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Kinetics > Renal Disease > Flashcards

Renal Disease Flashcards

1
Q

Ideal marker of GFR

A

-freely filtered, no clearance due to tubular secretion/reabsorption
-not metabolized by renal tissues
-no effect on renal function

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2
Q

Assessment of kidney function

A

-measuring GFR is gold standard (insulin, cystatin, markers)
-measure ClCr based on measured urinary clearance (urine collection)
-estimated ClCr or eGFR based on SeCr is widely used clinically

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3
Q

CG

A

-estimates creatine clearance, mL/min

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4
Q

CKD-EPI

A

-estimates GFR, mL/min/1.73m2

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5
Q

Estimated renal function

A

-CG (crcl ml/min)
-CKD-EPI (GFR, mL/min/1.73m2
-MDRD

-dif in units due to BSA

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6
Q

Cockcroft and Gault

A

-ClCr
-modified ClCr (adjusts for weight)
-formula sheet

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7
Q

Estimation of renal function

A

-eGFR most reliable (CKD-EPI methods)

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8
Q

FDA guidance on estimation of renal clearance

A

-eGFR corrected to BSA and reported as mL/min for use in drug dosing
-CG ClCr with IBW or AdjBW in overweight BMI>25
-prob gonna suggest eGFR in future and may even provide incentives to manufacturers

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9
Q

Limitations

A

-SeCr generated from muscle mass and diet
-amputees, body builders, vegans
-tubular secretion of SeCr (overstimulation of GFR esp at low ClCr)
-SeCr MUST be stable

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10
Q

Bottome line for estimation of renal function

A

-perform two estimates
-if estimates are dif selection of dose should be targeted risk/benefit
-TDM or conservative dose is narrow therapuetic index drug
-aggressive for wide therapuetic index
-actual measure of CrCl may be needed

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11
Q

Chronic kidney disease

A

-urine-albumin-creatine ration >30mg/g
-GFR <60mL/min for > 3 months

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12
Q

CKD staging

A
  1. GFR >90 ml/min/1.73m2
  2. 60-89
    3a.45-59
    3b. 30-44
  3. 15-29
  4. failure <15
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13
Q

CKD effect on Absorption

A

-no good data to suggest changes
-D-xylose absorption slowed
-likely reduced absorption and gastric emptying due to neuropathy
-reduced bioavailability due to gut wall edema, furosemide
-reduced due to drug interactions
-maybe reduced due to changes inc gas pH

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14
Q

Floroquinolone antibiotics-when admin with divalent cations

A

-when admin with divalent cations
-mg, ca
-form insoluble salts and reduce absorption

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15
Q

CKD effect on bioavailability

A

-alt metabolism/transport
-inc bioavailability of CYP
-dialysis may negate these effects
-suggesting uremic toxins may be responsible

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16
Q

CkD effect on distrivution

A

Vss=Vp + VT (fu/fu,t)
-any changes in those variables
-Vp and Vss change due to fluid overload
-see Di Piro for additional examples of Vd and protein binding changes

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17
Q

Alterations in plasma volume (Vp) drug distribution

A

-fluctuations in volume
-inc fluid admin
-hydrophilic drugs (aminoglycosides, cephalosporins)

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18
Q

Alterations in tissue binding (fu,t)

A

-dec tissue binding
-digoxin volume reduced in CKD stage 5 and HD pt
-actual dec due to dec tissue binding, acidosis or presence of DLIS

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19
Q

Drug distribution: protein binding

A

-inc binding of BASIC drugs to AAG
-CKD pt have more AAG
-dec binding of ACIDIC drugs to albumin

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20
Q

dec binding of drugs to albumin

A

-changes to albumin-binding sites
-accumulation of endogenous inhibitors of binding
-HYPOalbuminemia
-accumulation of competing metabolites

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21
Q

Phenytoin (anti-seizure)

A

-CKD alters relationship between total [DPH] and therapeutic and toxic effects
-narrow therapeutic index drug w non-linear or capacity limited PK
<10 mcg/mL

