kidney 2 Flashcards
Antihypertensive Agents
- ACE-Inhibitors, -Adrenergic blockers, Angiotensin II Receptor Blockers
- Can increase serum K levels
- Ca Channel Blockers
Diuretics
-K sparing or K losing, depending on type
Lipid Lowering Agents (people with chronic kidney desease are more at risk for coronary heart disease
e.g. Statins, Fibrates
Phosphorus Binders
–IF SERUM [PHOSPHATE] ELEVATED.
-Take with meals to bind phosphate and prevent its absorption from the GIT. —Aluminum Based -Amphojel & Basaljel —Calcium Based -Oscal & Tums —Non-Aluminum, Non-Calcium (NANC) Based -Renagel & Fosrenol
Vitamin D Analogues (often later stages)
e. g. Calcitriol
- as 1,25 dihydroxycholecalciferol since kidney cannot efficiently hydroxylate 25-OH cholecalciferol at the 1-postion.
Sodium polystyrene sulfonate
-a cation-exchange resin to bind K.
IF SERUM K IS HIGH.
Diuretics
- Potassium sparing (e.g. spironolactone/Aldactone)
- Potassium wasting (e.g. furosemide/Lasix)
Anemia Management SIGNIFICANT PROBLME IN CHRONIC KIDNEY DISEASE
-Causes:
treatment
a) erythropoietin production erythrocyte production = major cause
b) (later) blood losses associated with dialysis and laboratory tests may contribute.
c) dietary factors – poor intake-may contribute.
Treatment: —Human recombinant erythropoietin Eprex or Aransep —Adequate nutritional support for the increased erythrocyte production Iron B12 Folate
NUTRITIONAL CARE Nutritional recommendations vary for: • acute renal disease • chronic kidney disease -Stages 1-4 -Stage 5- renal replacement therapy -hemodialysis -peritoneal dialysis -renal transplantation Hemodialysis Renal transplantation
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-Objectives of nutritional care:
- Maintain optimum nutritional status.
- Minimize metabolic disorders & related symptoms:
i) reduce intake of substances that the kidney can no longer excrete well
ii) provide replacements for compounds lost in quantities. - Retard progression of disease: help people with overweight or obesity
Individualize guidelines for each patient throughout care. Based on blood work and history
Protein-energy malnutrition is a very common problem in those with advanced chronic kidney or in those undergoing dialysis.
There are many causes:
• Poor food intake due to:
o Anorexia caused by uremia (don’t feel like eating)
o Altered taste
o Unpalatable prescribed diets
• Catabolic response to the illness and chronic inflammation
• Dialysis causes loss of some nutrients and promotes protein catabolism
• Endocrine disorders of uremia (high wate products in the blood) (e.g. resistance to insulin and IGF [insulin-like growth factor])
• Accumulation of uremic toxins
Nutritional Care: Stages 1-4
= the stage prior to dialysis, transplantation.
Protein
HOW MUCH? CONSULT TABLES
Note the difference between Stage 3&4. – look at tables. Prn – as required
-With progression through stages 1 through 4, endproducts of protein metabolism are not being eliminated normally in the urine (uremia).
- Consider all sources of these endproducts:
1) Exogenous protein intake: with dietary protein
2) Endogenous protein breakdown.
-Factors that muscle catabolism uremia:
• inadequate energy intake
• inadequate protein intake
• unbalanced protein
-How do we deal with these metabolic alterations from a nutritional point of view?-Recommendations intended to:
- Aim: Do not provide excess protein to prevent accumulation of endproducts + maintain N balance.
- i.e. match the dietary protein to the workload capability of the kidneys.
- Note small increase in protein requirement in earlier stages related to issues described above for protein-energy malnutrition.
• prevent symptoms associated with uremia nausea, vomiting, fatigue.
• delay progression of kidney disease.
[evidence from Modification of Diet in Renal Disease (MDRD Study) and others].
Know the g/kg… on tables
Energy
HOW MUCH? CONSULT THE TABLES. BUT, assessment of individual energy requirement required- stays the same in each stage
WHY THE DIFFERENCE BY AGE?
How to assess whether you are meeting protein and energy needs:
BMR goes down
-protein recommendations assume energy needs are met by nonprotein sources.
-important to meet energy requirements and minimize endogenous protein catabolism to supply energy.
a) accumulation of protein breakdown products
e.g. serum [urea] –but note it is nonspecific, being affected by:
• renal function serum [urea]
• protein intake serum [urea]
• inadequate energy intake serum [urea]
b) nutritional assessment tests of protein and energy status
-biochemical and anthropometric assessment
-Appropriateness of level of protein intake is continually assessed and adjusted as required.
Biochemical and anthropometric assessment
Biochemical: would serum [albumin] be useful? Its going to go down so wont tell as much about nutritional status as we would like
Example of anthropometric measurement?
Fluid
HOW MUCH? NOTE CHANGE BETWEEN STAGES 1/2 AND 3/4. WHY?
½ stage: stay well hydrate
3- stay hydrated but restrict as needed
4- stay hydrated but restrict as needed
If dietary Na diminishes, thirst often decreases appropriately.
- IF DIETARY Na DIMINISHES, THIRST OFTEN DECREASES APPROPRIATELY.
- BUT, as urine output declines, may come a time when fluid has to be restricted to equal fluid loss. E. g. Volume of urine output for previous day + ~1000 ml to compensate for nonurinary losses.
