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Therapeutics II > Renal - Shepler > Flashcards

Renal - Shepler Flashcards

1
Q

Acute Kidney Disease Definition

A
  • short term

- one minute you’re good, the next, you’re not

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2
Q

CKD

A

Chronic Kidney Disease

Defined as abnormalities of kidney structures, present for >3 months with implications for health

Classified based on cause, GFR and albuminuria category

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3
Q

ESRD

A

End Stage Renal Disease

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4
Q

KDOQI

A

Kidney Disease Outcomes Quality Initiative

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5
Q

KDIGO

A

Kidney Disease Improving Global Outcomes

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6
Q

Incidence and Prevalence

A
  • 678,383 patients with ESRD as of December 31, 2014
  • 2,000,000 patients with ESRD estimated by 2030
  • 120,688 new cases of ESRD in 2014
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7
Q

Major Causes of CKD

A
  • Diabetes mellitus
  • HTN
  • glomerulonephritis (inflammation of kidney filters)
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8
Q

Prognosis of CKD

A

G1 = Normal or high (Best)

G2 = Mildly decreased

G3a = Mildly to modreately decreased

G3b = Moderately to severely decreased

G4 = Severely decreased

G5 = Kidney failure (Worst)

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9
Q

Glomerular filtration rate that indicates kidney failure

A

<15 ml/min/1.73m^2

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10
Q

Estimating the kidney function (Creatinine Clearance)

A

Cockroft and Gault formula, most commonly used in practice

*accurate for pts with stable kidney function

Good predictor of GFR and easy to use

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11
Q

Cockroft and Gault formula tends to _________ renal function

A

overestimate

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12
Q

Cockroft and Gault Equation

A

Men: CrCl = (140-age)IBW / (Scr x 72);

Women: CrCl x 0.85

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13
Q

CrCl measured in

A

ml/min

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14
Q

IBW measured in

A

kg

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15
Q

Scr measured in

A

mg/dL

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16
Q

SUN (serum nitrogen concentration) measured in

A

mg/dL

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17
Q

Alb measured in

A

gm/dL

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18
Q

Adjusted Body Weight (AjBW)

A

If pt is 130% of their IBW use AjBW = IBW + 0.4 (ABW - IBW)

ABW = Actual body weight

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19
Q

EGFR used to

A

stage disease

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20
Q

CrCl used to

A

dose drugs

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21
Q

Uremia Definition

A

Accumulation of waste molecules in the blood that are normally removed by the kidneys

Clinicians monitor the BUN to assess S/Sx

One possible effect on the body = Uremic frost = Crystals form = itchy

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22
Q

Fluid Retention

A

Pts develop edema (pitting and/or pulmonary) and BP increases

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23
Q

Fluid Restrict pts with retention?

A

Not normally necessary if Na is controlled. Large amounts of free water should be avoided

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24
Q

Fluid retention: Diuretics

A

-Used to treat volume overload and HTN in pts with renal insufficiency (those making some urine)

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25
Q

Fluid Retention: Loop Diuretic Treatment Option

A
  • all loops similar to one another, therefore a poor response to one will be a poor response to all
  • loops are REALLY good for fluid control
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26
Q

Fluid retention drug considerations

A
  • thiazides are ineffective when CrCl < 30ml/min
  • loops will work when CrCl < 30ml/min
  • furosemide bioavailability (10 - 100%) is usually about 50% — oral dose may be twice the IV dose
  • avoid potassium sparing diuretics
  • as renal function declines and loop diuretic dose is maximized, thiazide can be added to overcome the diuretic resistance

***DIURETICS ONLY WORK IF THE KIDNEY IS WORKING

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27
Q

Furosemide sporadic bioavailability

A

-oral bioavailability = 10 - 100

***might need to titrate

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28
Q

Ethacrynic Acid Note

A
  • risk of INCREASED ototoxicity

- still used, just an old drug

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29
Q

Complications associated with CKD + ESRD

A
  • uremia
  • fluid retention
  • electrolyte imbalances
  • mineral and bone imbalances (CKD-MBD)

—maybe more

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30
Q

Na Electrolyte Imbalances

A

No need to severely Na restrict pts beyond a no salt added diet UNLESS NEEDED FOR HYPERTENSION OR EDEMA (So <2g Na/day or <5g NaCl per day)

