, 2011, 350).

Sx of gout include acute pain, tenderness, warmth,
redness and swelling in affected areas (McCarty,
2011, 349.) Pain is often nocturnal. The areas most
affected is the metatarsophalangeal joint of the
great toe but it can occur in the hip, shoulder,
sacroiliac, sternoclavicular or cervical spine joints.
(McCarty, 2011, 350). Another site for tophi is the
helix of the ear (Winkler & Malone, 2012, 917). Tx
for gout includes anti-inflammatory drugs, treating
co-existing HTN, hyperlipidemia and obesity and
prevention of further deposition of crystals by
lowering serum urate level (McCarty, 2011, 352).

d. MNT for Gout

Gout has been traditionally treated by a low purine
diet, but has since been replaced by drugs, allowing
the diet to treat gout to become more liberalized
(Gomez & Kaufer-Horwitz, 2012, 917). It is not
recommended that pts follow a balanced diet c!
limited intake of animal foods, alcohol, avoidance
of foods high in purine, fructose and non-complex
carbohydrates. Portion control should also be
emphasized. Weight loss and glycemic control
can help to improve gout. High fluid intake (8-
16 cups daily) should be encouraged to help
excrete uric acid and minimize kidney stone
formation. Foods high in alkaline such as dairy,
eggs, vegetable proteins, cherries and coffee may be
protective against uric acid build up since the foods
are alkaline in nature (Gomez & Kaufer-Horwitz,
2012, 918).

E. Type 2 Diabetes Mellitus

Total carbohydrate intake eaten regardless of the
source is the primary determinant of postprandial
Type 2 diabetes mellitus (T2DM) is marked by
inadequate insulin secretion. While insulin levels
are high in Type 2, peripheral insulin resistance and

Pt. is a middle aged man at age 56.


Indicated for DM as well/in DASH Diet

Not indicated due to CKD.

" in hepatic glucose production make insulin
available inadequate to normalize glucose level
(Crandall, 2011, 867). T2DM accounts for 90-95%
of all DM cases; many undiagnosed (Franz, 2012,
678). Risk factors include genetic and
environmental factors, older age, obesity
(particularly intraabdominal), physical inactivity,
prior hx of gestational DM, race and ethnicity
(Franz, 2012, 678).

Blood glucose (BG) levels " after eating,
especially after a meal " in carbohydrate. BG
levels take longer to return to normal post-prandial
(Crandall, 2011, 867). Obesity and weight gain
contribute to insulin resistance. Adipose tissue "
plasma levels of free fatty acids and adipocytokines
impairing glucose transport and muscle glycogen
synthase activity (Crandall, 2011, 868).

Symptoms of DM during periods of hyperglycemia
include: frequent voiding of urine, polyuria and
polydipsia. Dehydration may occur. Weight loss,
nausea, vomiting, blurred vision and a
predisposition to bacterial or fungal infections may
occur (Crandall, 2011, 868).

Complications can result from poorly managed
DM, primarily vascular complications, that can
result in retinopathy, nephropathy and neuropathy.
Microvascular disease also impairs skin healing that
can compromise skin integrity. HTN and
dyslipidemia are commonly seen in patients with
DM (Crandall, 2011, 869). Screening for
complications related to DM should become five
years after diagnosis including food examinations,
funduscopic examinations, urine testing for
proteinuria and microalbuminuria and measurement
of creatinine and blood lipid profiles (Crandall,
2011, 871).

DM is diagnosed by monitoring fasting plasma
glucose levels but sometimes, oral glucose
tolerance testing (OGTT) is performed. OGTT is
more sensitive but less convenient and therefore
often only reserved for diagnosing gestational DM
(Crandall, 2011, 871). A random glucose test >

Fingerstick Glucose 138, 160, 168 mg/dL
2 hrs. post-prandial

Glucose 214 mg/dL on 2/10/14.

200 mg/dL may be diagnostic but it may also be
influenced by a recent meal and must be confirmed
by repeat testing if no other symptoms are present.
Hemoglobin (Hb) A
allows for a retrospective
look at glucose levels over the preceding 2-3
months. Urine glucose measurement is no longer
used (Crandall, 2011, 871).

