Download Renal Failure Case Study

Chronic Kidney Disease &
Renal Failure
A Case Study
McKinsey Wilson
NDFS 4560
Introduction
Patient (pt) KS was admitted to the hospital for hemodialysis (HD) treatment after being
diagnosed (dx) with renal failure due to a history of polycystic kidney disease. This case study
will address the pathophysiology of chronic kidney disease (CKD) along with the medical
history, treatment, and nutrition therapy for KS.
1. Patient Profile and Social History
KS is 21 year-old (y/o) Caucasian female with a weight (wt) of 59 kg and a height (ht) of
168 cm with no significant weight loss prior to admission (pta). KS is currently a college student
and living with roommates. She has strong family support at home with medical treatments and
relies on them for financial assistance. Due to a hectic lifestyle, diet adherence may be a
challenge once KS returns to everyday life.
2. Medical History
KS was diagnosed with polycystic kidney disorder June 2005 and has required close
monitoring of kidney function for the past seven years. Since then, KS has progressed to renal
failure and now requires HD treatment and a closely monitored diet that will be discussed in
more detail.
3. Chronic Kidney Disease- Literature Review
An estimated 13.1% of the US population is diagnosed with Chronic Kidney Disease (CKD),
and the prevalence of the disease is predicted to increase in the upcoming years (1). With such an
apparent health problem in the US today, it is important to understand the nature of the disease,
treatments, and nutrition therapy in order to better help those with CKD and reduce the risk of
others developing this disease.
Functions of the Kidney:
The kidneys have a variety of functions that are crucial to sustaining life. Kidneys are
primarily responsible for sodium regulation through sodium absorption during urine formation.
Aldosterone regulates sodium and potassium transfer in order to maintain balance. Closely
associated with sodium balance is fluid balance; the kidneys produce the hormone rennin that
promotes either fluid excretion or absorption to achieve electrolyte and fluid homeostasis (1,2).
Also regulated by the kidneys is plasma volume, which largely determines cardiac output and
blood pressure. Vitamin D is absorbed by the body, and the kidneys will then convert Vitamin D
to its active form, thus promoting calcium absorption. Erythropoietin (EPO), a hormone that
stimulates red blood cell (RBC) production, is produced by the kidneys, giving them a large
influence over iron levels and risk for anemia. The absorption of bicarbonate and release of
hydrogen ions by the kidneys help the body to keep pH balance. With CKD, all of the beforementioned functions can be significantly compromised and may lead to a variety of adverse
effects (1).
Pathophysiology:
Chronic Kidney Disease is a progressive disease that causes degenerative renal function
and ultimately leads to renal failure (2). Many of the symptoms and complications of CKD stem
from the loss of primary functions in the kidney. With decreased kidney function, sodium is not
reabsorbed effectively, which leads to sodium retention and edema (1). Edema disturbs the fluid
and plasma balance, which in turn increases the risk for hypertension and cardiovascular disease
(CVD) (3). Ascites and edema was noted for KS, which increases the patient’s risk for CVD.
Other electrolyte balances, especially potassium, are poorly regulated; the kidneys fail to excrete
excess potassium, and it begins to collect in the blood and causes hyperkalemia (1). According to
lab values, KS has hyperkalemia, and if the levels are high enough, it may result in arrhythmia
(1).
Urine formation declines with decreasing kidney function, and nitrogenous waste begins
to build up in the blood that later leads to azotemia (urea in the blood) and uremia (1). Iron
deficiency and microcytic anemia become major concerns with CKD patients; as EPO hormone
production slows, there is a reduction of total RBCs, and in turn, lower iron levels. KS’s
hematocrit and hemoglobin (h/h) levels are low due to a decrease in EPO production, putting the
patient at an increased risk for iron deficiency. With CKD, the kidneys are unable to excrete H
ions to maintain pH balance and metabolic acidosis can occur (1).
Parathyroid Hormone (PTH) is an essential part of the kidneys’ role in calcium
absorption and bone health. PTH controls calcium reabsorption, phosphorous excretion, and
Vitamin D activation. The kidneys are not sensitive to this hormone in CKD and will result in
hypocalcemia, hyperphosphatemia, and decreased bone strength (1). KS is currently receiving K
Hectoral, a medication to help with hypoparathyroidism. Because of the medication and related
lab values, it can be inferred that KS has a decreased PTH response and is susceptible to the
complications mentioned above.
