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CKD > CKD > Flashcards

CKD Flashcards

1
Q

Acute Kidney Injury

A

Sudden loss of kidney function due to non-renal conditions (drug).

Often reversible but can be permanent if precipitating factor is not corrected.

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2
Q

Common cause of AKI

A

Dehydration

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3
Q

Presentation of AKI

A

BUN: SCr ration greater than 20:1 plus

Decrease urine output

Dry mucus membranes

Tachycardia

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4
Q

Chronic Kidney Disease

A

A progressive loss of kidney function over months or years.

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5
Q

How is CKD severity measured?

A

Glomerular filtration rate (GFR)

Creatinine Clearance ( CrCl)

Albumin in the urine

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6
Q

End- Stage Renal Disease (ESRD)

A

Total and Permanent Kidney Failure

Fluid and waste accumulation

Dialysis or Transplant is needed

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7
Q

What are the most common causes Of CKD?

A

Diabetes

Hypertension

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8
Q

What is the function of the Nephron?

A

Control the concentration of sodium and water.

This regulate blood volume and in turn blood pressure.

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9
Q

What is the glomerulus ?

A

Large filtering unit that is located within the bowman capsule.

Afferent arteriole delivers blood into the glomerulus

Efferent arteriole unfiltered substance exit nephron here.

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10
Q

If the glomerulus is healthy?

A

Only substances less than 40,000 daltons including most drugs can pass through into the filtrate.

Large substance ( proteins and protein bound drugs) are not filtered and stayed in the blood.

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11
Q

If the glomerulus is damaged?

A

Some Albumin passes into the urine

Albumin + GFR assess CKD severity (nephropathy).

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12
Q

What is Proximal Tubule?

A

Entry point of nephron

Reabsorb filtered Na, Cl, Ca and water into bloodstream.

*Blood pH is regulated by the exchange of Hydrogen and Bicarbonate ions.

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13
Q

What is the Loop of Henle?

A

Descending limb (down): water is reabsorb

Ascending limb (up): Na and Cl ions are reabsorb

*If antidiuretic hormone (ADH) or Vasopressin is present water passes through the walls of the ascending limb and is reabsorbed into the blood; less water excreted in the urine (anti-diuresis)

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14
Q

Loop of Henle and Diuretics?

A

Loop diuretic inhibit the Na-K pump in the ascending limb ; less Na and Ca is reabsorb back into the blood.

Long term Ca depletion can decrease bone density.

Na concentration increase in filterate , less water is reabsorb and both are excreted in the urine.

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15
Q

What is the distal convoluted tubule?

A

The farthest point away from entry to nephron

Regulate K, Na, Ca and pH

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16
Q

Distal convoluted tubule and Diuretics?

A

Thiazide diuretic inhibit the Na-Cl pump

Thiazides( 5% Na reabsorb) is a weaker diuretic than loops (25% Na reabsorb).

Thiazides increases Ca reabsorption therefore long-term use has protective effect on bone.

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17
Q

What is the Collecting Duct?

A

Network of tubules and ducts that connects nephrons in each kidney to a ureter.

Involve with WATER and ELECTROLYTE balance affected by ADH and aldosterone

Urine Filtrate= Ureter to bladder then out the body via Urethra

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18
Q

Aldosterone role in distal convoluted tubule and collecting ducts?

A

Works in the tubule and duct to increase Na and water reabsorption but decrease K reabsorption.

Aldosterone Antagonist ( Spironolactone and Eplerenone) block aldosterone; more Na and water is excreted in the urine but serum K increases.

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19
Q

What is Drug Induced Kidney Disease (DIKD?

A

Linked to numerous medications

Acute and reversible; irreversible to CKD if drug is not stop.

Common in hospital setting and contributes to morbidity and mortality.

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20
Q

Drugs that cause kidney disease?

A

Aminoglycosides

Amphotericin B

Cisplatin

Cyclosporine

Loop diuretic

NSAIDS

Polymyxins

Radiographic Contrast Dye

Tacrolimus

Vancomycin

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21
Q

What are the two common laboratory markers use to estimate kidney functions and what do they measure?