Goals for glycemic control:
-BG 80-120 mg/dL during the day
-BG 100-140 mg/dL at bedtime
levels < 7% (Crandall, 2011, 872).

In the critically ill and hospitalized patients, blood
glucose levels should be ~110 mg/dL. Pts in
hospital will usually require IV insulin (Escott-
Stump, 2012, 548).

e. MNT for Type 2 DM

MNT for T2DM requires an individualized
approach. There is no single “diabetic” diet but a
diet prescription based on individual needs and
goals (Escott-Stump, 2012, 521). Pts should be
educated on self-management via diet and self-
monitoring of blood glucose (SMBG) (Franz, 2012,
684). Diet should be reduced in calories and fat,
carbohydrate counting or exchange lists with simple
meal plans, physical activity and behavioral
strategies should be incorporated in treatment
(Franz, 2012, 684).

glucose levels (Franz, 2012, 684). Carbohydrate
should contribute to 45-65% of total energy intake
(Escott-Stump, 2012, 546). Consistency in
carbohydrate intake eaten at each mealtime or snack
can help to improve glycemic control either solely
by diet therapy, or in combination with glucose
lowering medications or insulin regimens (Franz,
2012, 684). Carbohydrate counting considers 15 g
of carbohydrate to be 1 serving. Exchange lists
group foods into list depending on their
carbohydrate content. This method utilizes symbols
to identify foods high in fiber, fat or sodium (Franz,
2012, 685). Protein should contribute 15-20% of
total calories if renal function is normal. If the

No HbA
test ordered.

Pt’s FSBG WNL for hospitalized pt.
kidneys are affected, protein restriction to 0.8-1.0
g/kg is recommended (Escott-Stump, 2012, 546).
Fat can contribute 25-35% of total calories but
saturated fats should be restricted to 7-10%,
focusing on a higher intake of PUFAs and MUFAs
(Escott-Stump, 2012, 546). The DASH diet
principals are useful in planning a DM diet plan, as
it will help to manage HTN if present and reduce
NA+. Less than 2400 mg Na+ is recommended
(Escott-Stump, 2012, 546).

Testing pre-meal and post-meal glucose levels can
help pts to make adjustments to their meal planning
(Franz, 2012, 685). These diet plans are portion
controlled and can lead to weight loss. Moderate
weight loss of 5-10% can ! hyperglycemia,
dyslipidemia and hypertension (Escott-Stump,
2012, 546).

Part II: continued

Summary of Medical Text Findings Comparison of Patient to Text
d. Medications: list medication,
indication, effect of food and drug
interactions relative to nutrition: factors
that can affect nutrition
intake/GI/vitamins, minerals and labs.
B. Medications: how is medication
affecting patient? Is patient
experiencing any side effects?
1. Lovenox/heparin
Anticoagulant. May cause abdominal pain,
GI bleeding, constipation and black tarry
stools. Caution c! DM & ESRD. ! Platelets.
" AST, " ALT, " PT/INR (Pronsky, 2012,

2. Prinivil
Angiotensin Converting Enzyme (ACE)
inhibitor, antihypertensive. Used to treat left
ventricular dysfunction, CHF post MI, acute
MI, diabetic nephropathy. Insure adequate
fluid intake, ! Na, ! cal diet may be
recommended. Avoid salt substitutes, caution
c! K supplements. May cause anorexia. "K, !
Na (Pronsky, 2012, 36).

Heparin is giving prophylactically in hospital.
Not likely related to abdominal pain pt was

Dx: A-fib, CKD, DM

3. Humalog/insulin lispro
Antidiabetic, hypoglycemic. Use c! diabetic
meal plan to balance carbohydrate c! doses. "
wt. Avoid ETOH. Large wt. gain " insulin
needs. ! Glucose, ! HbA1
! K, ! Mg, ! P
(Pronsky, 2012, 167).

