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What is GFR for each of the 5 stages of CKD?
- 1: GFR > 90
- 2: GFR 60-89
- 3: GFR 30-59
- 4: GFR 15-29
- 5: GFR < 15 (on dialysis)
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What is the leading cause of CRF? The second leading cause?
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What is normal serum phosphorus?
2.7 to 4.5
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What is the goal for the Calcium x Phosphorus product? At what value does mortality increase?
< 55
72
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Medical issues resulting from hyperphosphotemia, hyperparathyroidism
- Alterations in lipid metabolism
- Insulin secretion
- Epo resistance
- Renal osteodystrophy
- Vascular calcification
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When treating Hyperparathyroidism why not give Vitamin D first?
Because it will increase the absorption of phosphorus in addition to the abs of calcium. You would increase the Ca x P product and get more vascular calcification. You have to get the P under control before giving Vit D.
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Why must patients take hyperphosphotemia meds with meals?
Because they bind Phosphate in the diet and it is excreted in feces
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Discuss Calcium Acetate (PhosLo)
- MOA: Binds dietary P and excretes in feces
- AEs: Constipation, N/V/D, abdominal pain, hypercalcemia
- DI: decreases FQs by 50%, interferes with abs of iron, zinc, PPIs, H2 antags
- Monitoring Parameters: Monitor P and Ca q2w during titration
- Place in therapy: Probably considered 2nd line now d/t potential for Ca deposits. However, it is cheap and should be used for patients who are paying cash. Also use if Ca is < 8.2
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Discuss sevelamer (Renagel)
- MOA: binds dietary P. Also lowers LDL and raises HDL.
- AEs: Constipation, N/V/D, abdominal pain, hypercalcemia
- DIs: Cipro, cyclosporine, omeprazole
- Monitoring parameters: P and Ca q2w during titration
- Place in therapy: First line agent. Preferred in pts @ risk for extraskeletal calcification - does not contain Ca. Generic. Lowers LDL, raises HDL.
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Discuss lanthanum (Fosrenol)
- MOA: Phosphate binder
- AEs: constipation, N/V/D, abdominal pain, hypercalcemia
- DIs: levothyroxine
- Monitoring parameters: P q2w during titration (then less often)
- Place in therapy: 2nd line. Pretty new - we have more experience with sevelamer. No generic yet.
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What are the parathyroid goals for stage 3, 4, and 5 CKD?
What is normal?
- 3: 35-70
- 4: 70-110
- 5: 150-300
Normal: 10-55
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Discuss Calcitriol for hyperparathyroidism
- MOA: Upregulates Vitamin D receptors. Suppresses PTH. Increases serum Ca. Increases GI abs of Ca and P.
- AEs: hypercalcemia, hyperphosphatemia
- DIs: Its abs is decreased by cholestyramine
- Monitoring Parameters: Vitamin D levels, Ca, P, PTH. Once stable, check q 12 mo in Stage 3 and q3mo in Stage 4
- Place in therapy: Used after getting the P conc and P x Ca product under reasonable control. Hold if Ca is > 10.2 or if PTH is under 150.
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Discuss Zemplar for hyperparathyroidism
- MOA: Suppress PTH, increases Ca and P abs from the GIT
- AEs: hypercalcemia, hyperphosphotemia
- DIs: CYP 3A4
- Monitoring Parameters: Check q 12 mo once stable in stage 3. Q 3 mo for stage 4
- Place in Therapy: Used after getting P conc and P x Ca under reasonable control.
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Discuss cinacalcet (Sensipar) for hyperparathyroidism
- MOA: calcimimetic - acts on Ca-sensing receptors, increasing the sensitivity to Ca and decreasing the secretion of PTH (decreasing serum Calcium)
- AEs: N/V, hypocalcemia
- DIs: CYP 2D6 and 3A4
- Place in therapy: Use as a 2nd line agent after Vitamin D replacement if PTH is still not controlled. (Don't start if Ca is 8.4 or less)
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List reasons pts with CRF can have anemia
- 1. Blood loss d/t blood draws
- 2. Blood loss d/t hemodialysis
- 3. Decreased RBC life span d/t uremia buildup
- 4. Iron deficiency
- 5. Decrease in Epo production (#1 cause)
- 6. Folate/B12 deficiency - taken off by dialysis because they are water soluble
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At what hemoglobin levels does workup for anemia start?
- For premenopausal women, < 12 g/dL
- For postmenopausal women and males, < 13.5 g/dL
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What is the normal hemoglobin level?
12 - 18
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What is the goal Hgb level for CKD?
11-12 g/dL
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At what Hgb level do we begin treatment for anemia?
9 g/dL
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What is the transferrin saturation goal?
>20%
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What is the serum ferritin goal?
> 100 ng/mL
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What is the serum iron goal?
65-185 mcg/dL
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What is normal MCV?
80-100
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Discuss "Epo" for the treatment of anemia secondary to renal failure
epoetin alfa, darbepoetin alfa (Epogen, Procrit, Aransep)
- MOA: stimulate erythroid progenitor cells and release reticulocytes from bone marrow into the bloodstream where they mature into RBCs
- Routes of Admin: IV or SC
- Directions for Admin: admin via venous line at the end of dialysis
- AEs: stroke, HTN, thrombosis, death
- Monitoring parameters: BP, Hct, Hgb, Iron before. After stable, monitor q 3 mo.
- Place in therapy: Anemia of chronic disease with Hgb < 9 g/dL. Hold if Hgb is > 13 g/dL. Increases risk of serious CV events
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Discuss iron in the treatment of anemia secondary to renal failure
- MOA: provides elemental Fe for Hgb production. Increases O2 transport to tissues
- Routes of Admin: PO, IV
- AEs: PO - C/N/cramps, dark urine. IV - HTN, HA, dyspnea, low back pain, anaphylaxis
- DIs: Antacids, antibiotics, levothyroxine, PPIs, H2 blockers, decreases abs of FQs
- Monitoring Parameters: Iron, Hgb, Hct. Q3mo after pt stable.
- Place in therapy: Patients with low iron (MCV, TSAT, Ferritin)
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Describe what happens in the body when the kidneys are not working properly in regard to Phosphorus, Calcium, Vitamin D, and PTH.
- Kidneys are not working properly
- Phosphorus is not getting excreted, so it increases
- Excess P binds with calcium, which decreases Ca in the blood
- This signals PTH to increase (tries to tell kidneys to pee out more P, but they won't respond because they aren't working right)
- Also, kidneys are not making active Vitamin D
- This is needed for Ca abs from the intestine, so Ca is not being absorbed from the GIT and it decreases
- This also activates PTH which causes more abs of Ca from the intestine, but P gets absorbed too
- The Ca x P product increases, leading to vascular calcification
- PTH also increases Ca reabsorption from the bone which leads to renal osteodystrophy
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