Etiology:
Chronic Kidney Disease is primarily caused by two other comorbid conditions, diabetes
(DM) and hypertension (HTN) (1,3). Hyperglycemia related to diabetes increases the risk of
diabetic nephropathy, which will slowly harden the kidney’s glomeruli. Kidney filtration will
begin to slow, and CKD will develop (1). Hypertension also increases the likelihood of
developing CKD or accelerates the deterioration of kidney function. Researchers from one study
concluded that patients with CKD and HTN had higher levels of proteinuria, an indicator of
decreased kidney function, than patients with CKD alone (4). Metabolic Syndrome, if diagnosed
with HTN and type 2 DM, is also a large contributing factor to CKD (2). Based upon laboratory
data, KS is at a high risk for CVD, so blood pressure, cholesterol, and lipid levels should be
monitored closely.
Diagnosis:
In diagnosing CKD, there are two areas that determine the level of kidney function:
Glomerular Filtration Rate (GFR) and the presence of proteinuria (3). According to the National
Kidney Foundation, the GFR is the standard for diagnosing CKD. GFR is the rate at which the
glomeruli are able to clear substances from the plasma that circulates through the kidneys (1,3).
Table 1 depicts the five stages of CKD that are defined by specific GFR ranges (1,2,5).
Proteinuria is a better indicator of kidney damage and disease progression (2,3).
Presence of protein in the urine increases as kidney function decreases, and the normal level of
protein excretion in the urine is 50mg/day. High proteinuria levels also tend to be more prevalent
in the diabetic population with CKD (3). Even though proteinuria is a good indicator of kidney
damage, GFR is most commonly used for diagnosis because there are clearly defined treatments
for each stage of CKD. Together GFR and proteinuria content provide an accurate prognosis on
overall kidney function.
The current patient was diagnosed with polycystic kidney disorder seven years ago, and
based upon GFR, has progressed to stage 5 kidney failure and will require the necessary medical
treatment which will be explained in the following section.
Table 1: 5 Stages of CKD and GFR
Stage 1
>90mL/min/1.73𝒎𝟐
60-89
Stage 2
30-59
Stage 3
15-29
Stage 4
<15
Stage 5- Renal Failure
Medical Treatment:
Treatment of CKD varies upon the stage of renal function. Before a patient reaches stage
5 of kidney disease, the primary focus of treatment is to control comorbid conditions, such as
diabetes and hypertension management, in order to prolong further kidney deterioration. If a
patient does have stage 5 kidney disease (renal failure), kidney replacement therapy is needed to
carry out the functions of the kidney, whether it be by kidney transplant or dialysis (3).
Hemodialysis (HD) and Peritoneal Dialysis (PD) are the two types of dialysis treatments
that are available to CKD patients. For patients who have HD, an arteriovenous fistula (AVF) in
the arm is used as a permanent access point for dialysis treatments. HD functions for the kidneys
by slowly removing the patient’s blood, filtering out waste, and returning the cleaned blood back
to the body. This process occurs three to four times a week, taking approximately three hours
each time. For PD, access point is surgically made into the peritoneum, where dialysate enters
through a catheter, changes the osmolarity, and causes the waste to be excreted through a
separate catheter (1). Patient KS requires HD three times per week, and his/her diet will need to
be modified to reflect the requirements for HD treatment.
Medical Nutrition Therapy:
Just as medical treatment is determined by the stages of kidney disease, medical nutrition
therapy is altered based upon the needs of the patient in a given stage of CKD. For Stages 1 & 2,
dietary control of comorbid conditions is recommended. This means strict glycemic control for
CKD patients with DM to help lower the risk of nephropathy (5). A cardiac diet for those with
HTN and at risk for CVD is recommended. Kidney degeneration is accelerated by CVD, so
maintenance of HTN is crucial (5). KS had a high triglyceride and cholesterol lab values and a
blood pressure (BP) of 220/80, indicating HTN and an increased risk of CVD; a cardiac diet
would be beneficial for this patient.
For Stages 3 & 4 of CKD, adequate nutrition is the main focus in order to prevent
malnutrition and to maintain lean body mass (1). A lower protein diet is recommended since the
kidneys have trouble with excreting nitrogenous waste. Protein needs should be calculated based
upon the level of kidney function (5). Continuation of comorbidity management is
recommended.