4. Lopressor/metoprolol
Antihypertensive, antiangina, CHF tx (XL), MI
tx. Beta-blocker. ! Na, ! Cal diet. Avoid
natural licorice. May cause dry mouth, N/V,
dyspepsia, diarrhea, constipation. Caution c!
DM as it may mask hypoglycemia/may !
insulin release. (Pronsky, 2012, 206).

5. Zosyn/penicillin
Antibiotic. May cause anorexia, dry mouth,
taste changes, N/V, epigastric distress.
Caution c! renal func. " K, " Na.

6. Lasix/furosemide
Anti-hypertensive, diuretic (K-depleting).
Used for tx of edema associated with CHF,
renal or hepatic disease. Take on empty
stomach, food ! bioavailability, but may take
with food/milk if GI upset occurs. Avoid
natural licorice. Limit alcohol. ! BP with
possible hypotension. Lab values may indicate
! K, ! Mg, ! Na, ! Cl, ! Ca and " glucose
(Pronsky, 2012, 110).

Vomiting likely not caused by medications.

Summary of Medical Text Findings Comparison of Patient to Text
C. Laboratory Tests: key tests and their
implications relative to patient’s
medical problems; include reasons for
increase and decrease for each lab.
e. Laboratory Tests: assess patient’s
laboratory values; refer to chart on first
page or use values from your facility;
note if any medications are affecting
lab values.
1. Red Blood Cell Count: Norm (F: 3.9-
5.5, M: 4.7-6.1 million/mm
" c! polycythemia, dehydration, severe
! c! anemia, hemorrhage, Fe def, systemic
disease (Pronsky, 2012, 352).

2. Mean Corpusal Volume: Norm (78-93)
" with megaloblastic anemia due to Fol or Vit
B12 def, liver disease, reticulocytosis,
Spurious with cold agglutinins.
! with Fe def anemia, hereditary,
spherocytosis, thalassemia minor, sideroblastic
anemia, Pyr-responsive anemia, lead poisoning
(Pronsky, 2012, p. 349).

3. Hemoglobin: Norm (12.1-15.6 g/dL)
" c! severe burns, polycythemia, shock
! c! anemia, blood loss, hemolysis, leukemia,
hyperthyroidism, cirrhosis, over hydration
(Pronsky, 2012, 346).

4. Hematocrit: Norm (34-45%)
" c! dehydration, polycythemia, CHF,
thalassemia, COPD, dehydration.
! c! anemia (<30), hyperthyroidism, cirrhosis,
many systemic diseases (eg. Leukemia, Lupus,
Hodgkin’s disease), HIV/AIDS (Pronsky,
2012, 346).

5. Albumin: Norm (3.5-5.0 g/dL)
" c! dehydration
! c! edema, hepatic disease, malabsorption,
diarrhea, burns, eclampsia, ESRD,
malnutrition, low pro intake, stress, over-
hydration, cancer (Pronsky, 2012, 340).

6. Calcium (Ca): Norm (8.4-10.2 mg/dL)

MCV ! (70.8, 69.1, 70.1)

! RBC (4.04, 3.86), ! Hgb (9.9 !, 9.6 !) and
! Hct (28.9, 27.9, 27.3) may be related to
CKD, blood draws for tests


Ca++ WNL
" c! cancer, hyperparathyroidism, adrenal
insufficiency, hyperthyroidism, Paget’s
disease, prolonged immobilization, excessive
Vit D or Ca intake, LT use of thiazide
diuretics, respiratory acidosis, milk-alkali,
Chronic renal failure, granulomatous disease
! c! hypoaluminemia, elevated phosphorus,
alkalosis, diarrhea, hypoparathyroidism, sprue,
osteomalacia, malabsorption, diarrhea, acute
pancreatitis, hypomagnesemia, starvation,
steroid use, vit D def (Pronsky, 2012, 342).

