Chronic Kidney DIsease

Question 1

why do ppl with CKD tend to bleed?

Answer 1

defects in platelet and von Willebrand factor interaction when forming a hemostatic platelet plug

Question 2

Does the degree of uremia correlate to bleeding risk?

Answer 2

no. Coagulation studies like PT/ PTT may be normal but bleeding time may be prolonged

Question 3

How do we treat pts with CKD or uremia and they have active bleeding?

Answer 3

may need DDAVP to increased release of Factor 8 von Willebrand factor polymers from endothelial storage sites Conjugated estrogen - from increased platelet reactivity Cryoprecipitate - for platelet aggregation

Question 4

What is most common treatment for bleeding in pts with CKD?

Answer 4

DDAVP simplest and least toxic treatment with acute bleeding and can be administered IV or subcut or intranasally and works within 1 hr of administration and lasts only 4 to 24 hrs. Repeat doses are less effective.

Question 5

Does dialysis work to help reverse platelet dysfunction and bleeding in CKD pts?

Answer 5

no because they need AC to prevent extracorporeal circuit and this can worsen epistaxis. Also a single dialysis session cannot reverse platelet defect.

Question 6

When do we used conjugated estrogen for bleeding in a CKD pt?

Answer 6

if DDAVP doesn’t stop and it’s a 2nd line treatment and takes about 4-5 days to reach peak levels and meant for controlling prolonged bleeding.

Question 7

When is there a benefit with transfusion and helping with bleeding in a CKD patient?

Answer 7

only really helpful with increasing a hematocrit when pts have less than 30%. Otherwise transfusions don’t help if HCT is >30%

Question 8

Why is cyroprecipitate not the 1st line treatment for reversal of bleeding in a CKD pt?

Answer 8

increased volume and possible exposure to blood borne pathogens.

Question 9

When to get a AV fistula?

Answer 9

get it when GFR is 15-20 because it takes up to 3 months to mature and AV fistula is preferred modality for dialysis

Question 10

renal replacement therapy and older adults?

Answer 10

need a risk benefit ratio because frail individuals with significant comorbitidies may only prolong or induce suffering. May need palliative care.

Question 11

CKD and HTN what to treat with?

Answer 11

start on ACEi and need close monitoring for BP, electrolytes.

Aim for proteinuria <1000mg/day in proteinuric CKD

Question 12

goal BP in pts who have proteinuric BP and those with CKD in non proteinuric CKD pts?

Answer 12

with proteinuria goal BP is 130/80 without proteinuria BP is 140/90

Question 13

which CCB are better with decreasing protein in urine for CKD

Answer 13

second line are diltiazem and verapamil or non dihydropyridine dihydropyridine CCB

amlodipine and nifedipine (dihydropyridine CCB) do not have anti-proteinuric effects

Question 14

what causes secondary hyperparathyroidism in CKD?

Answer 14

untreated or inadequately treated hyperphosphatemia and hypocalcemia in CKD.

Question 15

targets for dialysis for:

serum calcium,

serum phosphate,

and calcium phosphate product levels goal

intact PTH level

Answer 15

serum total corrected calcium: 8.4-9.5

serum phosphate: 3.5-5.5

calcium phosphate product should be <55

Intact PTH should be 150-300

Question 16

how do we correct or prevent hyperphosphatemia in CKD?

Answer 16

dietary phosphate restriction (<900 mg/day) Next step is to add phosphate binders (calcium carbonate/acetate or sevelamer/lanthunum)

Question 17

if serum phosphate remains uncontrolled in CKD what do next?

Answer 17

get serum PTH

if serum PTH is >300, need a vitamin D analog or calcimimetic depending on serum phosphate and calcium levels

Question 18

what do calcimimetics do?

Answer 18

they increase calcium sensitivity of the calcium sensing receptors of the parathyroid gland

This reduces serum PTH, calcium, and phosphate levels.

Question 19

what is an example of an calcimimetic medication?

Answer 19

Cinacalcet or Sensipar helps reduce fracture risk and improves symptoms of secondary hyperparathyroidism

Question 20

symptoms of secondary hyperparathyroidism?

what are the manifestations of this secondary hyperparathyroidism.

