CKD: complications and management II

Question 1

What are the goals of therapy for CKD in terms of phosphorus levels?

Answer 1

In stage 3-4, keep phsophrus less than 4.6 mg/dl. If high, restrict phosphorus intake to 800-1000 mg/day.
In stage 5, keep phosphorus less than 5.5 mg/dl. If high start phosphate binders with meals.

Question 2

What are the goals of therapy for CKD in terms of calcium levels?

Answer 2

Ca below 10.2 (mg/dl?)

avoid calcium conatining binder intake above 1500 mg/D. Avoid total Ca levels greater than 2000 mg/D.

Question 3

What are the goals of calcium X phosphorus product in CKD pts?

Answer 3

product under 55.

Question 4

What are phosphate binders? What are examples?

Answer 4

pills taken with meals to decrease the absorption of phosphorus. Some have calcium (Tums) but are less than ideal because of the potential for vascular calcification. Others like sevelamer and lanthanum don’t have calcium and are the first choices.

Question 5

Why are aluminum calcium binders contraindicated in CKD?

Answer 5

it can cause aluminum bone disease and dementia

Question 6

sevelamer

Answer 6

non-calcium containing phosphate binder. may cause nausea, vomiting, farting, abdominal pain.

Question 7

cinacalcet

Answer 7

effect way to reduce PTH. binds calcium sensing receptor in the parathyroid glands and fools them into thinking that there is more calcium than there is.

Question 8

What are the main ways of reducing PTH and/or phosphorus?

Answer 8

1. calcium containing phosphorus binders like Tums, calcium acetate.
2. non-calcium containing phosphorus binders like sevelamer and lanthanum
3. conacalcet: reduces PTH by mimicking Ca
4. parathyroidectomy
5. Vitamin D?

Question 9

Parathyroidectomy in CKD pts with mineral metab problems

Answer 9

good way to reduce PTH, but will cause hungry bone syndrome afterwards due to the rapid drop in PTH: must anticipate with a calcium drip as the bones deposit lots and lots of Ca from the blood.

Question 10

Anemia and CKD

Answer 10

erythropoeitin is secreted by fibroblasts in the interstitium of the kidney in response to tissue hypoxia. There is a decrease of erythropoeitan seen in CKD pts to varying degrees. Additionally, the lifespan of RBCs is lower in CKD, and RBCs are lost in hemodialysis. There is also significant iron deficienty, folate, and B12 deficiency.

Question 11

What are the agents that could replace erythropoeitin from the kidney?

Answer 11

erythropoetin: epogen and procrit, dosed 1-3X/wk
darbepoetin: aranesp, dosed monthly or weekly

Question 12

What do we know about the effects of erythropoetin stimulating agents in CKD?

Answer 12

no difference in time to first CV event among normal and low Hb groups in Europe; in US we saw a less time to first CV even in the group with normal Hb! For darbapoetin, there is no benefit to normal Hb group- and stroke risk was doubled. So, we don’t do much ESA (erythropoetin stimulating agent) therapy.

Question 13

Goals and management of ESA treatment

Answer 13

start ESA in pre-dialysis pts when Hb is less than 10, and aim for 10 in these pts.
In dialysis pts, goal is 10-11.  
Only goal is to prevent transfusions.
NO ESA for pts with Hb>12.  
Check CBC monthly and iron occasionally.

Question 14

What should I know about iron in CKD pts?

Answer 14

IV iron is more cost effective than po in iron deficient CKD pts if tsat is less than 20%