Lect 3 Flashcards
as kidney function declines there is ___
- hyperphosphatemia
- inhibition of renal activation of Vit D
- stim of PTH secretion
- Ca levels are maintained by bone resorption
- elevated Ca x P product can cause soft tissue calcification
as kidney function declines there is ___
- hyperphosphatemia
- inhibition of renal activation of Vit D
- stim of PTH secretion
- Ca levels are maintained by bone resorption
- elevated Ca x P product can cause soft tissue calcification
hypocalcemia
serum Ca less than 8.5 mg/dL
Ca x P product
less than 55 mg2/dL2
PTH ranges for Stage 4 and 5 CKD
above the normal range to prevent over suppression of PTH
hypocalcemia
serum Ca
Ca x P product
PTH ranges for Stage 4 and 5 CKD
above the normal range to prevent over suppression of PTH
PTH ranges for Stage 4 and 5 CKD
above the normal range to prevent over suppression of PTH
what is first line non-pharm intervention for CKD pts?
dietary phosphate restriction
800-1000 mg/day
parathyroidectomy
for pts with SEVERE CKD-MBD and nonresponsive to pharm therapy (PTH is higher than 800 picograms/mL)
MOA of phosphate binding agents
bind dietary phos in the GI tract and form an insoluble product that can be excreted in feces
lowers phos absorption
ex of phos binding agents
elemental Ca= lanthanum-, aluminum-, and magnesium-containing compounds
nonelemental= sevelamer carbonate
many times these are taken TID with a meal
calcium carbonate
TUMS
more soluble in acidic environments, thus given before meals
calcium acetate
PhosLo
binds 2X phosphorus as calcium carbonate
what phos binding agents are first line for control of both serum phos and Ca conc?
oral calcium compounds
what phos binding agent is approved for ESRD pts?
lanthanum carbonate
aluminum salts
restriction is limited to 4-week therapy
Potential for producing anemia
Mg containing antacid
use is limited in CKD pts due to GI side effects and potential for Mg accumulation
ADR’s of phosphate binding agents
- ALL are limited by GI side effects (constipation, diarrhea, N/V, abd pain)
- hypercalcemia
- CNS tox & worsened anemia= aluminum binders
- hyperMgemia and hyperKemia= Mg binders
Vit D therapy MOA
activated Vit D (calcitriol) suppresses PTH secretion by stim absorption of Ca by intestinal cells, proximal tubular cells, and through direct activity on parathyroid gland
examples of Vit D agents
- ergocalciferol (Vit D2) and cholecalciferol (Vit D3)= must be converted to active form by the kidney since they are Vit D precursors
- calcitriol (1,25 D3)= most active form
- paricalcitol or doxecalciferol= analogs
what Vit D agents are used in pts with severe kidney disease?
calcitriol or one of the analogs (since the rest need the kidney to convert them to active form)
which Vit D drug can be used either by oral or IV routes?
calcitriol
calcimimetics MOA
acts on the Ca-sensing receptor on the surface of the chief cells of the parathyroid gland to mimic the effect of extracellular ionized Ca and increase the sensitivity of the Ca sensing receptor
DOES NOT increase intestinal Ca/ phos absorption
example of calcimimetic
cinacalcet hydrochloride (Senispar)= tx for secondary hyperparathyroidism in ESRD pts and tx of hyperCaemia in pts w/ parathyroid carcinoma
efficacy of calcimimetics
signficantly decreased PTH and Ca x P product
ADR’s of calcimimetics
N/V
ADR’s of calcimimetics
N/V
PK of cinacalcet
Cmax reached in 2-6 hours
large vol of distribution and mostly protein bound so negligible removal by dialysis