7. Phosphorus: Norm (2.3-4.3 mg/dL)
" c! ESRD, hypocalcemia, hypervitaminosis D,
bone tumors, Addison’s, hypoparathyroidism,
acromegaly, sickle cell anemia
! c! hyperparathyroidism, alcoholism,
hypovitaminosis D, rickets or osteomalacia,
hyperinsulinism, acute gout, overuse of P
binders, Cushing’s syndrome, salicylate
poisoning, DM, alcoholism (Pronsky, 2012,

8. Blood urea nitrogen: Norm (8-23
" (azotemia) c! renal failure (> 50 = serious
impairment), shock, dehydration, infection,
DM, chronic gout, excessive pro
intake/catabolism, MI
! c! hepatic failure, malnutrition,
malabsorption, overhydration (excessive IV
fluids), pregnancy, SIADH (Pronsky, 2012,

9. Creatinine: Norm (0.4-1.2 mg/dL)
" c! acute & chronic renal disease, muscle
damage, hyperthyroidism, muscle mass,
starvation, diabetic acidosis, high meat intake,
gigantism, acromegaly.
! c! pregnancy (Pronsky, 2012, 344).

10. Sodium (Na): Norm (136-144 mEq/L)
" (hypernatremia) c ! dehydration & low fluid
intake, diabetes insipidus, Cushing’s
syndrome, coma, primary aldosteronism.
! (hyponatremia) c ! edema, severe burns,

Phos WNL

BUN" (136, 145, 154)

Creat " (5.3, 5.6)

Na+ ! (129, 128, 126)

Lasix Rx’d
severe diarrhea/vomiting, diuretics, SIADH,
water intoxication, Addison’s disease, severe
nephritis, starvation, hyperglycemia,
malabsorption, AIDS (Pronsky, 2012, 352).

11. Potassium (K): Norm (3.5-5.0 mEq/L)
" (hyperkalemia) c! renal failure, tissue damage,
acidosis, Addison’s, uncontrolled DM, internal
hemorrhage, overuse of K suppl, acute AIDS.
! (hypokalemia) with GI loss, IV fluid with
without K suppl, alcohol abuse, malabsorption,
malnutrition, diarrhea, vomiting, chronic stress
or fever, K depleting diuretic, steroid,
estrogen use, hepatic disease with ascites,
excessive licorice intake, renal disease
(Pronsky, 2012, 351).

12. Glucose: Norm (70-109 mg/dL)
" c! DM, Cushing’s syndrome, Thi def,
acromegaly, gigantism, chronic hepatic
dysfunction, severe infections,
hyperthyroidism, pancreatitis, chronic hepatic
disease, prolonged physical inactivity, chronic
hepatic disease, prolonged physical inactivity,
chronic malnutrition, K def drugs (eg
corticosteroids), high dose, antihypertensives,
! c! insulin overdose, islet-cell carcinoma,
bacterial sepsis, hypothyroidism, Addison’s
disease, extensive liver disease, glycogen
storage disease, alcohol abuse, starvation,
vigorous exercise, pancreatitis, oral
hypoglycemic drugs (Pronsky, 2012, 345).

13. Magnesium (Mg): Norm (1.3-2.1
" c! renal failure, diabetic acidosis,
hypothyroidism, Addison’s, dehydration,
overuse of Mg supplement or antacid.
! c! chronic diarrhea, alcoholism, pancreatitis,
renal disease, hepatic cirrhosis, toxemia of
pregnancy, hyperthyroidism, malabsorption,
ulcerative colitis, K-depleting diuretics,
malnutrition (Pronsky, 2012, 348).

14. Chloride (Cl): Norm (98-107 mEq/L):

K+ ! (3.0)

Glu " 214, ! 56

Rx’d Lasix, Prinvil, Lopressor

Insulin given in hospital, not routinely used @

Mag 1.8 WNL

" c ! dehydration, eclampsia, anemia,
hyperventilation, cardiac decompensation,
renal insufficiency, aspirin toxicity, diarrhea,
diabetes insipidus
! c ! diabetic acidosis, fever, acute infections,
metabolic alkalosis, protracted vomiting, K
deficiency, chronic respiratory acidosis,
SIADH (Pronsky, 2012, 343).