  • use saline containing IV solutions with caution
  • make outpatients aware of hidden high Na content foods (hot dogs, canned soups)
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31
Q

K goal for pre-dialysis K concentration

A

4.5 - 5.5 mEq/L

might seem high BUT these patients are resistant to effects of hyperkalemia

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32
Q

K Electrolyte Imbalance

A

Restrict to 3gm/day

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33
Q

K Electrolyte Imbalances

A
  • avoid high potassium foods (tomatoes, dried fruits, salt substitutes, fresh fruits)
  • treatment for hyperkalemia
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34
Q

3 parameters impacting PTH gland

A
  • Increased phos
  • Decreased Ca
  • Decreased Vit D
  • ALL INCREASE PTH
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35
Q

Long term impact of increased Ca

A
  • Ca in blood
  • pulls Ca out of blood
  • bone fractures in vertebrae
  • painful
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36
Q

Different types of parathyroidism

A
  • Primary = tumor on gland

- Secondary = hyperparathyroidism (nothing is really wrong, affected by many things)

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37
Q

Hyperphosphatemia

A
  • problem for nearly all ESRD pts
  • nearly all pts receive phosphate binders
  • agents bind dietary phosphate which is ingested in food. the chelate is eliminated in feces
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38
Q

Difference between phosphate and phosphorus

A
  • phosphate = describes dietary intake

- phosphorus = the portion of phosphate that is measured in the blood

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39
Q

phosphate binders are

A

GIVEN WITH MEALS

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40
Q

Key points of calcium and phosphorus ish

A
  • hyperphos is an issue
  • decreased vitamin is an issue
  • hypo Ca is an issue. Must consider Ca, phos, vit D and the intact PTH
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41
Q

Phosphate Binder Examples (Calcium containing)

A
  • Ca carbonate (TUMs)

- Ca acetate (PhosLo

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42
Q

Calcium carbonate (TUMs)

A
  • 40% elemental Ca
  • Dose = TID w/ meals
  • SE = constipation
  • DO NOT EXCEED 1500mg/day of elemental Ca
  • cheap!
  • problem = has calcium, some will go into blood
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43
Q

Calcium acetate (PhosLo)

A
  • 25% elemental Ca
  • BID - TID with meals
  • DO NOT EXCEED 1500 MG DAILY
  • Phoslo 667 mg = 169 mg elemental calcium
  • when given at the same elemental dose, calcium acetate will bind twice as much phosphate compared to calcium carbonate
  • Ca acetate produces fewer hypercalcemia events
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44
Q

Non-calcium containing phosphate binders

A
  • sevelamer carbonate (Renvela)
  • lathanum carbonate (Fosrenol)
  • sucroferric oxyhydroxide (Velphoro)
  • Auryxia (ferric citrate)
  • Aluminum hydroxide (amphojel)
  • Magnesium carbonate (Mag-Carb)
  • Nicotinic acid and nicotinamide
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45
Q

Sevelamer (Renvela)

A
  • AE: GI upset, N/V, diarrhea
  • ***decreased LDL by 15 - 30%
  • always take with food
  • not absorbed. low risk of systemic toxicity
  • decrease uric acid serum concentrations –> good for gout
46
Q

Lanthanum carbonate (Fosrenol)

A
  • ***dosed daily with meals
  • may titrate this drug
  • eliminated in the feces
  • no long term accumulation
  • SE: mainly GI
  • efficacy at diff pHs
  • **pH 3 = 97.5% phos bound
  • **pH 5 = 97.1 % phos bound
  • **pH 7 = 66.6% phos bound
47
Q

Sucroferric oxyhydroxide (Velphoro)

A
  • minimal effect on iron stores

- SE = may cause DARKENED stools due to iron content

48
Q

Auryxia (ferric citrate)

A
  • for CKD pts on dialysis
  • each tablet has 1g ferric citrate
  • may cause DISCOLORED feces
  • DOES impact iron levels
  • increases ferritin
  • increases TSAT
49
Q

Aluminum hydroxide (Amphojel)

