Uremia

Question 0

Ways in which the GI system is affected in uremia? (including anything involving eating..)

Answer 0

Decreased appetite.
Altered taste.
Bad breath (uremic fetor).
Esophagitis/motility problems.
GI bleeding.
Diverticular disease and constipation.

Question 1

Simplest definition of uremia?

Answer 1

Symptomatic renal failure.

Question 2

How is anemia caused by uremia characterized? (in MDTI terms, for cell size and color)

Answer 2

Normochromic normocytic anemia.

with hypoproliferative bone marrow and decreased reticulocytes.

Question 3

3 primary drivers of anemia in uremia?

Answer 3

Reduced EPO production.
Shortened RBC lifespan.
Inhibitors of erythropoeisis accumulate.

Question 4

What cells in the kidney actually make EPO?

Answer 4

A population of interstitial fibroblasts (Type I interstitial cells)

Question 5

Several aggravating factors for anemia of uremia?

Answer 5

Fe or B12/folate deficiency.
Blood loss (via GI tract or from dialysis).
HyperPTH.

Question 6

Drawback to EPO or synthetic EPO therapy for anemia of uremia?

Answer 6

There’s increased risk of adverse CV events…

One should aim for an Hg of 10-11, not 14.

Question 7

Why do patients with uremic syndrome bleed more easily?

Answer 7

Impaired platelet aggregation.

Some toxin appears to be inhibiting IIb/IIIa, but we don’t know what that is

Question 8

Treatment options for uremic syndromes with bleeding?

Answer 8

Treat anemia with EPO.
DDAVP (synthetic AVP aka ADH) -> vWF release.
Cryoprecipitate.
Estrogens.
Dialysis.

Question 9

Unique CVD risk factors that uremic patients have? (they’re not all entirely unique…)

Answer 9

Anemia.
Increased homocysteine.
Thrombogenic state.
Ca++ intake.
HyperPTH.
Persistent inflammatory state.
Toxins.

Question 10

Why are CV events often not aggresively treated in pts with CKD?

Answer 10

People are afraid of drugs / procedures in pts with CKD.

Question 11

What’s the most common lipid abnormality associated with uremia?

Answer 11

High TGs - due to decreased clearance from bloodstream.

due to reduced function of lipoprotein lipase, reduced hepatic lipase, increased retention a lipase inhibitor…

Question 12

Cholesterol changes in uremia?

Answer 12

Decreased HDL.

Increased apolipoprotein A1.

Question 13

Is sexual dysfunction a big problem in CKD?

Answer 13

Yes. But you can still get pregnant with triplets sometimes.

Question 14

Most important factor in predicting fetal outcome in CKD?

Answer 14

HTN

Question 15

Is transplant or dialysis better if you want to have a baby?

Answer 15

Transplant, generally.

Question 16

2 problems that occur more frequently in the pregnancies of women with CKD?

Answer 16

Pre-eclampsia.

Fetal growth retardation.

Question 17

What happens to phosphate levels in CKD?

What does this lead to?

Answer 17

More phosphate is retained.
Hyperphosphatemia -> FGF-23 -> hypocalcemia and secondary hyperPTH -> Vit D activation.
Bone reabsorption, calcium deposition in tissues.

Question 18

It wasn’t really emphasized in other lectures, but what enzyme activates 1-OH-D (calcidiol) to 1,25-(OH)2-D (calcitriol)?

Answer 18

1-alpha-hydroxylase

Question 19

At the end of all the pathways… how are serum phosphate, FGF-23, calcium, Vit D, and PTH in advanced CKD?
(It’s confusing because there are mutually antagonistic effectors floating around.)

Answer 19

Phosphate: high
FGF-23: high
Calcium: low
Vit D: very low
PTH: very high

Question 20

What high-turnover bone disease happens in pts with CKD? What mediates the disease?

Answer 20

hyperPTH -> osteitis fibrosa

Question 21

What effect does low Vit D have on bone?

Answer 21

Osteomalacia.

Question 22

Why is secondary hyperPTH from CKD especially bad for kids?

Answer 22

It causes really bad growth retardation.

Question 23

4 ways to treat these mineral/hormone imbalances of CKD?

Answer 23

Restrict phosphate / give phosphate binders (which have lots Ca++).
To suppress PTH:
-Calcitriol.
-Calcimimetics. (activate CaSR)
-Parathyroidectomy.