15. Serum Iron (Fe): Norm (F: 30-160, M:
50-170 µg/dL)
" c ! excessive Fe intake, hemolytic anemias,
hepatic disease, estrogen use, hemochromatosis
c ! Fe def anemia, chronic diseases, infections,
hepatic disease, surgery, MI (Pronsky, 2012,

16. Ferritin: Norm (F: 12-150, M: 30-320
" c! inflammatory diseases, chronic renal
disease, malignancy, hepatitis, Fe overload,
! c! Fe def anemia (Pronsky, 2012, 344).

17. Folic Acid: Norm (2.8-40 ng/mL)
! with megaloblastic or hemolytic anemia,
malnutrition, folate antagonist drug (eg.
Anticonvulsant, methotrexate, oral
contraceptives), malabsorption (eg. Sprue,
celiac disease), alcoholic hepatic disease,
hyperthyroidism, vit C def, dialysis, febrile
states, pregnancy, cancer (Pronsky, 2012, 345).

18. Vitamin B12: Norm (210-91 pg/mL)
" (> 1100 pg/mL) with hepatic disease, some
leukemias, cancer (especially with hepatic
metastasis), pregnancy, oral contraceptives
! (< 100 pg/mL) with pernicious anemia,
malabsorption syndromes, primary
hypothyroidism, ! gastric mucosa (eg.
gasterectomy or stomach cancer), vegetarian
diet, achlorhydria (Pronsky, 2012, 354).

19. Creatine clearance GFR: Norm (M: 85-
125, F: 75-115 mL/min)

Cl ! (85, 84) (K ! on 2/10/14)

Fe ! (31)

Ferritin WNL

Folate WNL

Vit B

GFR 14
" in acromegaly and burns
! in CHF, glomerular disease, eclampsia,
gout, multiple myeloma (Pronsky, 2012, 344).

Part III: Nutrition History:

A. Food Intake Pattern/Nutrition History
Directions: Record food intake over a 24-hour period including time eaten and portion sizes. Include all
food, condiments, alcoholic and carbonated beverages. If eating pattern differs each weekend or due to
different work shifts, record on a separate sheet. Food intake can be calculated by hand or computer.

Usual intake at Home or Hospital (circle one)

Meal Intake/Amt
Breakfast 2 eggs c! 2 slices cheese, made in bacon fat or salted butter (1 pat)
Plus 1 T ketchup
2 slices white toast c! salted butter, 1 T grape jelly
4-5 slices bacon
Sometimes: 1 orange or 1 glass ~12 oz. orange juice/apple juice
Coffee c! cream and sugar
Lunch 2 Egg salad sandwiches c! regular mayonnaise on white bread
1 can Sprite soda
2-3 handfuls potato chips, usually sour cream & onion or plain flavor
Snack 2 shortbread cookies & tea made c! whole milk and sugar
Dinner 5 Pork roast medallions or 1 large breast of fried chicken
Mashed potatoes made c! cream, butter (large portion of late, ~2 cups)
Green beans (~15 pcs)
Dessert 1 slice apple pie c! vanilla ice cream (1 scoop)

B. Nutritional Analysis

Protein meets recommended quantity, but due to GFR should be restricted from 0.8 to 0.6 g/kg. Na+ is
significantly higher than recommended (2.3g/day) (Escott-Stump, 2012, 869). Phosphorus intake is " by
599 mg. K intake is under recommended daily allowance of 2.4 g/day (Escott-Stump, 2012, 869). Pt
chooses foods " in fat and does not utilize carbohydrate counting to maintain blood glucose control.

