CKD pt 2 Flashcards
Shepler 9-14
Vit D and secondary hyperparathyroidism (SHPT)
hyperphosphatemia + lack of kidney function –> no activation of Vit D –> decrease in calcium serum concentration –> triggers parathyroid gland –> more PTH secreted –> increase calcium mobilization
treatment of SHPT drugs
ergocalciferol (stage 3/4)
calcitriol, paricalcitol, doxercalciferol (stage 5)
increase vit D concentrations and decrease PTH concentrations through negative feedback mechanism
ergocalciferol (calciferol)
UNACTIVATED vit D2
for vit d insufficiency in CKD stage 3/4
cholecalciferol
UNACTIVATED vit d3
for vit d insufficeincy in ckd stage 3/4
calcitriol
activated vit d3 for CKD stage 5 and some stage 3/4
approved for pediatric usage
greatest risk of hypercalcemia (monitor for signs)
cheap
signs and symptoms of hypercalcemia
fatigue
weakness
headache
NV
muscle pain
constipation
paricalcitol
activated d2
same monitoring parameters as calcitriol
over 30% reduction in PTH
approved for peds
most favorable ADE profile
less calcemic activity
doxercalciferol
activated vit D2
prodrug activated in the liver (so don’t use in pts with hepatic issues)
produced a more even serum concentration
over 30% reduction in PTH
higher incidence of hyperphosphatemia
lower incidence of hypercalcemia in comparison to calcitriol
calcimimetic drugs
cinacalcet (sensipar)** type 2
etelcalcetide
contraindicated in hypocalcemia (do not use if Ca is below 7.5, wait until it reaches 8mg/dL
cinacalcet (sensipar)
TYPE 2 calcimimetic agent
mimics the action of Ca by binding to Calcium sensing receptor (CaR) and inducing a conformational change to the receptor to trigger decrease PTH secretion via PT gland
etelcalcetide
sensipar but via IV
erythropoietin (EPO)
promotes production of mature red blood cells in the bone marrow
when there is too many red blood cells, it is suppressed via the hypoxia-inducible factor
anemia occurs when too few RBCs are circulating leading to increased transcription of EPO to account for it
mechanisms of anemia development
decreased production EPO
uremia causes a decreased life span of RBCs
vitamin losses during dialysis (like folate, B12, and B6)
dialysis with loss of blood through dialyzer (hemolysis)
signs and symptoms of anemia
fatigue
dizziness
headache
decrease cognition
low MCV
iron deficiency
aluminum toxicity
high MCV
folate deficiency
B12 deficiency
normal MCV
could be signs of chronic disease
GI bleed
EPO deficiency
treatment goals of anemia
reverse signs and symptoms of tissue oxygen deprivation and left ventricular hypertrophy
increase exercise tolerance and capacity
optimize survival
increase or quality of life
monitoring parameters of anemia
Hb is best due to stability
should be monitoring annually in 3, biannually in 4, and q3m in 5 unless previously diagnosed
males - under 13
females - under 12
iron supplementation in anemia
recommended if TSAT is under 30% and serum ferritin is under 500 ng/mL
monitor q3m
best absorbed in an acidic environment
food decreases absorption
should be separate from other meds by 2 hours
SE – stomach upset
oral iron
will likely not be sufficient in correcting and maintaining iron stores for HD patients
may be used for CKD or PTD patients
NOT FOR STAGE 5
drugs –> ferrous salts (sulfate, gluconate, and fumerate)
hepcidin
destroys FPN make it so that iron cannot be moved out of the duodenum
IV iron
preferred route for CKD
drugs –> iron dextran, sodium ferric gluconate, iron sucrose, ferric carboxymaltose, ferumoxytol (feraheme)
iron dextran
IV iron
test dose of 25mg needs to be done as dextran is a common allergy
feraheme
interferes with MRI so should not be used for up to 3 months after second injection
ESA
erythropoiesis stimulating agents
used after all other correctable causes of anemia have been addressed
although QOL benefits increase as the Hb increases, the incidence of CV AE also increases so do not use ESA to push Hb above 11.5 g/dL
decrease dose by 1/2 if the pt has hepatic impairment
do not give with strong CYP2C8 inhibitors (genefobrizil)
ESA in stage 3-5ND
Hb under 10 g/dL
Hb falling at a rapid rate
needed to avoid blood transfusion
ESA in stage 5D
start when Hb is between 9 and 10 g/dL
ESA drugs
recombinant human erythropoietin (epogen)
darbepoetin alfa (aranesp)
methoxy polyethylene glycol - epoetin beta (mircera)
ESA SE
pure red cell aplasia (PRCA)
HTN
PRCA with ESAs
antibodies develop to erythropoietin
discontinue drug permanently
HTN with ESAs
23% of patients will seen an increase
not a reason to not give the drug even if they have pre-existing HTN (more important to keep them alive with this)
causes of ESA therapy failure
lack of vitamins or iron
aluminum toxicity
active bleed
drug induced bone marrow suppression
acute inflammation or infection
new therapy for anemia of CKD
HIF inhibitors, PHI inhibitors, or HIF-PHIs
Daprodustat
for patients who have been on dialysis for at least 4 months
daprodustat
approved in feb 2023
injection leads to more adherence
increased CV effect thugh
acid base disorders
ESRD patients cannot excrete H+ ions and develop metabolic acidosis
treatment of acid base disorders
1) dialysis - increase bicarbonate in dialysate (usually corrects problem)
2) Shohl’s solution
3) sodium bicarbonate tablets
4) administer over several days
uremic bleeding
common complication of CKD patients
not fully understood but could be partially due to impaired binding of Von Willebrand factor to platelet membrane glycoprotein receptors
diabetic kidney disease
excess glucose in the blood enters the glomerular cells and alters ability of glomerulus to filter waste products from blood appropriately
microalbuminuria
best predictor of DKD (also risk factor for heart attack and stroke)
treatment of DKD
SGLT2 inhibitors (flozins) and metformin to control BG if eGFR is above 30
life style mods
HgbA1 below 6.5 to 8% in non-dialysis dependent CKD
antihypertensives (ACE-i and ARBs to decrease proteinuria in addition to lowering BP)
HTN in CKD
target SBP below 120 mmHg (weak evidence)
salt intake below 2 g/d of sodium or 5 g/d of sodium chloride
drug of choice: 1) ACE inhibitors 2) ARBs 3) diuretics
hyperlipidemia
common in CKD patients due to altered metabolism of serum lipoproteins
elevated serum LDL concentrations
