Pharmacotherapy Of Renal Disease

Front 1

T/F:
Its not uncommon to see a patient on 15 to 20 drugs when suffering from AKF or CKF.

Back 1

True, not uncommon usually 15-20 drugs

Front 2

What is the focus of renal disease?

Back 2

Management of complications and prevention of consequences

Front 3

Name the organ systems effected by renal failure (5)

Back 3

cardiac, vascular, dermatological,CNS, hematological, endocrine

Front 4

What is the definition from the slides of chronic renal failure?

Back 4

Progressive deterioration in renal function ultimately leading to irreversible nephron structural damage

Front 5

CRF is based off the presence of ___/_____ for >3 months + a GFR of <_____ml/min/1.73m2

Back 5

CRF is based off the presence of _proteinuria_/_albuminuria_ for >3 months + a GFR of <_90_ml/min/1.73m2

Front 6

What are the GFR's for the 5 stages of CKD?

Back 6

Stage 1: <90
Stage 2: 60-89
Stage 3: 30-59
Stage 4: 15-29
Stage 5 (ESRD): <15

Front 7

What is the Cockcroft-Gault method of approximating GRF/CrCl?

Back 7

Males:
(140-age)(TBW)/SCr72
Females multiple by .85
TBW up to 120% of IBW
otherwise use ABW:
IBW + [0.40(TBW-IBW)]
IBWM= 50+2.3(inches > 5ft)
IBWF=45+2.3(inches>5ft)

Front 8

What is the equation for the 24 hour urine collection?

Back 8

CrCl=UV/Pt
U=urine Cr
V=urine Volume
P=plasma Cr
t=time of collection

Front 9

What are the most common causes of CKD in the US? (4)

Back 9

DM, HTN, Glomerular nephoritis (GN), Polycystic kidney disease (PKD)

Front 10

What are some susceptibility factors for CKD? (4)

Back 10

Advanced age, low income or education (2), racial/ethnic minority

Front 11

What are some initiation factors of CKD mentioned on the slide?

Back 11

DM, HTN, GN, infections, ADRs and others

Front 12

What are some progression factors that further kidney deterioration? (6 from slide)

Back 12

Proteinuria, Hyperlipidemia, HTN, DM, obesity, Tobacco use

Front 13

DM increasing the risk of developing CKD by what percent? What about Type 2?

Back 13

40-50%
Type 2 have a 12 fold greater risk than nonDM

Front 14

Agressive therapy in DM has been associated with a decrease in ____________

Back 14

Agressive therapy in DM has been associated with a decrease in _risk for albuminuria_

Front 15

What combo of factors leads to a 6 fold > risk of ESRD?

Back 15

HTN+DM

Front 16

T/F:
Early and agressive tx of HTN is associated with a decrease in progression of CKD

Back 16

True that

Front 17

What is considered nephrotic syndrome with proteinuria?

Back 17

>5 gms/qd

Front 18

When does treating proteinuria benefit the most?

Back 18

With high levels of proteinuria

Front 19

What are 2 characteristics of nephrotic syndrome as mentioned?

Back 19

Proteinuria and hyperlipidemia

Front 20

T/F:
The prevalence of hyperlipidemia decreases and renal function declines

Back 20

False
The prevalence increases

Front 21

What are some CV clinical presentations of CKD? (4)

Back 21

HTN, hyperlipidemia, HF, angina pectoris

Front 22

What are some CNS clinical presentations of CKD? (3)

Back 22

Clouded sensorium, coma, seizures

Front 23

What are some hematological presentations of CKD? (2)

Back 23

Anemia, hemorrhage

Front 24

What are some M.S. presentations of CKD? (2)

Back 24

Renal osteodystrophy, osteoporosis

Front 25

During ESRD what are some clincal presentations mentioned in the slides? (5)

Back 25

decrease in thyroid, decrease in glucose (unable to clear insulin in ESRD), acidosis, DM, increase in PTH

Front 26

T/F:
Some clincal presentations of CKD include: uremic syndrome, pruritus, altered fluids and electrolytes.

