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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)
What is the leading cause of CRF? The second leading cause?
What is normal serum phosphorus?
2.7 to 4.5
What is the goal for the Calcium x Phosphorus product? At what value does mortality increase?
Medical issues resulting from hyperphosphotemia, hyperparathyroidism
- Alterations in lipid metabolism
- Insulin secretion
- Epo resistance
- Renal osteodystrophy
- Vascular calcification
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.
Why must patients take hyperphosphotemia meds with meals?
Because they bind Phosphate in the diet and it is excreted in feces
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
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.
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.
What are the parathyroid goals for stage 3, 4, and 5 CKD?
What is normal?
- 3: 35-70
- 4: 70-110
- 5: 150-300
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.
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.
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)
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
At what hemoglobin levels does workup for anemia start?
- For premenopausal women, < 12 g/dL
- For postmenopausal women and males, < 13.5 g/dL
What is the normal hemoglobin level?
12 - 18
What is the goal Hgb level for CKD?
At what Hgb level do we begin treatment for anemia?
What is the transferrin saturation goal?
What is the serum ferritin goal?
> 100 ng/mL
What is the serum iron goal?
What is normal MCV?
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
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)
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