A
  • old

- only use short term, if at all (< 4wks) — why? Al is eliminated by kidney, could build up. SE = ALUMINUM TOXICITY

50
Q

Magnesium carbonate (Mag-Carb)

A

-dosed with meals

51
Q

Dietary Restrictions of Phosphorus

A

-800-1000 mg/day if:

  • **Phos >4.6 mg/dL (CKD stage 3 and 4)
  • **Phos >5.5 mg/dL (CKD stage 5)
  • **Phos > target range for stage 3,4 or 5
52
Q

Foods that contain high phosphorus

A
  • meat
  • nuts
  • dairy
  • dried beans
  • colas
  • bear
53
Q

If someone has kidney disease they should _____ using NSAIDs

A

STOP

54
Q

Hyperphosphatemia and the kidney’s inability to activate vitamin D lead to

A

a decrease in Ca serum concentrations. Triggers the Parathyroid gland to secrete more PTH to increase the Ca mobilization from the bone

55
Q

Vitamin D (ergocalciferol) and active vitamin D sterols (calcitriol and paricalcitol and doxercalciferol) are used to treat

A

SHFP. They increase vitamin D concentrations and decrease PTH concentrations through negative feedback mechanism

56
Q

25-hydroxyvitamin D [25(OH)D] and 1,25(OH)2D3

A

25-hydroxyvitamin D [25(OH)D] is converted by the kidney to 1,25(OH)2D3. CKD stage 3 and 4 patients usually have enough kidney function left to run this conversion on their own. Stage 5 ESRD patients often do not and require the already active (converted) forms of vitamin D.

57
Q

Vitamin D synthesis overview

A

7-dehydrocholesterol in skin

–> sun exposure

–> cholecalciferol (D3)

–> 25 hydroxylase in liver

–> 25-hydroxyvitamin D

–>1-alpha-hydroxylase in kidney

–> 1,25-dihydrovitamin D (active)

–> binding to vitamin D receptors

–> biological actions

58
Q

Vitamin D (D2 and D3 require activation) Drugs

A

Ergocalciferol (calciferol) and Cholecalciferol are both for stage 3 and 4 patients (pts still have some kidney function left)

59
Q

Ergocalciferol is D_

A

D2

60
Q

Cholecalciferol is D_

A

D3

61
Q

Activated vitamin D compounds are for

A

CKD stage 5 and some CKD stage 3 and 4 patients

62
Q

Activated vitamin D Examples

A
  • Calcitriol (Rocaltrol and Calcijex)
  • Paricalcitol (Zemplar)
  • Doxercalciferol (Hectorol)
63
Q

Calcitriol (Rocaltrol and Calcijex)

A

-approved for use in pediatrics

***carries greatest risk of hypercalcemia

-cheap

64
Q

Paricalcitol (Zemplar)

A
  • 30% reduction in the PTH
  • Approved for pediatrics
  • most favorable ADE profile
  • less calcemic activity compared to calcitriol
  • $$$
65
Q

Doxercalciferol (Hectorol)

A
  • $$$
  • prohormone that becomes activated in the LIVER but if someone has liver failure (or maybe an alcoholic) –> the drug wont work
  • > /= 30% reduction in PTH
  • higher incidence of hyperphosphatemia (but still rare)
  • lower incidence of hypercalcemia compared to calcitriol
66
Q

Calcium homeostasis and secondary hyperparathyroidism (1 class of drugs)

A

Cinacalcet (Sensipar) - Oral

Etelcalcetide (Parsabiv) - IV

67
Q

Cinacalcet is a type

A

II calcimimetic agent

mimics the action of calcium but does so by binding to the cacium sensing receptor (CaR) and inducing a conformational change to the receptor, triggering the parathyroid gland to decrease PTH secretion.

68
Q

Etelcalcetide (Parsabiv) is (-)

A

Contraindicated in hypocalcemia. If Ca is <7.5 mg/dL, withhold cinacalcet/etelcalcetide until Ca is = or > 8 mg/dL.

69
Q

Anemia 4 key points

A

Nearly all ESRD patients will develop anemia by one or more of the following mechanisms.