Iron (mg) 8.00 Do not exceed 45 mg *
Magnesium (mg) 420.00 Do not exceed 350 mg by supplement *
Phosphorus (mg) 700.00 Do not exceed 4000 mg *
Potassium (mg) 4,700.00
Sodium (mg) 1,300.00 Less than 2300 mg - lower for some
people +
Zinc (mg) 11.00 Do not exceed 40 mg *
* Dietary Reference Intakes - For Adult 19-70 years, non-pregnant
+ 2010 Dietary Guidelines for Americans
Bar Graph Report
The Bar Graph Report displays graphically the amount of the nutrient consumed and compares that to the
dietary intake recommendations.
0 50 100 Percent Nutrient Value 150 DRI Goal
Basic Components
Calories 3,579.35 110 % 3,249.22
Calories from Fat 1,596.97 176 % 909.78
Calories from SatFat 545.99 187 % 292.43
Protein (g) 110.23 110 % 99.79
Carbohydrates (g) 383.46 86 % 446.77
Sugar (g) 176.93
Dietary Fiber (g) 19.29 42 % 45.49
Soluble Fiber (g) 1.73
InSoluble Fiber (g) 2.57
Fat (g) 177.44 176 % 101.09
Saturated Fat (g) 60.67 187 % 32.49
Trans Fat (g) 1.30
Mono Fat (g) 47.19 131 % 36.10
Poly Fat (g) 15.85 49 % 32.49
Cholesterol (mg) 1,049.98 350 % 300.00
Water (g) 2,145.88 58 % 3,700.00
Vitamin A - RAE (mcg) 811.95 90 % 900.00
Vitamin B1 - Thiamin (mg) 1.73 144 % 1.20
Vitamin B2 - Riboflavin (mg) 2.39 184 % 1.30
Vitamin B3 - Niacin (mg) 33.56 210 % 16.00
Vitamin B6 (mg) 2.47 146 % 1.70
Vitamin B12 (mcg) 4.00 167 % 2.40
Vitamin C (mg) 182.30 203 % 90.00
Vitamin D - mcg (mcg) 3.59 24 % 15.00
Vitamin E - Alpha 12.06 80 % 15.00
Folate (mcg) 377.93 94 % 400.00
Calcium (mg) 915.99 92 % 1,000.00
Iron (mg) 13.74 172 % 8.00
Magnesium (mg) 249.95 60 % 420.00
Phosphorus (mg) 1,599.01 228 % 700.00
Potassium (mg) 3,694.54 79 % 4,700.00
Sodium (mg) 5,499.66 423 % 1,300.00
Zinc (mg) 9.73 88 % 11.00
Omega-3 (g) 0.98
Omega-6 (g) 7.02
Alcohol (g) 0.00
Caffeine (mg) 90.72
Spreadsheet Report
The Spreadsheet shows all the values for all nutrients. Nutrients are displayed horizontally, with totals at the
bottom of the list.
Item Day Meal Amount Cals FatCal SatFatCal Prot (g)
Fri 01-24-
Breakfast Eggs, whole, lrg, fried (USDA each 2 180.3 126.7 35.5 12.5
Cheese, American, past, proc, each 2 157.5 118.1 74.3 9.3
Butter, salted (USDA SR-21) tbsp 2 203.8 207.3 131.3 0.2
Ketchup (USDA SR-21) tbsp 1 14.6 0.4 0.1 0.3
Bread, white, soft, slice (USDA each 2 133.0 14.8 3.1 3.8
Jelly, concord grape (J.M. tbsp 1 50.0 0.0 0.0 0.0
Bacon, brld/pan fried/rstd, med piece 5 216.4 150.3 49.0 14.8
Juice, orange, 100%, cnd/btl oz 16 206.2 0.0 0.0 0.0