Once a patient reaches Stage 5 Renal Failure, dietary needs and restrictions become much
more specific to prevent deficiencies or toxicities. Major nutrients of concern include: protein,
potassium, phosphorous, sodium and fluid, and additional vitamin/mineral supplementation.
Specific needs will vary between PD and HD.
Stage 5 patients have higher protein requirements because protein loss and catabolism
increases to roughly 10-12g of amino acids per day. Protein requirements increase to 1.2-1.5g/kg
for patients on PD and 1.2-1.4g/kg for patients on HD (1). Patients with PD have an increased
risk for peritonitis, which increases protein losses up to 50-100%. Additional protein is needed
until inflammation subsides (1).
Potassium recommendations vary greatly between HD and PD patients. HD patients are
restricted to 2-3g/day to prevent hyperkalemia, but PD patients do not require any restrictions
because kidney filtration is daily and more direct. Supplementation may even be needed if PD
patients become hypokalemic. High potassium foods to avoid include: legumes, bran, leafy
greens, milk, bananas, and chocolate. Low potassium foods to suggest include: rice, pasta,
apples, grapes, peaches, peas, and peppers (1).
Phosphorous can accumulate in both HD and PD patients, so the recommendation for
phosphorous is 800-1000mg/day or <17mg/kg body weight. Phosphate binders may also be
needed to decrease the availability of phosphorous in the blood. High phosphorous foods to
avoid include: dairy products, legumes, nuts, seeds, and whole grain products (1). Obtaining
adequate calcium can be difficult, because most high calcium foods are also high in
phosphorous. It is recommended that calcium be supplemented in the diet to reach calcium
requirements without increasing phosphorous levels (1).
Fluid and sodium recommendations often go hand in hand. Sodium should be restricted
to 2-4g/day to prevent fluid retention and edema. Fluid needs are based on urine output, meaning
low urine output may decrease recommended fluid intake. HD patients should be limited to 1L
fluid/day while PD patients can have up to 2L/day. PD patients are allotted more fluids because
dialysis occurs on a daily basis (1).
To minimize micronutrient deficiencies, supplementation of a few key vitamins and
minerals are recommended. Due to a lack of Vitamin D activation, Vitamin D should be
supplemented in the diet. Iron supplementation is needed with decrease EPO production to help
prevent iron deficiency (1). Other water soluble vitamins may become deficient during dialysis
and should be monitored on a regular basis. Fat soluble vitamins tend to accumulate in CKD
patients and can quickly reach toxic levels if supplemented. Because of this high risk,
supplementation of any fat soluble vitamins is not recommended (5). All of the above mentioned
recommendations for HD patients should be applied in the nutrition intervention for KS.
Conclusion:
Chronic Kidney Disease is a degenerative disease that will ultimately lead to kidney
failure. The goal in treatment is to prolong disease progression by treating comorbidities,
implementing a diet that will lighten the kidneys’ burden, and preventing possible nutrient
deficiencies. This diet includes limited phosphorous, potassium, salt, fluid, and protein intake.
Once CKD has progressed to kidney failure, the diet must be based off of pertinent lab values
because some of these nutrients can build up to toxic levels quickly, so phosphorous, potassium,
sodium, BUN, and creatinine are some of the labs that should be monitored closely. Nutrition
therapy plays an essential role in the treatment, and together with appropriate medical treatment,
can improve the patient’s quality of life.
4. Treatment and Progress
KS will continue to receive HD treatments three times per week until otherwise indicated
by the nephrologist. KS also received education on the renal diet for HD from the Registered
Dietitian (RD). The RD also prescribed a vitamin/mineral supplement that meets requirements
for HD patients. KS then had a two week follow-up appointment with RD to assess diet
adherence. To treat anemia, KS received EPO at 30 units/kg. KS receives Hectoral, a medication
to treat hypoparathyroidism and dialysis patients, four times per day, three days a week. KS is
responding well to treatments, and based upon 24-hour recall, demonstrated understanding of
renal diet.
5. Nutritional Status
Anthropometrics:
Upon admit, the patient’s weight was 59 kg with a height of 168 cm, giving KS a body
mass index (BMI) of 21. KS is at a healthy weight and reports no significant weight gains or
losses prior to admission. After discharge, KS experienced a 2.3 kg wt loss after two weeks of
diet adherence, giving the pt a new wt of 56.7 kg and a BMI of 20. A 4% loss of total body
weight within two weeks is of moderate concern, so increasing energy intake may be necessary
to prevent further weight loss.