Back 26

True, these are some "misc" clinical presentations

Front 27

Generally, what are some emphasis on therapies known to slow renal deterioration? (3)

Back 27

delay hemodialysis (improve pts QOL)
avoid tx that hasten renal det.
DC or minimize use of nephrotoxins

Front 28

What is an important non drug tx approach in CKD?

Back 28

decrease intake of PO4 and protein

Front 29

For CKD treatment a no salt added diet is more restrictive in what risk factors?

Back 29

HTN and edema

Front 30

In Na restriction you can use what pharmalogical approach?

Back 30

Use loop +/- a thiazide

Front 31

Which thiazide is preferred in Na restriction?

Back 31

Metolazone, it retains its diuretic properties even when CrCl is <30 ml/min

Front 32

When is H2O restriction unnecessary when treating CKD?

Back 32

If Na intake is "contolled" and stage < 5

Front 33

T/F:
H2O restriction should be avoided in CKD when a pt is oliguric/anuric or ESRD.

Back 33

True

Front 34

What is the goal of K restriction in CKD?

Back 34

50 to 80 mEq/day

Front 35

When should avoid and not avoid NaHCO3 when restricting K in CKD?

Back 35

Avoid: if pt is HTN or hyperkalemic
Not Avoid: when pt has acidosis

Front 36

What is an approach to restricting K in CKD mentioned in the slide?

Back 36

D/C or limit K retaining meds

Front 37

T/F:
Loop diuretics are effective in restricting K in CKD

Back 37

False, theyre actually ineffective

Front 38

What is the agressive goal of bp for HTN in CKD w/o DM or proteinuria? What about with those disorders?

Back 38

130/80 for just HTN
W/ DM or proteinuria its 125/75 mmHg

Front 39

A goal of therapy in HTN in CKD is to minimize or eliminate ______

Back 39

A goal of therapy in HTN in CKD is to minimize or eliminate _proteinuria_

Front 40

These pharmacological treatments are 1st line in treating HTN in CKD while slowing the decline of renal function.

Back 40

What is ACEI's and ARB's

Front 41

ACEI's and ARB's are especially beneficial in these pt's, w/ or w/o HTN in CKD.

Back 41

What is DM

Front 42

Why should pt's be monitored in CKD in regards to HTN meds?

Back 42

They can lead to ARF

Front 43

What CCB is preferred in HTN for CKD? What are two examples of these class?

Back 43

NDHP, diltiazem and verapamil

Front 44

Why should an alpha agonist be avoided when taking a BB?

Back 44

Can cause rebound HTN w/ poor compliance and sever bradycardia

Front 45

What were then examples given of ACEI's?

Back 45

Captopril, Enalapril, Lisonipril, Fosinopril, Trandolapril

Front 46

What were then examples given of ARB's?

Back 46

Losartan, Valsartan, Ibersartan, Candesartan

Front 47

T/F:
BB mayb exacerbate renal dysfunction but are not really contraindicated in the tx of HTN in CKD.

Back 47

True

Front 48

What is the main MOA of BB in the tx of HTN in CKD?

Back 48

decrease CO to decrease renal blood flow

Front 49

Using water soluble agents such as ________ and _______ should be avoided when using BB to tx HTN in CKD because they can do what in the kidneys?

Back 49

Using water soluble agents such as _atenolol_ and _nadolol_ should be avoided when using BB to tx HTN in CKD because they can _accumulate_ in the kidneys

Front 50

ACEI's block the conversion of?

Back 50

ANGI --> ANGII

Front 51

ARB's block what receptor?

Back 51

AT1

Front 52

SCr is going to increase or decrease with a HTN medicine in CKD?

Back 52

Increase up to 30-40% over 1st 3 months

Front 53

When would you stop using an Rx for HTN in CKD in regards to CKD?

Back 53

If increase in K developes

Front 54

When do you start measuring Cr every 6 months when using a HTN Rx in CKD?

Back 54

After check Cr and K every 1 to 4 weeks after starting until stable levels then every 6 months

Front 55

What is metabolic acidosis?

Back 55

Decrease in net acid excretion leading to acid accumulation

Front 56

At what stage of CKD is metabolic acidosis clinically significant?