  1. Decreased production of erythropoietin
  2. Uremia causes a decreased life span of red blood cells
  3. Vitamin losses during dialysis – folate, B12, B6
  4. Dialysis – loss of blood through dialyzer (hemolysis)
70
Q

Anemia S/Sx

A
  • HA
  • fatigue
  • dizziness
  • decreased cognition
71
Q

Anemia treatment goals

A

i. reverse signs and symptoms of tissue oxygen deprivation and left ventricular hypertrophy
ii. increase exercise tolerance and capacity
iii. optimize survival
iv. increase or quality of life

72
Q

Hemoglobin is _____ stable than a hematocrit

A

MORE

Hb is the best assessment parameter for anemia due to its increased stability over the hematocrit (Hct).

73
Q

Anemia monitoring standards

A

i. Hemoglobin (Hb)
Hb is the best assessment parameter for anemia due to its increased stability over the hematocrit (Hct).

ii. Hb vs. Hct

iii. KDIGO guidelines recommend monitoring Hb annually in CKD 3, twice/year in CKD 4-5ND, and every 3 months in CKD 5D as a means to screen for anemia.
If patients have existing anemia, then monitor Hb for CKD 3- 5ND every 3 months and CKD 5D monthly.

iv. Diagnosis of anemia and further workup should be initiated when:
Hb < 12g/dL in females
Hb <13g/dL in males

v. What is the goal Hb? This depends on if you are using an ESA – see below.

74
Q

Diagnosis of anemia in men vs women

what is normal

A
  • Hb < 12g/dL in females (normal = 14g/dL)

- Hb <13g/dL in males (normal = 15.5 g/dL)

75
Q

Anemia treatment comparisons

A
  • Ferritin = storage form of Fe (warehouse)

- TSAT = Transferring saturation (delivery truck of Fe)

76
Q

Define erythropoiesis

A

the generation of new red blood cells requires iron.

77
Q

KDIGO suggests that

A

iron supplementation if TSAT <30% and serum ferritin is <500 ng/mL.

78
Q

Monitor TSAT and ferritin

A

every 3 months. There is no longer a specific range for targeting TSAT and ferritin. KDIGO further recommends that iron should not be given if TSAT
>30% and/or ferritin is >500 ng/mL.

79
Q

Oral Iron

A

Will not likely be sufficient for correcting and maintaining iron stores for hemodialysis patients

May be used for CKD patients or peritoneal dialysis patients

Drug products include ferrous salts (sulfate, gluconate, and fumerate); various other products are available as well.

***Dose = 200 mg of elemental iron per day at least! Heme iron

-SE: stomach upset (hurts to absorb). Best absorbed in an acidic environment

80
Q

What to consider when giving iron?

A
  • food increases stomach pH
  • Enteric coating interferes with absorption
  • pts on meds increase pH
81
Q

Heme iron

A

Greater absorption, different absorption site –> not subject to 200 mg/day rule

82
Q

Heme iron examples

A
  • Proferrin ES

- Proferrin Forte

83
Q

IV route ______ route for CKD 5D patients

A

PREFERRED

84
Q

IV Iron Agents

A
  • Iron Dextran (infed, dexferrum)
  • Sodium ferric gluconate (Ferrlicit)
  • Iron Sucrose (Venofer)
  • Ferric carboxymaltose (Injectafer)
  • Ferumoxytol (Feraheme)
85
Q

Iron sucrose

A

indication for patients not yet on dialysis

86
Q

Feraheme

A

interferes with magnetic resonance(MR) imaging for up to 3 months after the second injection. MR imaging should be completed prior to starting ferumoxytol.

87
Q

Low molecular weight vs. high molecular weight iron

A

Low molecular weight = Infed

High molecular weight = Dexferrum

***BOTH ARE DEXTRAN

88
Q

Pts with high MW iron had

A

higher rate of anaphylaxis

89
Q

Erythropoiesis Stimulating Agents (ESAs) used

A

used after all other correctable causes of anemia have been addressed

90
Q

When suggested to use ESAs?