Biochemical: Lab Data
The following abnormal lab values are determinants of KS’s medical status. All abnormal
values are related to decreased kidney function.
Lab
Admit Normal Values
8.6
12-15
Hgb
34
37-47
Hct
88
80-100
MCV
110
Platelets
150-400 x 103 𝑚𝑚2
130
136-145mml/L
Sodium
5.8
3.5-5.5 mmol/L
Potassium
3.4-4.5mg/dL
Phosphorous 2.9
36
23-35 mmol/L
Total CO2
69
8-18 mg/dL=
BUN
12
0.6-1.2 mg/dL
Creat
1.8
0-0.4 mf/dL
Billi
10.3
11-16 sec
PT
10
15-60 pg/mL
Vit D
99
160-700 ng/dL
Folate
18
60-130mcg/dL
Zinc
220
120-199 mg/dL
Chol
200
35-135
TG
Low h/h levels, along with a normal MCV indicate normocytic anemia, but KS is still at
risk for an iron deficiency due to a decrease in EPO production. Decreased EPO production also
caused low platelet count. KS has high BUN and Creatinine levels, which according to the
National Kidney Foundation, indicate kidney failure (3). Phosphorous and sodium are currently
low, but since these are nutrients of concern with CKD, should be monitored closely and still
may need to be restricted in the diet. Phosphorous may also be falsely low due to a Vitamin D
deficiency (6).
Vitamin D, Folate, and Zinc deficiencies were noted. These micronutrient deficiencies
may be due to malnutrition prior to admission. Vitamin D may also be low due to a decrease in
responsiveness to PTH. Folate deficiency also increases the risk of Vitamin B12 deficiency.
Supplementation of the following micronutrients may be required (1,6).
KS’s cholesterol and triglyceride levels are high, which puts the patient at an increased
risk for HTN and CVD. Since HTN and CVD are common comorbidities of CKD, a cardiac diet
may be helpful in reducing additional risks for KS. Diabetes is the other is also a comorbidity of
CKD, and although, the patient’s blood glucose levels are normal, they should be monitored on a
regular basis to prevent the onset of DM (1).
Medications:
KS is currently receiving EPO (r-HuEPO) hormone treatment at 30 units per kg body
weight, and this drug requires iron, Vitamin B12, and Folate supplementation. Iron deficiency is
a common concern with this medication. EPO may increase blood pressure (BP) and cause
nausea and vomiting (n/v). BP should be monitored closely, since KS is already at has HTN and
an increased risk for CVD (7).
KS also receives Hectoral at 2.5 mcg four times a day, three times per week. This
medication may cause weight loss and decreased thirst response. Vitamin D and magnesium
supplementation is not recommended with this medication. Hectoral can also increase serum
calcium, phosphorous, magnesium, cholesterol, BUN, and Creat. KS’s renal function should be
monitored closely (7).
Captopril, an antihypertensive medication, may decrease food absorption up to 30-50%.
If patient’s weight begins to decline, increased energy needs may be required. KS may also
experience anorexia and weight loss as a side effect to this medication (7).
Clinical:
Upon admission, KS appeared pale and lethargic, which may be a marker for nutrient
deficiencies. Pitting edema was noted in the knees as well ascites in the abdominal area. The pt’s
apparent dry skin and lethargy may be due to dehydration or fluid imbalances. KS’s skin appears
yellowed due to bilirubin accumulation. Vitals taken showed KS was hypertensive with a BP of
220/80. Aside from the HTN, the heart rate (HR) was rapid but regular at 86 beats per minute
(BPM). A 24-hour urine collection was performed while KS was in the hospital. KS had a very
low urine output of 0.3ml/kg, and no protein or glucose was found in the urine.
Dietary:
Prior to admission, KS was consuming approximately 1900 Calories (kcals), 60g of
protein, and fluid intake not known, but KS reports to “just drink when thirsty.” KS’s calcium,
iron, phosphorous, and potassium intakes were already within the recommendations for HD
patients. Even though intake of phosphorous and potassium were at normal levels, excess dairy
and whole grains were noted in the diet and should be eaten more sparingly. Low fruit and
vegetable intake was also noted. Protein, fiber, and sodium intake did not meet the
recommendations for the renal diet. During meal planning the RD and KS should find food
sources that are higher in protein and fiber. Processed and other higher salt foods were noted in
the diet; it would be important for KS to focus on whole foods and cooking from scratch more
often.
