CKD and ESRD Flashcards

1
Q

Define chronic kidney disease and end stage renal disease.

A

Chronic kidney disease is the progressive degeneration of the kidneys and loss of function over several months to years. End stage renal disease is a term used to describe a patient’s condition when renal failure has reached stage 5 (GFR < 15mL/min).

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2
Q

Differentiate the 5 stages of CKD based on kidney function (GFR).

A
Stage 1 = >90mL/min
Stage 2 = 60-89 mL/min
Stage 3 = 30-59 mL/min
Stage 4 = 15-29 mL/min
Stage 5 = <15 mL/min
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3
Q

Other than by GFR, what is one other method by which different levels of kidney disease can be differentiated?

A

albuminuria

A1= <30 mg/day
A2= 30-300 mg/day
A3= >300 mg/day
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4
Q

Explain how diuretic resistance develops and how it can be overcome.

A

Diuretic resistance often develops with long-term use of loop diuretics. As higher levels of sodium are continuously delivered to the DCT, sodium channels are working hard to accommodate by increasing reabsorption. Over time, DCT cells hypertrophy and express more sodium channels. This can eliminate the effect of the loop diuretic. To overcome this, the loop diuretic can be combined with a thiazide, which acts in the DCT.

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5
Q

What is the Cockroft-Gault equation, and what is it used for?

A

used for calculation of CrCl for drug dosing purposes and ESTIMATING kidney function

CrCl=((140-age)IBW)/(SCr72)

if female, multiply by 0.85

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6
Q

What is the MDRD equation, and what is it used for?

A

MDRD calculates GFR and is used for staging kidney disease.

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7
Q

If the Cockroft-Gault equation is going to be used for CrCl calculation, what must be true of the patient’s kidney function?

A

It must be STABLE. Patients with rapidly changing kidney function (those with AKI) cannot have CrCl estimated by this equation.

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8
Q

Explain why the Cockroft-Gault equation tends to overestimate kidney function in patients with moderate to severe kidney disease.

A

When GFR drops significantly, creatinine can still be disposed of, to an extent, by secretion to accommodate the loss of filtration. Our measured creatinine clearance would suggest that filtration is better than it actually is due to increased secretion.

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9
Q

When the kidneys cannot excrete metabolic wastes from the blood, the resulting condition is called ________.

A

uremia

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10
Q

What are some of the systemic effects of uremia? (hint: think about each body system and how it is affected by excess wastes or fluid)

A

CNS: encephalopathy
EENT: uremic fetor (pee breath)
pulmonary: non-cardiogenic edema from fluid overload
CV: Na retention–>volume overload–>LVH
GI: anorexia, constipation, metallic taste
musculoskeletal: restless leg syndrome and metabolic bone disorder
hemodynamic: anemia due to EPO deficiency
skin: uremic frost

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11
Q

Damaged kidneys cannot properly regulate the levels of ______ and ______ in the body, so patients are often fluid overloaded.

A

water and salt

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12
Q

What are the guidelines for fluid restriction in patients with fluid retention issues due to CKD?

A

Fluid restriction is not really necessary in these patients as long as their sodium intake is controlled. It is, however, recommended that these patients avoid large quantities of water.

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13
Q

Why don’t diuretics work in patients without functioning kidneys?

A

Diuretics work by increasing the amount of urine produced. If a patient can’t produce urine, the diuretic will have no effect.

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14
Q

________ diuretics will work when CrCl is <30 mL/min, but ________ diuretics will not.

A

Loop, thiazide

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15
Q

Why are thiazide diuretics less effective at very low CrCl levels? (<30 mL/min)

A

As CrCl gets below 30 mL/min, a greater percentage of sodium is reabsorbed in the PCT because there is less of it being filtered out and delivered to this segment. With more reabsorption in the PCT, there is less delivery to the DCT, where thiazides act. So, their effect is negated.

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16
Q

What are the dietary restrictions for sodium and potassium in patients with CKD?

A

NMT 2g of Na/day
NMT 5g of NaCl/day
NMT 3g of K/day

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17
Q

What is the treatment protocol for hyperkalemia?

A

will differ according to site, but usually involves:

  • calcium chloride/gluconate to stabilize myocardium
  • insulin/dextrose to push potassium back into cells
  • nebulized albuterol
  • potentially bicarb (but not for ESRD pts)
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18
Q

What are the 3 key points of mineral and bone disease that we can pharmacologically target?