Answer 20

in Secondary Hyperparathyroidism we see increased PTH released via the parathyroid glands due to CKD.

see pruritis, bone pain, fractures, calciphylaxis and avascular necrosis

Question 21

what does cinacalcet do long term for pts who have secondary hyperparathyroidism?

Answer 21

it helps decrease need for parathyroidectomy by 50% reduce cardiovascular risk in pts >65 yrs. decreases bone turnover from secondary hyperparathyroidism and so reduces risk for osteitis fibrosa development.

Question 22

when should we not use cinacalcet (senispar) or who is this medication contraindicated in?

Answer 22

pts who have hypocalcemia as this can cause seizures and prolong QT C

Question 23

cinacalcet (senispar) side effects:

Answer 23

hypocalcemia and GI disturbances

Question 24

hyperphosphatemia in ESRD pts

Answer 24

increased PTH levels result from reduced calcium excretion and increased phosphorus excretion by the kidneys.

in early CKD, PTH induced increase in renal phosphate excretion allows for normal serum phosphate levels despite reduced renal excretory capacity.

as CKD progresses, kidney is unable to compensate for increased phosphorus and so phosphorus levels rise. THis creates a vicious cycle of increased PTH production.

Question 25

Management of HTN in proteinuria CKD (algorithm)

Answer 25

Question 26

Proteinuria is defined by:

Answer 26

proteinuria >500 mg/day

Question 27

target BP for CKD pts is

If pt has proteinuria what med do you use first?

If they continue to have uncontrolled (above goal BP), what do you use in addition as secondline?

What if there’s edema?

Answer 27

<140/90

1st line choice to use: ACEi or ARB if there’s proteinuria

2nd line if uncontrolled: use non dihydropyridine calcium channel blocker: diltiazem or verapamil)

Can use diuretics if there’s edema

Question 28

Do we use diuretics in CKD pts?

Answer 28

no thiazide diuretics are less effective in pts with CrCl<30 and should have loop diuretics brought on board. If loop diuretics are not effective a thiazide may added again to improve diuresis.

Question 29

contrast induced nephropathy (CIN) is caused by:

When do you see this develop and what is on labs?

who is at risk for CIN?

Answer 29

this is likely from cytotoxicity and renal vasoconstriction.

See AKI within 24-48 hrs of contrast administration and pts have a low FENA<1% in the absence of clinical volume depletion

Low risk for CIN in normal renal function. also higher risk with CKD and older 1st generation contrast agents.

Question 30

how to minimize risk for contrast induced nephropathy CIN?

Answer 30

avoidance of NSAIDs

periprocedural infusion of NS

use smallest amount of (volume wise) of contrast media

Try to use later generations of contrast medium

Question 31

What do you see with chronic vitamin D deficiency?

Answer 31

see osteomalacia, and inaccessible calcium stores in bone (unmineralized osteoid) and eventual hypocalcemia.

They can develop pseudofractures, bone pain and deformity

Question 32

how do we have normal serum Ca when there’s vitamin D deficiency caused by uncontrolled Celiac dx?

Answer 32

See increased PTH released from secondary hyperparthyroidism and this causes more reabsorption of urinary Ca and low phosphate.

Question 33

Best treatment for slowing progression of CKD with pts who have >1g/day of protein in urine

Answer 33

ACEi and ARBs

decrease intraglomerular pressure throught dilation of both efferent and afferent glomerular arterioles and decrease proteinura as much as 35-40%

helps prevent the rapid decline of GFR regardless of what the cause was of primary renal dysfunction or initial GFR

Question 34

what also can help with decreasing proteinuria in CKD?

Answer 34

1st line: ace inhibitors or ARBs

can combine with spironolactone to help but increases risk of hyper K

2nd line is non dihydropyridine calcium channel blockers (verapamil, diltiazem) block spilling of protein (more so than dihydropyridine CCB like amlodipine or nifedipine)

Question 35

management of hyperphosphatemia in CKD pts

Answer 35

Question 36

how does CKD cause hyperphosphatemia?

Answer 36

the kidneys do a lot of metabolic work and as they fail, they also lose the ability to excrete phosphorus.

The higher concentration of phosphorus causes CKD related mineral bone disease: osteitis fibrosa, osteomalacia, and adynamic bone dx

Question 37

how does CKD related hyperphosphoratemia (high phosphorus) lead to secondary hyperparathyroidism?