2 Week Follow-Up:
KS met with RD two weeks after discharge to assess adherence to the renal diet. KS kept
a food log for the past two weeks and expressed the challenges that she faced in implementing
the diet. Some of the days were close to meeting the nutritional requirements while other days
KS had an energy intake well below the recommended intake, which led to inconsistency in the
diet. KS did meet protein needs, but with such a frequent intake of eggs, cholesterol intake was
too high for a cardiac diet. KS was unable to increase fiber intake, so a fiber supplement may be
needed to meet recommendations. Calcium intake lowered with the decrease in dairy
consumption; alternative calcium sources or calcium supplementation may need to be added to
the diet. Phosphorous, potassium, and sodium intake were all within HD renal diet
recommendations. Fruit and vegetable consumption increased and saturated fat intake decreased.
KS made substantial improvement in her diet, but further alterations need to be made to better
promote kidney and heart health.
6. Summary and Conclusions
After receiving HD treatment and nutrition education on the renal diet for HD patients,
KS was discharged from the hospital. KS was also treated with EPO hormone therapy and was
prescribed medications to help with HTN and dialysis management. KS verbalized
understanding of renal diet and made noticeable changes in her diet. Calorie, fiber, and calcium
intake need to be increased and should be monitored upon the next follow-up appointment. KS is
encouraged to continue HD treatments and the renal diet. Pertinent lab values will continue to be
monitored closely.
7. Nutrition Notes
ADIME: (at discharge)
A: 21 y/o pt, KS dx w/ renal failure d/t polycystic kidney disorder. Edema noted in knees and
ascites in abdomen. Very low urine output noted from 24-hr collection and dry skin may be
possible dehydration or fluid imbalance. Apparent yellowed skin indicates bilirubin
accumulation. Pt hypertensive w/ BP 220/80. Pt c/o n/v. HD prescribed 3x/wk per MD and renal
diet education w/ vit/min recommendations by RD. Labs of concern: low h/h, platelet count,
reticulocyte, folate, and high bilirubin d/t decrease in EPO production. Folate def inc risk of Vit
B12 deficiency. Na low d/t hypervolemic state and edema. K high r/t dec kidney fxn of K
excretion. Vit D low d/t dec PTH fxn. Phos low d/t Vit D def. Zn low d/t malnutrition and dec
abs. High CHOL, TG, and BP inc risk of CVD. Medications to note: Captopril can dec food abs
30-50%. EPO inc BP and Fe, Vit B12, and folate supp recommended. Hectoral- adequate Ca and
no Vit D supp recommended. Anthros: ht: 168cm, wt: 59kg, BMI: 21 w/ no significant wt loss
PTA. All abnormal lab values associated w/ renal failure. Estimated needs based upon ABW:
1830kcal (1900 kcal for meal plan), 71-83g pro, 1020 ml, (2000ml for meal plan) fluid, may
need restriction. P: 800-1000mg/day, Na: 2g/day, K: 2-3g/day.
Medical hx includes polycystic kidney disease dx 7 yrs ago. Diet hx before renal diet indicates
adequate Ca, K, P intake. Fiber intake low and sodium exceeds renal diet recommendations. F/v
intake low, and dairy and whole grain intake high for HD diet. Family and social hx non
contributory to dx at the time.
D: Altered nutrition-related lab values (NC-2.2), r/t kidney failure, AEB low h/h, folate, Zn, Vit
D, and high K, BUN, and Crea.
I: Nutrition Education- Nutrition relationship in health/disease (Kidney failure) (E-1.4)
 Educate pt on Renal Diet
o Nutrients of concern:
 Potassium: 2-3g/day – provide food examples
 Fluid: 1L/day – fluid restriction and thirst quenching recommendations
 Na: 2g/day – no added salt
 Phos: limited to 800-1000mg/day – provide food examples and educate on
phosphate binders
 Ca: <2000mg/day – supp required
o Together w/ pt, come up w/ 3-day meal plan that meets Renal Diet requirements.