Back 56

Stage 4

Front 57

What are the clinical presentations of metabolic acidosis, mentioned in the slides? (5)

Back 57

Exacerbates renal osteodystrophy
Decrease in Vit D synthesis
Fatigue (impairs O2 delivery)
Decrease in contractility (ionotrophic)
Increase in protein catabolism

Front 58

What are the goals of tx in metabolic acidosis?

Back 58

Normalize systemic pH (7.35-7.45) and HCO3 (22-26 mEq/L)

Front 59

What is the normal pH range for a patient?

Back 59

7.35-7.45

Front 60

What is the normal HCO3 range in a patient?

Back 60

22-26 mEq/L

Front 61

What can be used to treat metabolic acidosis in a pt with CKD?

Back 61

Citrate/citric acid solutions

Front 62

Shohl's, Bicitra, Polycitra all cause an increase in what electrolyte to decrease metabolic acidosis?

Back 62

Potassium

Front 63

Citrate increases ______ when being used to treat M.A. in CKD.

Back 63

Citrate increases _HCO3_ when being used to treat M.A. in CKD.

Front 64

Citric Acid is converted to these two chemical compounds that allow the decrease in metabolic acidosis.

Back 64

What is H2O and CO2

Front 65

What should be avoided when using any citrate/citric acid solution?

Back 65

Al

Front 66

When using NaHCO3 in metabolic acidosis, what must be true of the pt in regards to HTN?

Back 66

Their HTN must be controlled

Front 67

What is renal osteodystrophy?

Back 67

Soft tissue mestatic calcification (in the joints, blood vessels, kidneys, intestine, and eyes, etc)
Ca ppt into tissue causing hypocalcemia
PO4 is elevated in the blood causing hyperphosphotemia
This then leads to an increase in PTH which then causes Ca to be removed from the bones leading to osteodystrophy

Front 68

What are some pulmonary consequences of renal osteodystrophy? (3)

Back 68

decrease in pulmonary function test
pulmonary fibrosis
pulmonary HTN

Front 69

What is a vascular consequence of RO?

Back 69

organ ischemia

Front 70

What are some M.S symptoms of RO?

Back 70

pain, bone pain, myopathy, fatigue, tendon rupturre

Front 71

What are some pulmonary sx of RO?

Back 71

SOB, CP (chest pain)

Front 72

What are some cardiac sx of RO?

Back 72

CP, AMI, death

Front 73

T/F:
The evidence of RO is amenable due to the quick onset of symptoms.

Back 73

False:
The evidence of RO is not amenable, the onset is too slow and when symptoms come about its too late

Front 74

What are the risk factors for RO? (4)

Back 74

Hyperphosphatemia
Ca-P product > 55mm2/dL2
2ndary hyperparathyroidism
Excessive Ca intake

Front 75

How is the Ca-P product calculated?

Back 75

Ca level * PO4 level

Front 76

What is the Ca-P product level at which mortality risk is increase?

Back 76

<70 mm2/dL2

Front 77

What 4 things mentioned in the slide can lead to excessive Ca intake, a risk factor of RO?

Back 77

Diet
Dialysis
Ca containing P binding agents
Ca supplement

Front 78

What are 3 general pharmacological tx for RO?

Back 78

PO4 binders, Vit D, and calcimimetic

Front 79

At what level of CrCl should a pt be at to initiate dietary PO4 restriction in regards to RO and CKD?

Back 79

CrCl <60 ml/min

Front 80

In PO4 restriction, other than protein, what can a pt limit in their diet?

Back 80

meats, dairy, beans, dark cola, peanut butter, beer, and chocolate

Front 81

What is the name of the surgery involved in RO for those pts resistant to therapy?

Back 81

Parathyroidectomy

Front 82

What needs to be done with PO4 binding agents in order to have maximal effect?

Back 82

Take just before or with a meal

Front 83

What is the MOA of a PO4 binding agent?

Back 83

Bind to and sequester PO4 in the GI lumen so its not absorbed and thus excreted

Front 84

What are some examples of PO4 binding agents (PBA)?

Back 84

Ca salts
Aluminum salts
Non Ca/Al/Mg

Front 85

When does Ca carbonate, a Ca salt (PBA), have a max effect? What do you do if there are ADR?

