Chronic Kidney Disease Mineral Bone Flashcards
(42 cards)
Calcium Role
99% in bone
Bone, Kidney, Intestine maintain homeostasis of Calcium
Phosphate Role
Maintain mineralization of Bone
Bone, Kidney, Intestine maintain homeostasis of Phosphate
Vitamin D3 Role
Inactive Form
- First hydrolyzed by the liver
- Then activated by the kidneys to produce Calcitriol
Calcitriol Role
Active Form
- Intestines: Increases absorption of Calcium and phosphate
- Bone: Promotes resorption of Calcium and phosphate
- Parathyroid: Inhibits PTH production
–> Increased calcium production will inhibit PTH secretion
Summary:
- Increases Calcium and Phosphate
- Decreases PTH
Parathyroid Hormone
- Production
PTH is produced when
- Low calcium (Main regulator)
- High phosphate
- Low calcitriol
Parathyroid Hormone
- Role
Kidney:
- Increases Phosphate excretion
- Increases Calcium reabsorption (Decreased Calcium excretion)
Bone:
- Increases Calcium and Phosphate resorption
Intestinal:
- Increases Calcium and Phosphate reabsorption
Calcitriol:
- Increases production of Calcitriol (More Calcium and Less Phosphate)
- Inhibits itself (Less PTH)
Summary:
- Increase Calcium
- Decrease Phosphate
- Increase Calcitriol
FGF-23 Role
- Production
FGF-23 is produced when
- High Calcitriol
- High Phosphate
FGF-23 Role
- Role
Decreases Phosphate
- Less Phosphate reabsorption
- More Phosphate excretion
Decrease Calcitriol
- Decrease production
- Increase catabolism
Inhibits PTH
Summary:
- Decrease Phosphate
- Decrease Calcitriol
- Inhibit PTH
Secondary Hyperparathyroidism and CKD
- Kidney decreases in function leading to reduced phosphate excretion
–> Increased Serum Phosphate - High Phosphate suppresses Calcitriol
- High Phosphate leads to more FGF-23 leading to low Calcitriol
- Reduced kidney mass leads to less Calcitriol production
- Decreased Calcitriol with reduced Calcium absorption leads to Hypocalcemia
- Steps 1-5 lead to more PTH and proliferation of parathyroid cells
Mild Hyperparathyroid-Related Bone Disease
Bone Turnover
- Medium
Bone Mineralization
- Normal
Advanced Hyperparathyroid-Related Bone Disease (Osteitis Fibrosa)
Bone Turnover
- High
Bone Mineralization
- Normal
Adynamic Bone Disease
Caused by oversuppression of PTH by medicines that lower PTH (Calcium, Active Vitamin D)
Bone Turnover
- Low
Bone Mineralization
- Normal
Secondary Hyperthyroidism
- Causes what to develop
Medium-High Bone Turnover
Secondary Hyperthyroidism
- Management
Reducing Hyperphosphatemia
Normalizing Calcium Levels
Suppressing PTH
Adynamic Bone Disease
- Management
Allow PTH to rise and return to increase bone turn over
Reduce Vitamin D analogues and Calcimimetics
Osteomalacia
Results from aluminium deposition
- Stop aluminium phosphate binders
Phosphate Binder Considerations
Use only if patient has excessive Phosphate levels (In CKD 3-5 patients)
Must be taken in with food to maximize efficiency
Calcium Salt
- What are they
Most commonly used
% of Elemental Calcium
- Citrate < Acetate < Carbonate
Give bigger dose with larger meals
Calcium Salt
- Adverse Effects
Hypercalcemia
GI Side Effects
- Nausea
- Constipation
Interacts with the absorption of Iron and Fluoroquinolone Antibiotics
Sevelamer
- What is it
Non-Calcium based Phosphate Binder
- Can be used in patients with hypercalcemia
- Can be used along with other phosphate binders
Also decreases LDL Cholesterol
Sevelamer
- Adverse Effects
Metabolic Acidosis
GI Side effects
Lanthanum
- What is it
Dissociates in upper GI into ions which bind phosphate
Can be used with other phosphate binders
Lanthanum
- Adverse Effects
Unknown Long-Term Safety (Can accumulate in bone and tissues)
GI Side Effects
Aluminium Salt
- What is it
Used for acute treatment of severe hyperphosphatemia
Limit to only 4 weeks
No longer first line therapy