Lunch Sandwich, egg salad, w/white each 2 757.6 430.6 68.5 18.8
Soda, Sprite (Sprite) oz 12 136.1 0.6 0.2
Chips, potato, sour cream & each 2 320.0 180.0 18.0 4.0
Dinner Fried Chicken, breast, each 1 217.6 78.2 21.6 31.2
Mashed Potatoes, prep f/recipe cup 2 474.6 159.1 78.2 7.9
Snap Beans, green, ckd, drained cup 1 43.7 3.1 0.5 2.4
Snack Cookies, shortbread, plain, 1 each 2 80.3 34.6 8.6 1.0
Tea, brewed w/tap water (USDA oz 16 4.5 0.2 0.1 0.0
Sugar, white, granulated (USDA tbsp 1 48.9 0.0 0.0 0.0
Milk, whole, 3.25% (USDA SR-21) tbsp 2 18.3 8.9 5.1 1.0
Apples, pie spiced, w/natural cup 1 140.0 0.0 0.0 0.0
Ice Cream, vanilla (USDA SR-21) oz 3 176.1 84.2 52.0 3.0
Day Total -- 3579.4 1597.0 546.0 110.2
Average Day Total -- 3579.4 1597.0 546.0 110.2
Item Day Meal Carbs (g) Sugar (g) Fiber (g) Fib-S (g) Fib-I (g) Fat (g)
Fri 01-24-
Breakfast Eggs, whole, lrg, fried (USDA 0.8 0.8 0.0 0.0 0.0 14.1
Cheese, American, past, proc, 0.7 0.2 0.0 0.0 0.0 13.1
Butter, salted (USDA SR-21) 0.0 0.0 0.0 0.0 0.0 23.0
Ketchup (USDA SR-21) 3.8 3.4 0.0 0.0 0.0 0.0
Bread, white, soft, slice (USDA 25.3 2.1 1.2 1.6
Item Day Meal ExOth ExStar ExVeg ExFat
Fri 01-24-
Snack Ice Cream, vanilla (USDA SR-21) 1.3 1.8
Day Total 5.5 12.6 1.7 23.7
Average Day Total 5.5 12.6 1.7 23.7
Calories and Fat
The Calories and Fats report is useful for quickly seeing the calorie and fat breakdowns of your intake. The
Source of Calories window shows graphically the percentage of calories from protein, carbohydrates, fat, and
alcohol. The Source of Fat window shows the breakdown of fat (saturated, monounsaturated, polyunsaturated,
and other fats).
Source of Calories Calori Gram Percent
Protein 12 %
Carbohydrates 43 %
Fat (Total) 45 %
Alcohol 0 %
Total 3579
Saturated Fat 546 60.7 15%
Mono Fat 425 47.2 12%
Poly Fat 143 15.9 4%
Trans Fat 12 1.3 0%
*The N/A Fat category includes the glycerol portion of the
fat molecule (typically 5%), as well as any unavailable
values for saturated, mono, poly, and trans fats.
P:S ( Poly Fat / Saturated Fat ) 0.26 : 1
Potassium : Sodium 0.67 : 1
Calcium : Phosphorus 0.57 : 1
CSI ( Cholesterol / Saturated Fat ) 113.77
Source of Fat (approx.) Fat (g) Percent
Saturated Fat 34 %
Mono Fat 27 %
Poly Fat 9 %
Trans Fat 1 %
Total (g) 177.4
*The N/A Fat category includes the glycerol portion of the
fat molecule (typically 5%), as well as any unavailable
values for saturated, mono, poly, and trans fats.
Starch 12.60
Other Carbs 5.53
Very Lean Meat
Fruit 5.56
Vegetables 1.74