Back 85

At acidic gastric pH
Give with a meal

Front 86

What drugs should be avoided when using Ca carbonate (PBA)?

Back 86

H2 receptor blocked and PPIs

Front 87

What are the 3 Ca salts that are PO4 binding agents?

Back 87

Ca carbonate, Ca acetate, Ca citrate

Front 88

T/F:
Ca carbonate binds twice as much PO4 as Ca acetate.

Back 88

False
Ca ACETATE binds twice as much PO4 as Ca CARBONATE

Front 89

What is the advantage of Ca acetate over Ca carbonate in regards to gastric pH?

Back 89

Ca acetate is more effective over a wider range of gastric pH than Ca carbonate

Front 90

Why is there a greater likelihood of hypercalcemia with Ca acetate compared to Ca carbonate?

Back 90

Ca acetate has greater systemic absorption

Front 91

Ca citrate has _____ PO4 binding capacity and _____ Al absorption

Back 91

Ca citrate has _Low_ PO4 binding capacity and _increased_ Al absorption

Front 92

What therapeutic agent is used in combo with Ca salts that is also a PBA?

Back 92

Non Ca/Al/Mg such as sevelamer and lanthanum carbonate (fairly expensive!)

Front 93

When would a non Ca/Al/Mg PBA be used?

Back 93

When pt arent responding to Ca salts or if the pt becomes hypercalcemic

Front 94

The Al salt PBA are considered 3rd line. When should a pt be prescribed them?

Back 94

If there is severe hyperphosptemia or in combo with Ca compounds or Sevelamer when response to the other single agents are inadequate

Front 95

What is the limit of duration for Al salt PBAs?

Back 95

</= 4 weeks

Front 96

What are some consequences of Al salts?

Back 96

Osteomalacia, encephalopathy, and anemia

Front 97

During CKD and onward to RO, _______ can be used to increase GI absorption of Ca, decrease PTH, and increase renal PO4 absorption

Back 97

During CKD and onward to RO, _Vitamin D therapy_ can be used to increase GI absorption of Ca, decrease PTH, and increase renal PO4 absorption

Front 98

Vitamin D therapy minimizes the likelihood of?

Back 98

hypercalcemia and hyperphosphotemia

Front 99

What stage of CKD should Vitamin D be started?

Back 99

Stage 3 or after

Front 100

Can Vitamin D (such as calcitriol, paricalcitriol, or doxercalcefitriol) be administered with a calcimimetic (such as cinacalet)?

Back 100

Yes

Front 101

T/F:
Cinacalet, a calcimemtic, is approved for any stage of CKD.

Back 101

False,
Only approved for Stage 3 and greater in CKD

Front 102

What is the MOA of a calcimemetic?

Back 102

Increases the sensitivity of calcium- sensing receptors of the PT gland to Ca thus supressing PTH secretions

Front 103

Can cinacelet (calcimemetic) be administered with Ca salts (PBA) and sevelamer (PBA)?

Back 103

Yes

Front 104

What are the cutoffs of Hb for male and female for anemia?

Back 104

Male <13mg/dl
Female <12mg/dl

Front 105

Anemia in CKD is defined as?

Back 105

The inability to produce erythropoeitin (EPO) due to renal insuffieciency

Front 106

How much circulating EPO is produced by a normal functioning kidney?

Back 106

90%

Front 107

Hypoxia or a decrease in Hct leads to and increase in __________ production

Back 107

Hypoxia or a decrease in Hct leads to and increase in _EPO production_

Front 108

If Fe, FA, and B12 are WNL the inability to produce EPO results in a ____chromic, _____cytic anemia

Back 108

If Fe, FA, and B12 are WNL the inability to produce EPO results in a _normo_chromic, _normo_cytic anemia

Front 109

What GFR does anemia usually develope at?

Back 109

</ 50-60 ml/min

Front 110

The lifespan of a RBC in anemia is _______

Back 110

The lifespan of a RBC in anemia is _shortened_
(from 120 days to 60 days)

Front 111

What are some s&s of anemia?