22
Q

Phenytoin healthy vs CKD

A

-normal fu=0.08
-CKD fu=0.16
-Cl int is same

23
Q

Clinical considerations for protein binding

A

-measure of unbound concentrations are desired in CKD pt
-highly protein bound drugs
-some have sut point of fu<0.2
-narrow therapeutic index drugs
-marked variation in fu

24
Q

CKD effect on elimination and metabolism

A

-ClT = ClR + ClNR +Cl…
-reduction in ClR obv
-what happens to ClNR?
-most drugs are metabolized prior to excretion
-acute vs chronic
-hepatic and non-hepatic metabolism may be altered
-complex

25
Q

As renal impairment increases, enzyme function

A

decreases

26
Q

Metabolism in CKD

A

-CYP3A allegedly lower
-reduced Cl of CYP3A substrates
-likely reduction in ClNR in numerous enzymes

27
Q

drug transport in CKD

A

-impaired
-OATP, P-glycoprotein reduced
-Fexofenadine

28
Q

Metabolism and transport bottome line

A

-impact of given drug is difficult to guess
-no strategy for making predictions even in the same drug class
-qualitative strats may be employed by knowing the enzyme or transporter involved

29
Q

CKD effect on metabolite accumulation

A

-inc side effects
-esp morphine, allopurinol, propoxyphene, procainamide, meperidine
-esp polar coumpunds in kidney

30
Q

Renal clearance

A

-ClR = [GFR*fu] + [Clsecretion - Cl reabsorption]
-assume all renal drug elimination processes decline in parallel

31
Q

Renal excretion graphs

A

-no ClR = straight line at 100% Cl
-no Cl NR = goes all the way down to zero

32
Q

Grouping based on ClCr

A

-as CrCl inc, ClT inc
-ClT = slope + b(ClCR)

33
Q

Relationship between Cl and renal function

A

-ClT = ClCR
-ClT = ClR + ClNR
-linear

34
Q

too much H2 blocker (cimetidine) in elderly

A

-dementia side effect

35
Q

Drug dosage adjustment in CKD

A

-collect
-assess
-plan
-monitor follow uppp

36
Q

Drugs that require special consideration

A

-antibiotics
-lithium and digoxin
-cyclophosphamide
-metformin
-DOACs

37
Q

Antibiotic special consideration in CKD

A

-aminoglycosides, vancomysin (NTI drugs)
-beta-lactam (penicillins, cephalosporins, etc)

38
Q

Lithium and digoxin special considerations in CKD

A

-NTIs
-extensively removed renally
-significant toxcities

39
Q

Cyclophosphamide special considerations in CKD

A

-active metabolites may accumulate

40
Q

Metformin special considerations in CKD

A

-associated w development of lactic acidosis, if doses not adjusted in CKD

41
Q

DOACs (direct oral anticoagulants)

A

-surpassed warfarin as ACs used most commonly
-variable renal excretion
-significant toxicities

42
Q

Individualization of drug therapy

A

-determine dose adj factor (Q)
-determine dose and/or interval change (dec dose, inc interval)
-low Q = greater change in regimen

43
Q

If fe is 1

A

-all drug eliminated by kidney

44
Q

If fe is 0

A

-all drug is metabolized

45
Q

low Q =

A

greater change in regimen

46
Q

Dose pt =

A

-Q * normal dose
-dec dose

47
Q

Interval pt =

A

-interval normal/Q
-inc interval

48
Q

Renal dosage adj assumptions

A

-ClCr is good assessment and declines linearly w ClCr
-drug does NOT follow linear PKs
-unaltered drug absorption, protein binding and ClNR

49
Q

Cefazolin ex

A

-has own equation for ClCR estimating

50
Q

Limitations

A

-nonlinear assumptions
-NTI drugs should use TDM and estimation of Cmax and Cmin

51
Q

Narrow Therapeutic Index drugs

A

-akikacin
-gentamicin
-tobramycin
-vacnomycin
-digoxin
-phenytoin

Kinetics (22 decks)

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