(see attached meal plan)
 Educate on heart healthy diet
o Low sat/trans fat, inc MUFA and PUFA
o <2 g Na
o Inc f/v, fiber
Goals:
- Pt verbalizes understanding of Renal Diet and food options
- Pt intake PO 100%
- Pt lab values will be WNL on f/u appt
- Pt will maintain wt w/ diet implementation
Food and Nutrient Delivery- Vitamin and Mineral Supplement (ND-3.2)
 Renal MVI (ND-3.2.1)
 Vitamins (ND-3.2.3)
o Vit B12 (11)
 Minerals (ND-3.2.4)
o Ca (1): Ca Citrate @ 1500mg/day
M/E: F/u w/ pt in 2 weeks to monitor adherence to diet by using 24hr recall. Monitor the
following lab values to assess nutrition status: h/h, K, Ca, Na, Vit D, Folate, Zn, CHOL, and
TRIG. Make adjustments to diet plan if labs still abnormal. Monitor I/O in case of need for fluid
restrictions.
Day 1
Breakfast
Snack
Lunch
Snack
Dinner
Frosted flakes
Milk 1%
Strawberries
White toast w/ jelly
Grape Juice
Apple w/ dip
Chicken Wrap
Tortilla- white flour
Chicken, cooked w/
canola oil and spices,
pepper
Low sodium cheese
Lettuce
Lemonade
Crackers, LS
Squash and Herb
Pasta
Meatballs, LS
Lemon garlic
asparagus
Jello w/ whipped
topping
1 cup
4 oz
½ cup
1 slice
1T
6 oz
1 med ¼ cup
dip
1 each
2 oz
1 oz
½ cup
10 oz
15 each
1 cup
3 Day Meal Plan
Day 2
Breakfast
Snack
Lunch
4 oz
6 spears
Dinner
½ cup
Day 3
Breakfast
Snack
Lunch
Rice Chex
1 cup
Milk 1%
4 oz
Pears, canned
½ cup
Apple Cider
8 oz
Bagel- blueberry
½ each
Cream cheese
2T
Turkey Sandwich
White bread
2 slices
Turkey, LS
2 oz
Mozarella, LS
1 oz
Mustard
To taste
Lettuce
3 leaves
Fruit smoothie
6 oz
Strawberry/blueberry
Dinner
Snack
Chicken Fajitas
Chicken, grilled w/ cumin
3 oz
Onion
1/8 cup
Olive oil
1T
Peppers
¼ cup
Garlic
½ clove
Spanish rice (recipe)
½ cup
Mixed vegetables
½ cup
Tortilla- white
1 each
Berry cobblerhomemade- LS
½ cup
Snack
English muffin w/
margarine
Scrambled egg
Peaches, canned
Apple Juice
Yogurt, Greek
Graham crackers
Taco Pasta Salad
(recipe)
Applesaucecinnamon
Homemade tortilla
chips, LS
Homemade Corn
Chowder (recipe)
Dinner roll, white
Salad
LS dressing
Cranberry juice w/
diet Sprite
Raspberry sherbet
1 each
1T
2 large
½ cup
6 oz
4 oz
4 squares
1 cup
½ cup
15 each
1 cup
1 each
1 cup
2T
8 oz
½ cup
8. References
1. Nelms M, Sucher K, Lacey K, Roth S. Diseases of the Endocrine System. In: Nutrition
Therapy & Pathophysiology. 2nd ed. Belmont, CA: Wadsworth, Cengage
Learning; 2011:302,471-519.
2. Porter R, Kaplan J. The Merck Manual. 19th ed. Whitehouse Station, NJ: Merck Sharp &
Dohme Corp; 2011.
3. National Kidney Foundation. Definition and Classification of Stages of Chronic Kidney
Disease. Am. J. Kidney Dis. 2002;39(2):46-75.
4. Peterson J, Adler S, Burkart J, et al. Blood Pressure Control, Proteinuria, and the
Progression of Renal Disease. Ann. Intern. Med. 1995;123(10):754-762.
5. Beto J, Bansal V. Medical Nutrition Therapy in Chronic Kidney Failure: Integrating
Practice Guidelines. J. of ADA. 2004;104(3):404-409.
6. Bakerman S. ABC’s of Interpretive Laboratory Data. 4th ed. Scottsdale, AZ: Interpretive
Laboratory Data, Inc; 2002.
7. Pronsky Z, Crowe J Sr. Food Medication Interactions. 17th ed. Birchunville, PA: FoodMedications Interactions; 2012.