Back 111

dypsnea, fatigue, dizziness, HA, pallor, angina, CHF, mental state changes

Front 112

What is the adaption phenomenon in anemia?

Back 112

Where there are no symptoms present

Front 113

If the RBC present as hypochromic (pale) and microcytic (smaller) then what kind of anemic deficiency does the pt have?

Back 113

Fe deficiency

Front 114

When RBC present as macrocytic (very large and immature) what type of anemic deficiency does the pt have?

Back 114

B12 and/or FA (folic acid)deficiency

Front 115

What are the goals of therapy for anemic pts with CKD?

Back 115

Increase the O2 carrying capacity of RBC and minimize symptoms

Front 116

In iron deficiency anemia (IDA) Serum Fe is insenstive
Transferrin sat'n is ___ normal
Ferretin is ____
TIBC is ____

Back 116

In iron deficiency anemia (IDA) Serum Fe is insenstive
Transferrin sat'n is _below_ normal
Ferretin is _low_
TIBC is _high_

Front 117

What are 4 oral iron tx for treating anemia in CKD?

Back 117

Ferrous sulfate
Ferrous gluconate
Polysaccharides
Heme iron polypeptides

Front 118

When is absorption best for oral iron agents?

Back 118

On an empty stomach

Front 119

What are some ADRs of oral iron agents? (4)

Back 119

Constipation
Nausea
Abdominal cramping
Black stools

Front 120

When are iron oral agents not useful?

Back 120

When there is functional iron deficiency, w transferrin sat'n less than 20% but normal or elevated ferritin

Front 121

What iron tx can be given IV?

Back 121

Ferric gluconate, iron sucrose, iron dextran

Front 122

What is the preferred route of administration in functional iron deficiency?

Back 122

IV

Front 123

IV iron tx can lead to what ADRs? (5)

Back 123

allergic rxn (iron dextran)
hypotension
dizziness
dypsnea
HA

Front 124

What should be given with Fe to prevent an Fe overload?

Back 124

Deferoxamine

Front 125

For megablastic (macrocytic) anemia, what should be prescribed?

Back 125

FA and B12 supplement

Front 126

What is the DOC for long term management of anemia?

Back 126

ESA (epoetin alfa, darbepoetin)

Front 127

What comorbidities are resistant to ESA tx? (8)

Back 127

Fe deficiency, Al toxicity, bleeding, malnutrition, CA, chemo, HIV, infections

Front 128

What are 2 ADRs of ESA?

Back 128

HTN, seizures

Front 129

What is the normal dosing for epoetin alfa?

Back 129

50-100 units/kg IV/SC 3 times a week

Front 130

What is the normal dosing for darbepoetin?

Back 130

0.45 mcg/kg/week

Front 131

Transfusion for anemic pts are reserved for what occassions? (3)

Back 131

Acute symptoms
Major blood loss
Before surgery

Front 132

T/F:
Hyperlipidemia slows the rate of decline of CrCl

Back 132

True

Front 133

T/F:
There is no known reversal therapy for established ARF

Back 133

True

Front 134

What is the focus of tx for ARF?

Back 134

Supportive therapy, managing other diseases, D/c nephrotoxins

Front 135

What is the definition of ARF?

Back 135

Decrease in GRF over hours to days and accumulated waste products including Cr in urea
Abrupt increase of SCr >50%
or
Abrupt decrease of GFR >25%
Reduction in urinary output >6 hrs

Front 136

Why is the cockcroft-gault equation not useful in ARF?

Back 136

Because weight and CrCl is rapidly changing

Front 137

What are the risk factors for ARF? (7)

Back 137

age>60,preexisting renal, liver, CV/vascular, or lung disease, infection, hemorrhage, volume depletion, DM, male, nephrotoxins

Front 138

What medications are considered nephrotoxic in ARF? (11)

Back 138

Contrast media dyes, NSAIDs, chemo, ACEI or ARB, antiviral medicine, diuretics,cyclosporine/tacrolimus,AntiBs,amphoterecin B, metformin

Front 139

What complication of ARF is the most common cause of death?

Back 139

Infection

Front 140

What type of CV complications are associated w ARF? (3)

Back 140

CHF, increase/decrease of BP, Arrythmias

Front 141

What are the electrolyte complications associated w ARF?