A

BUN( blood urea nitrogen): measure amount of nitrogen in the blood that come from urea, a waste product of protein metabolism

SCr ( serum creatinine) : waste product of muscle metabolism

As kidney function declined BUN and SCr increases.

SCr Normal Range: 0.6 - 1.3 mg/dL

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22
Q

What common equation is use for CrCl?

A

Cockcroft Gault Equation

CrCl (mL/min) = (140-age)/(72*Scr) ×weight x 0.85 (female)

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23
Q

What weight to use to calculate CrCl?

A

Use Actual Body weight if less than calculate Ideal Body Weight

Use Ideal Body Weight if BMI is in normal range

Use Adjusted Body Weight if BMI is in overweight range

IBW = ( 45.5 or 50 kg) + 2.3kg (inches over 5ft)

AdjBW= IBW + 0.4(TBW - IBW)

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24
Q

What’s calculate CrCl use for?

A

To determine dosing adjustments and medication contraindications.

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25
Q

Calculate CrCl accuracy is decreased?

A

When a patient has very low muscle mass (frail elderly patients)

Low muscle mass = low Scr

Overestimate CrCl

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26
Q

Calculate crockcroft gault CrCl can be inaccurate in patients with ?

A

Obesity

Liver disease

Pregnancy

High muscle mass

Very young children (crockcroft gault not preferable)

ESRD or unstable kidney function (crockcroft gault not preferable)

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27
Q

Drug dosing is usually base on CrCl but sometimes is base on GFR.

Which drug dosing can be base on GFR?

A

SGLT2 inhibitor

Metformin

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28
Q

How is GFR Calculated?

A

Calculated using the Modification of Diet in Renal Disease (MDRD) and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI).

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29
Q

What is albumin in relation to CKD?

A

The primary protein that is measured in the urine to assess kidney disease.

Known as Albuminuria or Proteinuria

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30
Q

What is KDOQI guidelines recommendations?

A

Use GFR and degree of ALBUMINURIA (levels in urine) along with cause of CKD to Determine the degree/ stage of renal impairment.

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31
Q

Which levels of GFR and/or Albumin suggests a patient have CKD?

A

GFR less than 60 mL/ min/1.73m3

Albuminuria greater than or equal to 30 mg/mmol

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32
Q

ACE and ARBs role in CKD?

A

ACE and ARBs are FIRST- LINE drugs to prevent progression of disease in patients with CKD, Diabetes, and/or HTN if Albuminuria is present.

Works by inhibiting RAAS causing efferent arteriolar dilation.

Reduce pressure in the glomerulus, decrease Albuminuria and provide cardiovascular protection.

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33
Q

What to expect in SCr when starting treatment with ACE inhibitor or ARBs?

A

Scr can increase up to 30%

If more than 30% increase D/C medication and referred patient to nephrologist.

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34
Q

What should be monitored when on ACE Inhibitor and ARBs?

A

Scr and K. 1 to 2 weeks after initiating

NEVER use both class together

They increase Potassium (K)

Advice pt to avoid K supplement and salt substitutes (KCl)

MAXIMIZED Dose for Renal protection

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35
Q

What is KDIGO Guidelines Recommended BP goal for CKD patient?

A

No Proteinuria: Less than 140/90 mmHg

Proteinuria: Less than 130/80 mmHg

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36
Q

Reasons to MODIFY DRUG THERAPY in CKD

A

Drug is Eliminated through the Kidneys: modify to avoid accumulation and SE/toxicity; Reduce dose and/or extend interval

The drug can cause or worsen kidney disease( Nephrotoxic)

Drug become less effective as kidney function declines (ex. Thiazide, and Nitrofurantoin)

Drug is CONTRAINDICATIONED at a specific level of kidney impairment because accumulation is unsafe. (Ex. Bleeding risk with anticoagulants)