Part IV: Nutrition Care Process: Assessment, Diagnosis, Intervention, Monitoring and
Evaluation (ADIME)

S: Pt. came to the ED c! abdominal pain, nausea and vomiting. Pt. reports that he has a
RD that he sees on an outpt basis but admits he has difficulty following his diet at home. Pt.
finds it difficult to follow his diet because it is restrictive at times. As a pastor, he attends a lot of
events (such as weddings, funerals) that serve catered foods " in carbohydrate and fat. Food
being offered to him is hard for him to turn down. He tries to avoid sugar and soda and has
attempted to " his vegetable intake. In the hospital, pt has a good appetite and he says he has ate
>75% of all meals served.
O: 56 y/o #. Dx: acute on chronic kidney disease. PMH: A-fib (pacemaker), HTN,
Gout, DM Type 2, CKD Stage 4. Rx: Lovenox, Prinivil, Humalog, Lopressor, Zosyn and Lasix.
Ht: 68” Wt: 275# (2/10/14). UBW: 270s. %IBW: 179%. %UBW: 100%. BMI: 43, Class III
Obesity. Diet Rx: K2gm, ! Na, ! Chol, 2000 kcal DM providing 1870 kcal, 99 g PRO. Labs:
(2/10/14): RBC 4.08 WNL, Hbg 9.9 !, Hct 28.9 !, MCV 70.8 !, Alb 3.6 WNL, Ca++ 9.6 WNL,
BUN 136", Creat 5.3", Na+ 129!, K 3.0 !, Glu 214", Cl 85!. (2/11/14) RBC 4.04!, MCV
69.1!, Hgb 9.9!, Hct 27.9!, Alb 3.5 WNL, Phos 3.7 WNL, BUN 145", Creat 5.3", Na+ 128!,
Mag 1.8 WNL, Fe 31!, Ferritin 246 WNL, Folate 12.2 WNL, Vit B12 1174 WNL. (2/12/14)
RBC 3.86!, MCV 70.1!, Hgb 9.6 !, Hct 27.3!, Ca++ 9.4 WNL, Phos 2.8 WNL, BUN 154",
Creat 5.6", Na+ 126!, K+ 3.7 WNL, Glu 56!, Mag 1.8 WNL, Cl 84!. GFR 14.
A: PES #1: Not ready for renal/DM diet change related to disinterest in applying
knowledge and lack of self-efficacy for making change evidenced by negative body language
and defensiveness when discussing renal/DM diet.
PES #2: Excessive sodium and phosphorus intake related to lack of application of knowledge of
renal diet evidenced by 24-hour diet recall and verbalization of difficulty following renal diet at
Calorie needs 35 kcal/kg using IBW of 77 kg ~2700 kcal/daily. Current usual intake,
evidenced by 24-hour recall provides 3579 kcal/daily: 133% of EEN. Protein needs in CKD
Stage 4 are 0.6 g/kg of IBW until initiation of HD. Protein needs are 46 g/day; current diet
intake is " in protein providing 240% of protein needs. Protein needs when HD is initiated will "
to 77-100 g daily (1.0-1.3 g/kg). Fluid needs are 750-1000 mL. Na+ should be limited to 2.3
g/day and currently Pt is taking in 3.7 g. Phos should be limited to 0.8-1 g, pt’s diet recall
reveals 1.6 g of phos intake. Guidelines for K+ are 2.4 g/daily. K+ intake is within guideline
limits; K+ lab values trended up and are now WNL. Pt is at high nutritional complexity due to
advancement of CKD to Stage 5 and impending initiation of HD. No edema or s/s of
dehydration are noted in this pt, however, his abdomen appears to be distended.
Due to ! H&H and ! MCV, Fe deficiency anemia is likely and may be related to CKD or
due to blood losses from tests performed while in hospital. BUN/Creat " likely due to renal
insufficiency. Gout can also " BUN. ! Na+, ! Cl and ! K+ may be due to Lasix Rx and
possibly exacerbated by AKI. Glucose indicates poor glycemic control.

Part IV: Nutrition Care Process continued (Intervention, Monitoring and Evaluation)

Goal 1:
Lower serum Na+ and Phos to WNL
Plan 1:
-Provide reinforcement of nutrition education
regarding high/low Na+ and Phos foods
-Work c! pt to come up with sample menu
including food prefs
-Educate for self-monitoring strategies
including food diary
-Recommend Phoslo phosphate binder
-Monitor serum Na+ and Phos on lab reports

Goal 2:
" H&H and MCV to WNL
Plan 2:
-Recommend Epogen & Venofer

Goal 3:
Maintain glucose between 80-120 mg/dL

Plan 3:
-Provide education reinforcement of
carbohydrate counting, incorporating
carbohydrates into renal meal plan (mentioned
-Encourage self-monitoring of blood glucose

Long Term (if pt. returns to outpatient clinic):

Goal 4:
Encourage 10% wt loss (~30#), 1-2# per week.

Plan 4:
-Encourage portion control in combination c!
renal & DM diet recommendations
-Provide pt c! benefits of wt reduction in Tx of


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