A

(1) hyperphosphatemia
(2) hypocalcemia
(3) decreased vitamin D

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19
Q

What class of drugs is indicated for hyperphosphatemia? How do they work?

A

phosphate binders

They bind phosphate in the GI tract to prevent its absorption.

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20
Q

When MUST phosphate binders be taken, and why?

A

with meals, once phosphate has been absorbed in the blood, there is nothing we can do about it

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21
Q

What is the most common side effect of phosphate binders?

A

constipation

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22
Q

What is the maximum amount of elemental calcium that can be consumed per day?

A

1500 mg

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23
Q

calcium carbonate= _______

calcium acetate= _______

A

TUMS, PhosLo

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24
Q

Which calcium-containing phosphate binder binds more phosphate in the GI tract?

A

calcium acetate (PhosLo) – binds twice as much phos as TUMS

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25
Q

Velphoro=__________

A

sucroferric oxyhydroxide

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26
Q

What are some common side effects noted with Renvela (sevelamer carbonate)?

A

N/V, diarrhea

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27
Q

What are the positive characteristics of Renvela that make it the “gold standard” for non-calcium phosphate binders?

A

(1) decreases LDL by 15-30%
(2) decreases serum uric acid
(3) not absorbed-low toxicity rate
(4) no ADRs noted even with therapy way above suggested dosages

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28
Q

Which non-calcium phosphate binder is suggested for patients with CKD on dialysis?

A

Auryxia (ferric citrate)

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29
Q

Which compound contains iron that binds phosphate so tightly that none of the iron is absorbed?

A

Velphoro (sucroferric oxyhydroxide)

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30
Q

Fosrenol=_________

A

lanthanum carbonate

31
Q

Which two non-calcium phosphate binders can cause stool discoloration?

A

Velphoro (sucroferric oxyhydroxide)
Auryxia (ferric citrate)

both contain iron

32
Q

How is lanthanum carbonate (Fosrenol) excreted?

A

in the feces, so there is no long-term accumulation of this drug

33
Q

While calcium-containing phosphate binders are 0% effective at low pH, _______ is highly effective (97.5%) at pH 3.

A

lanthanum carbonate (Fosrenol)

34
Q

What are some side effects associated with Fosrenol?

A

GI symptoms

35
Q

What effect do Velphoro and Auryxia have on TSAT and ferritin?

A

Auryxia increases both, while Velphoro has no effect on either.

36
Q

If dietary restriction of phosphorus is necessary, how much should patients limit their intake to?

A

800-1000 mg/day

37
Q

Which foods are high in phosphorus?

A

meats, nuts, dairy, dried beans, colas, beer

38
Q

How does hyperphosphatemia affect vitamin D and calcium levels?

A

Hyperphosphatemia inhibits the kidneys’ ability to activate vitamin D. Because vitamin D is crucial for calcium absorption, serum calcium levels decrease.

39
Q

What is the kidneys’ role in activation of vitamin D?

A

conversion of 25-OH vitD to calcitriol, the active form of vit D

40
Q

Why is it preferred to give inactive forms of vitamin D to patients with some remaining kidney function?

A

Anytime the patient can use their organs to convert only the amount of drug needed, this is the kind of therapy we want to provide. If we give active vitamin D, the patient has no control over how much is produced and may end up getting more than is actually needed by the body.

41
Q

What are the two inactive vitamin D compounds used therapeutically to lower PTH levels by a negative feedback mechanism?

A

Ergocalciferol (vitamin D2)

Cholecalciferol (vitamin D3)

42
Q

At which stages of kidney disease are patients still able to receive inactive vitamin D for conversion by the kidneys?

A

stages 3 and 4

43
Q

When is it necessary to give patients active vitamin D?

A

stage 5 renal failure (ESRD)

44
Q

Calcitriol (active vitamin D) is marketed under which names?

A

Rocaltrol (PO dosage form)

Calcijex (IV dosage form)

45
Q

Which two active vitamin D compounds are approved for pediatric use?

A

calcitriol and paricalcitol

46
Q

Which active vitamin D compound has the best ADR profile, causes greater than 30% decrease in iPTH, and has less calcemic activity compared to calcitriol? (and does NOT require activation by the liver)

A

Zemplar (paricalcitol)

47
Q

Hectorol=_________

A

doxercalciferol

48
Q

Which active vitamin D compound is a pro hormone?

A

Hectorol (doxercalciferol)

49
Q

Hectorol has an increased incidence of ___________ compared to Zemplar, but a lower incidence of ___________ compared to calcitriol.