A

When not on dialysis yet

CKD 3-5ND Hb < 10 g/dL; Hb falling at a rapid rate; needed to avoid blood transfusion

CKD 5D Start when Hb is between 9 and 10 g/dL

91
Q

ESA improves quality of life but

A

increases risk of cerebral vascular events

92
Q

HARD cut-off of ESA at

A

11.5 g/dL

93
Q

Recombinant human erythropoietin (rHuEPO, epoetin alfa, Epogen, Procrit, EPO)

A

stimulates erythroid progenitor cells

94
Q

Epogen was the _____ drug

A

FIRST

95
Q

Recombinant human erythropoietin has an ___ preferred route

A

SC!

96
Q

Darbepoetin alfa (Aranesp)

A

samed concept as recombinant human erythropoietin

***dosed ONCE per week IV or SC

97
Q

Methoxy polyethylene Glycol

A
  • extended half-life

- dosed once every two weeks

98
Q

ESA adverse effects (Epogen, Aranesp, and Mircera)

A

Pure Red Cell Aplasia PRCA: antibodies develop to erythropoietin; DC drug permanently

HTN: Most common, increase in BP by 23% in patients

99
Q

Causes of ES therapy failure

A

***Lack of vitamins or iron

Aluminum toxicity Active bleed

Drug induced bone marrow suppression

Acute inflammation or infection

100
Q

Acid Base Disorders: ESRD pts cannot

A

excrete H+ ions and develop metabolic acidosis.

101
Q

Acid Base treatment usually starts when

A

bicarb is <20 mEq/L

102
Q

Treatment options

A

a) Dialysis – increase bicarbonate in dialysate (usually always corrects the problem in dialysis patients)
b) Shohl’s solution – contains 1 mEq sodium and 1 mEq bicarbonate (as sodium citrate) per ml of solution.

c) sodium bicarbonate tablets 325mg and 650mg strengths
1 gram of sodium bicarbonate contains 11.9 mEq of sodium and 11.9 mEq of bicarbonate.

d) Dose(mEq) = Vd bicarb(0.5 L/kg) x wt(kg) x (24mEq/L – HCO3),
administer over several days

103
Q

Most common treatment option of acid base disorders

A

Sodium bicarbonate tablets

104
Q

Nutrition for acid base disorders

A
  1. Protein and energy requirements (ESRD vs CKD) ***Protein: 0.8 g/kg/day if GFR < 30 ml/min

CKD 3,4

  1. 2 g/kg/day if have ESRD
  2. Water soluble vitamin replacement Nephrocaps,
    - B + C for dialysis patients (Potential intervention to put pts on this)

Nephron FA

105
Q

Uremic bleeding is a _____ complication of chronic kidney disease pts

A

common

mechanism is not fully understood. due partially to impaired binding of von willebrand factor to platelet membrane glycoprotein receptors

106
Q

Signs of uremic bleeding

A

purpura, ecchymoses, epistaxis, and bleeding from hemodialysis access sites.

107
Q

Treatment of uremic bleeding

A

a) red cell transfusions
b) cryoprecipitate (fraction of blood containing factor VIII, fibrinogen, fibronectin)
c) DDAVP
d) conjugated estrogens

108
Q

Single most important cause of ESRD worldwide

A

DKD - diabetic kidney disease

109
Q

DKD mechanism of action

A

excess glucose in the blood enters the glomerular cells and through multiple biochemical mechanisms alters the ability of the glomerulus to filter waste products from the blood appropriately.

110
Q

Microalbuminuria

A

a) one of the best predictors of DKD; also a risk factor for heart attack and stroke
b) ACR value between 30-300 mg/g = microalbuminuria
c) 2-3 consecutive ACRs in this range is “persistent” microalbuminuria
d) all diabetic patients should have an ACR annual spot urine check for microalbuminuria
e) Target HbA1c approximately 7%

111
Q

***Treatment of DKD

A

a) SGLT2 inhibitors and metformin - control blood glucose (if eGFR >30)
b) HgbA1c <6.5 – 8.0% in non-dialysis dependent CKD
c) lifestyle modifications – weight loss
e) protein requirements CKD stage 1-4 = 0.8 g/kg/day
f) antihypertensives – ACE inhibitors and ARBs because they decrease proteinuria in addition to their blood pressure lowering effects.
g) hypertensive DKD CKD patients may require multiple drug combinations. ACE I and ARB combination therapy may increase hyperkalemia and acute kidney injury. NEJM 2013;369:20

Therapeutics II (12 decks)

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