Answer 37

elevated serum phosphate triggers release of fibroblast growth factor 23 from bone and lowers calcitriol (1,25 vit D or active vit D) production and intestinal calcium absorption.

PTH senses low calcium and high phosphorus causes parathyroid gland to secrete extra PTH to try to raise Ca levels.

Question 38

how to treat CKD related hyperphosphatemia?

Answer 38

early dietary phosphorus restriction is needed for pts with CKD.

Phosphate binders are needed as dietary restriction generally isn’t enough.

Can use calcium containing or non calcium containing though calcium containing are better tolerated.

Question 39

why do we not like aluminum hydroxide as a phosphorus binder in pts who have high serum phosphate in CKD?

Answer 39

becaue while it works it can cause adynamic bone dx and nonreversible encephalopathy

avoid in all CKD pts.

Question 40

When do we avoid using calcium based phosphate binders in CKD and high phosphorus levels?

Answer 40

when pat already has high calcium level because excessive serum Ca levels will cause coronary arterial calcification and so non calcium containing binders are preferred.

Pick sevelamer or lanthanum.

Question 41

calcium containing phosphate binders are preferred in

Answer 41

hypocalcemic or normocalcemic pts

Question 42

non calcium containing binders are preferred in

Answer 42

hypercalemic pts, low PTH, vascular calcification, or those with suspected adynamic bone dx

Sevelamer - renvela or renagel

lanthanum - fosrenol

calcium acetate - phoslo

Question 43

peritoneal dialysis surivival rate? i

Answer 43

s the same survival rate for those with chronic peritoneal dialysis and generally is comparable to chronic HD but not better than transplant

Ok for people who have stable cardiovascular dialysis

Question 44

what is happening when some who has CKD and is on EPO and improving anemia and now has worsening anemia?

Answer 44

They have erythropoietin reisstance due to iron deficiency anemia.

This can be due to absolute iron deficiency through blood loss (GI, blood draws, vigorous hematopoiesis during ESA therapy)

Functional iron deficiency - impaired mobilization of iron due to elevated hepcidin levels (anemia of chronic dx) and Fe cannot be rapidly mobilized to keep up with hematopoiesis after ESA administration.

Treatment of this is with IV iron.

Question 45

what do we see in early stages of Iron deficiency?

Answer 45

before microcytosis develops can see normocytic anemia.

Question 46

Diagnosis of Fe deficiency in CKD is hard but we look at:

Answer 46

low transferrin saturation (<20%)

ferritin <200 in HD pts

all pts with ESRD on EPO threapy should be treated with iron regardless of iron studies unless ferritin >500.

If replete needs to be evaluated for GI bleeding

Question 47

5 year survival rate for pts on HD from DM2 is

Answer 47

30-40%

>50% death from CAD dx

after transplant kidney 5 year survival is 67-77% and better quality of life.

Question 48

best candidate for donar of kidney in ESRD is

Answer 48

living donor transplant but cadaveric transplant also offers increased survival in diabetic pts See improved survival in all pts including those >70 yrs old

Question 49

When to start sodium bicarbonate in CKD pt?

Answer 49

when Bicarb <22 and CKD 4-5 as it helps to reduce progression of chronic kidney disease

as kidney becomes weaker it loses ability to excrete H+ and so need to have bicarbonate present to help maintain pH of kidney.

Question 50

Sevelamer is a

Answer 50

non calcium containing phosphate binder - meant to help lower phosphate levels.

Question 51

what is the best pain for someone who has ESRD?

Answer 51

hydromorphone

Don’t use these following medications.

morphine - can create a toxic metabolite. Morphine, codeine and meperidine are all contraindicated

tramadolol is contraindicated

gabapentin - is not helpful for acute pain.

Question 52

what medication should be avoided in CKD pt?

Answer 52

NSAIDs

CKD pt s are sensitive to nephrotoxic effects of NSAIDs and these medications are a frequent cause of AKI.

Tx OA with exercise and tylneol. weight loss. Topical NSAIDs are safer,

Question 53

cinacalcet is a

Answer 53

calcimimetic that decreases PTH levels and is FDA approved in pts who undergo dialysis and used as off label for secondary hyperparaythryoidism associated hypercalcemia where vitamin D analogue has led to hypercalcemia.