A

hyperphosphatemia, hypercalcemia

50
Q

A physician approaches you and asks for a recommendation for a patient with hyperparathyroidism that is not controlled by vitamin D related compounds (D2, D3, or active vitamin D). What is another drug class (and an example) you could recommend?

A

a type 2 calcimimetic agent

only one approved–Sensipar (cinacalcet)

51
Q

Describe the mechanism of action of Sensipar.

A

Sensipar is a type 2 calcimimetic agent, meaning it binds somewhere on (not in) the PT receptor that senses blood calcium levels. It is able to induce the same shape change as calcium and signal a decrease in PTH production.

52
Q

There are four ways by which nearly all ESRD patients can become anemic. What are they?

A

(1) decreased erythropoietin production
(2) loss of blood through dialysis
(3) loss of vitamins through dialysis
(4) uremia (shortens RBC lifespan)

53
Q

What is MCV? What is the normal lab value?

A

MCV-mean corpuscular volume, aka the average size of an RBC

80-96 cubic micrometers

54
Q

What is RDW? When is it necessary to know?

A

RDW-red cell distribution width, the range of sizes of RBCs in circulation

RDW is good to know if a patient has several vitamin deficiencies that may cause both microcytic and macrocytic anemia, which would yield a normal MCV even though the patient is still anemic.

55
Q

What are the signs and symptoms of anemia?

A

fatigue, dizziness, palor, HA, cognition issues

56
Q

What is the optimal monitoring parameter to assess a patients anemic status?

A

Hgb (better that Hct due to increased stability)

57
Q

How is oral iron (used for tx of anemia) best absorbed?

A

in an acidic environment

58
Q

What are some counseling tips and monitoring parameters for patients using oral iron for anemia?

A

take with OJ to keep stomach acidic
do not take with food
separate from oral calcium by 2 hours

monitor for drugs that increase pH (PPI, H2 antagonists, antacids)

59
Q

What are TSAT and ferritin levels used to detect?

A

TSAT=transferrin saturation–aka amount of iron being transported in the blood

ferritin=stored iron levels

60
Q

How often should TSAT and ferritin be monitored? At what point should oral iron therapy be discontinued in regards to these levels?

A

at least every 3 months

D/C when TSAT>30% or ferritin>500ng/mL

61
Q

When should therapy with an erythropoiesis stimulating agent (ESA) be initiated?

A

when all other anemia treatments have failed

CKD 3-5 patients when Hgb <10 g/dL or
CKD 5 patients when Hgb 9-10 g/dL

62
Q

ESA treatment should stop with Hgb reaches _______.

A

11.5 g/dL

63
Q

What are two ESA currently in use for anemia?

A

recombinant human erythropoietin (ProCrit, epoetin alfa, Epogen)

darbepoietin alfa (Aranesp)

64
Q

ESA use is associated with several adverse effects, including: (6 total)

A

pure red cell aplasia (development of ABs against RBCs)
stroke
seizures
hypertension
cardiac arrest
exacerbation of comorbidities (HTN, CHF, AMI)

65
Q

ESA doses are titrated according to what monitoring parameter? How often should this be monitored?

A

hemoglobin, monitored every week during initiation, then every 4 weeks

66
Q

What is the goal for Hgb increase during ESA therapy?

A

1-2 g/dL/month

67
Q

ESRD patients often develop _________ (an acid base disorder) due to their inability to _________.

A

metabolic acidosis due to inability to secrete H+ ions

68
Q

How can acidosis be corrected in ESRD patients?

A

(1) increase bicarb in dialysate
(2) oral bicarb therapy with Stohl’s solution or tablets
(3) IV bicarb administered over several days

69
Q

Which vitamins may need replaced in patients on dialysis?

A

water-soluble B&C (fat soluble not removed by dialysis)

70
Q

What are the major causes of CKD?

A

DM, HTN, glomerulonephritis, PKD, HIV nephropathy

71
Q

How often should hemoglobin be monitored at the start of ESA therapy? How often can you change the dose if you desire?

A

monitor hemoglobin weekly, but do not change dose more than once every 4 weeks

72
Q

Many (23%) of CKD patients using an ESA experience this adverse effect:

A

HTN

73
Q

What are the goal protein amounts for CKD patients with CrCl < 30 mL/min? for ESRD patients?

A
  1. 8 g/kg/day if CrCl < 30 mL/min

1. 2 g/kg/day if ESRD