Back 141

Increase K, PO4, Mg
Decreased/increased Na
Metabolic acidosis

Front 142

What hematological complications are associated with ARF?

Back 142

Hemorrhage (GI), anemia

Front 143

What complication of ARF results in anorexia, N/V, MS changes and seizures or comas?

Back 143

Uremic syndrome (the clinical syndrome associated with uremia)

Front 144

Azotemia is a complication of ARF, what exactly is azotemia?

Back 144

Elevation in circulating concentrations of nitrogenous waste products (i.e Cr and BUN)
Can have no clinical sx

Front 145

What is functional ARF characterized by?

Back 145

Decrease in GFR due to decrease in glomerular hydrostatic pressure
No structural damage

Front 146

What is a common cause of functional ARF?

Back 146

ACEI or ARB usage

Front 147

T/F
Pre-renal ARF is considered azotemia

Back 147

True

Front 148

What are the characteristics of pre renal ARF?

Back 148

renal parachymal hypoperfusion w/ or w/o hypotension

Front 149

T/F:
In post renal ARF Na and Fe are elevated suggesting there is structural damage to the tubules

Back 149

False,
Na and Fe are normal suggesting there is NO structural damage to the tubules

Front 150

What are the compensatory responses in pre renal ARF? (4)

Back 150

SNS, RAAS, afferent arteriolar vasodilation, efferent arteriolar vasoconstriction

Front 151

If presented with Pre renal ARF, a pt should be administered fluid and/or D/C of offending meds except?

Back 151

HF, cirrhosis, RAS

Front 152

What type of ARF has direct structural damage to the kidney?

Back 152

Intrinsic ARF

Front 153

What in the lab values tells you that there is structural damage to the kidney?

Back 153

Na and FE are increased showing no reabsorption taking place

Front 154

What is the most common intrinsic ARF?

Back 154

ATN (Acute tubule necrosis)

Front 155

What is the flow of damage when tubular injury occurs?

Back 155

cell necrosis-->loss of cells--> decrease in filtration--> fluid/electrolyte imbalance--> dilute urine--> decrease in Na reabsorption--> decrease in GFR

Front 156

In ATN there is a ____ in Scr and a ____ in urine output

Back 156

In ATN there is a _increase_ in Scr and a _decrease_ in urine output

Front 157

What are the clinical phases of ATN? (4)

Back 157

Polyuria
Oliguria
Maintenence/diuresis
Recovery

Front 158

How does post renal ARF develop?

Back 158

When theres an obstruction from the renal tubule to the urethra

Front 159

What are some causes of Post renal ARF? (4)

Back 159

Malignancy, BPH, neprolithiasis, tumor lysis syndrome

Front 160

What drugs are related to the cause of post renal ARF?

Back 160

Indinavir (HIV), sulfonamides, acyclovir, probenecid

Front 161

For ARF, what could you do to decrease the nephrotoxicity of amphoterecin B if the pt needed to be on it?

Back 161

Limit the use/slow infusion
use liposomal formulation
use fluconazole or itraconazole

Front 162

T/F:
Aminoglycosides should be used 2-3 times a day for pts w ARF?

Back 162

False, should be d/c or down to once a day

Front 163

What is really important for pts to do before getting a cardiofxn scan with radiocontrast dyes?

Back 163

Rehydration!
Na load w/ 5% dextrose better
D/C Metformin!

Front 164

What does NAC (N-acetylcysteine) help prevent? What are the doses and circumstances?

Back 164

Helps prevent ARF IF there is previous renal impairment
600mg po bid 2-4 days
1200 po bid 2 day

Front 165

What are some non pharmalogical therapies for ARF? (4)

Back 165

Fluid restriction
Remove obstruction (postrenal)
electrolyte management
Renal replacement tx (dialysis)

Front 166

What are 2 renal replacement tx?

Back 166

hemodialysis and peritoneal dialysis

Front 167

What role does dopaminergic agonist play in ARF? What are the dosings?

Back 167

Improve renal blood/plasma flow, not necessarily outcome
Dosing 0.5-3 ug/kg/min