Documente Academic
Documente Profesional
Documente Cultură
Serum Na: 136 - 145 mmol/L Urine Protein: 6.4 - 8.3 g/dL
2. AKI can be classified into the following 3 categories. Define each one and list 1 or 2
examples of possible etiologies.
Pre Renal: inadequate renal perfusion - severe dehydration / circulatory collapse.
Post Renal: urinary tract obstruction - carcinoma of the bladder or prostate / bilateral ureteral
stones and obstruction.
Intrinsic: diseases within the renal parenchyma - acute tubular necrosis / nephrotoxicity (drugs
or contrast agents).
3. List the general medical nutrition therapy guidelines followed in acute kidney injury. Note
possible reasons for deviation from these guidelines.
Sodium: 2-3g/day for anuric/oliguric phase based on blood pressure and edema. During the
diuretic phase, replace based on urine output, edema, need for dialysis, and serum Na levels.
Potassium: 2-3g/day for anuric/oliguric phase. Replace losses depending on urine volume,
serum potassium levels, and need for dialysis or medication during the diuretic phase.
Fluid: 500 mL + total output for the anuric/oliguric phase. Large volume of fluids may be needed
during the diuretic phase (assess frequently).
Calories: 25-35 kcal/kg or use indirect calorimetry. Consider stress level and include energy
from RRT if applicable.
Part III: Chronic Kidney Disease (CKD)
A. The progression of chronic kidney disease can be divided into 5 stages based on GFR and
results in complications prior to the initiation of renal replacement therapy. These stages, as
defined by the National Kidney Foundations K/DOQI (Kidney Disease Outcomes Quality
Initiative), were released in January 2002. It is important to be familiar with these guidelines to
know when nutritional intervention should begin. Please refer to the chart in the appendix to
these worksheets.
2. List the changes in blood chemistries that occur with uremia. What is the end product of
protein breakdown?
There is an unacceptable level of nitrogenous wastes in the body, fluid and electrolyte
disturbances, and glucose intolerance. The end product of protein breakdown is amino acids,
which have nitrogen in their makeup. The nitrogen is normally excreted by the kidney in the form
of urea, but remains in the body with CKD.
3. What is the etiology of the metabolic acidosis associated with uremia and why is it important to
correct?
The etiology is the impaired kidney function not excreting the nitrogen/urea as it should and
impaired catabolism of protein substances which the kidney normally breaks down.
2. Describe the parameters used to identify when a patient with CKD should be instructed to
restrict protein. What is the KDOQI recommendations for protein?
Protein restriction should begin at a GFR < 50. Protein restriction depends on stage of
CKD, diabetes, dialysis, HBV, and whether the person is catabolic. The KDOQI
reccomendations say 0.8g/kg body weight per day
(https://www2.kidney.org/professionals/KDOQI/guideline_diabetes/guide5.htm).
4. Describe high biological value; list food source of HBV; and explain how it
is used with patients with chronic kidney disease. What percentage of the protein
prescription is recommended as high biological value?
Protein that has all of the essential amino acids and a high protein digestibility corrected amino
acid score. 50-60% of protein should be from sources of HBV to allow for optimal protein use.
5. List the vitamins that may be inadequate in a diet with < 60 gm protein/day.
Vitamin E and B vitamins, including niacin, thiamin, riboflavin, and vitamin B6
(https://www.choosemyplate.gov/protein-foods-nutrients-health).
6. What are the indications for restricting sodium and potassium for CKD Stage 3-4? What
sodium restriction is recommended for CKD Stage 3-4?
Sodium restriction of 2.4 g/day according to the EAL. Potassium should be restricted to
less than 2.4 g/day.
7. What are the KDOQI recommendations for phosphorus allowed in the diet for CKD Stage
3-4?.
EAL: 800mg to 1,000mg per day or 10mg to 12mg phosphorus per gram of protein.
(Could not find KDOQI guidelines)
8. How and when the decision to restrict phosphorus is made?
Controlling phosphate is important in the early stage of the CKD. Those with a GFR less
than 60 are evaluated for bone disease and benefit from phosphorus restriction.
1. In Peritoneal dialysis (PD) waste products are removed from the blood by the process of
diffusion across a semi-permeable membrane down a chemical concentration gradient. The
lining of the peritoneal cavity is used as the semi-permeable membrane and dextrose solutions
are used as the dialysate. What 3 things determine the amount of fluid and solute removed
during PD?
Concentration of dextrose, the rate of equilibration between the dialysate and the blood, and
dwell time.
Part V: Hemodialysis
1. What are the KDOQI protein recommendations for a patient on hemodialysis? What is the
rationale for this protein allowance? What percentage of protein that should be HBV?
KDOQI guidelines recommend 1.2 g/kg standard body weight per day with at least 50%
being HBV. The rationale: protein is lost through HD, so the recommendations are designed to
compensate these losses.
2. What is the preferred weight gain between hemodialysis treatments? How are fluid
recommendations determined? .
1 kg/day or less. It should not exceed 5% of the patients body weight between dialysis
treatments. The recommendations should be individually assessed based on the patients
comorbid conditions, age, activity level, and body size.
3. State the amount of sodium recommended and explain the reason for sodium
restriction in hemodialysis patients.
2-3 g/day. Hypertension in CKD is usually salt sensitive and lowering sodium intake to 2
g/day lowers thirst, extracellular fluid volume, weight, proteinuria, and blood pressure while
enhancing the effects of antihypertensive medications (Byham-Gray, Stover, & Wiesen, 2013,
p. 57).
1. State the normal range for hematocrit/hemoglobin. Why is hemoglobin x3 a better reflection
of anemia in CKD than hematocrit? Explain the etiologies of anemia in
dialysis patients. Provide possible treatment options to reduce or minimize the
occurrence of anemia.
Current target hemoglobin levels are 10-12 g/dl. In CKD, anemia is often caused by
depressed EPO, which decreases hemoglobin levels. Hematocrit levels are more susceptible to
hydration changes, so the hemoglobin is a better indicator of anemia. Other etiologies of anemia
in dialysis patients include insufficient iron supply in bone marrow, blood loss through the GI
tract, blood sampling, and blood loss through access sites and dialyzer leaks. Anemia can be
treated with EPO stimulating agents (ESA) and iron supplementation.
3. List the acceptable laboratory values for the dialysis patients in the center to
which you are assigned.
his is the excessive secretion of parathyroid hormone in response to low blood calcium levels.
T
The failing kidneys to not convert enough vitamin D to its active form nor do they excrete
phosphate adequately. Therefore, calcium phosphate forms in the body and removes calcium
from the blood.
2. State the GFR level at which the plasma phosphorus begins to increase.
Explain the importance of dietary intervention to limit phosphorus at this critical
stage.
6. What are the KDOQI recommended maximum amounts of oral/dietary Calcium that a
dialysis patient should ingest? Why?
No more than 2,000 mg, so your body can get the vitamin D it needs.
VIII: Transplant
Chapter 3
Read: Adult Kidney Transplantation by Linda S. Blue, MS, RD, FADA
In Comprehensive Guide to Transplant Nutrition, Jeanette M. Hasse, PhD, RD, FADA
and Linda S. Blue, MS, RD, FADA, editors
1. Renal transplant patients require immunosuppressive agents for the rest
of their lives. The most common three agents are tacrolimus, prednisone
and Cellcept. List the common side effects of each and how they are
treated.
3. What are the four most common long-term adverse nutritional side effects
of the immunosuppressive meds? List them and how they are treated.
5. W
hat are the three categories of kidney transplant patients?
6. N
ame three common diseases that cause chronic kidney disease?
7. W
hat is ATN and what causes it?