Drug can cause further kidney damage ( ex. NSAIDS)

Drug can cause more harmful effects than usual when kidney function is reduced (ex. Hyperkalemia with aldosterone antagonist)

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37
Q

Dose Adjustments may be required or necessary when:

A

CrCl is less than 60 mL/min (1/2 of normal)

CrCl is less than 30 mL/min (1/4 of normal; additional adjustments may be needed or drug may be CONTRAINDICATED)

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38
Q

Related disorders associated with CKD

A

Anemia

Hypertension

Acid-Base and ELECTROLYTE disturbances

Bone mineral metabolism disorder ( management of PTH, PO4, Ca and Vit D levels)

39
Q

What is CKD Mineral and Bone Disorder (CKD-MBD)?

A

Common in renal impairment pt and almost in all pt receiving dialysis.

Associated with fractures, cardiovascular disease and increase mortality.

40
Q

In relation to CKD-MBD patient with advanced kidney disease require monitoring for

A

Parathyroid Hormone (PTH)

Phosphorus (PO4)

Calcium (Ca)

Vitamin D levels

41
Q

Explain the interaction of Ca, PO4, Vitamin D and EPO in CKD

A

PO4 increase bc kidneys cannot eliminate

Vitamin D cannot be activated by kidney causing Calcium absorption to decrease

High PO4 and low Ca cause increase release of PTH (usually increase Ca reabsorption via feedback)

PTH pull Ca from bone causing demineralization and increase fracture

High PO4 levels( hyperphosphatemia) continued to stimulate PTH (secondary hyperparathyroidism) and hypercalcemia persist causing calcification and cardiovascular disease

Kidney produce less erythropoietin (EPO) resulting in decrease RBC production in the bone marrow which causes anemia.

42
Q

Hyperphosphatemia must be treated to prevent bone disease and fractures. Treatment is focused on;

A

Restricting dietary phosphate

Avoid dairy products, cola,chocolate and nuts

43
Q

What is the MOA of Phosphate Binder?

A

Block absorption of dietary PO4 by binding to it in the intestine.

Missed dose ( food is absorb) = Skipped till next meal or snack

3 types: Aluminum-based, Calcium-based and
Aluminum and Calcium free drug

44
Q

Aluminum based Phosphate Binders:

*Potent but Rarely Use due to Aluminum accumulation/ toxicity

A

Aluminum Hydroxide Suspension

300-600 mg TID

SE : *Dialysis Dementia

Aluminum toxicity due to accumulation cause nervous system and bone toxicity

Osteomalacia

Constipation

Nausea

MONITOR: Ca, PO4 , PTH, S/SX ALUM.TOX

45
Q

Calcium base Phosphate Binders:

*FIRST LINE

A

Calcium Acetate (Phos-lyra, Phos-lo): bind more

Calcium Carbonate (Tums)

Daily Calcium less than 2000 mg

SE: *Hypercalcemia (especially with concomitant use of Vit D due to increased calcium absorption )

Constipation

Nausea

MONITOR: Ca*, PO4, PTH

46
Q

Alu/Ca Free Phosphate Binders:

Sucroferric Oxyhyroxide (Velp-Horo)
Ferric Citrate (Aury-Xia)
Lanthanum Carbonate ( Fos-Renol)

*MORE Expensive; *Less hypercalcemia; *No Aluminum accumulation

A
  • Sucroferric Oxyhyroxide (Velp-Horo)
  • Ferric Citrate (Aury-Xia)

WARNING: *Iron absorption occurs with ferric citrate ( reduce IV iron dose; store out of reach of children)

SE: Diarrhea, Constipation, discolored black feces

MONITOR: Iron, ferritin, Tstat (ferric citrate), PO4, PTH

  • Lan-tha-num Carbonate ( Fosrenol)
  • Chew tab thoroughly to reduce severe GI adverse effects.

CONTRAINDICATIONS: GI obstruction, fecal impaction, illeus

WARNING: GI perforation

SE:* NVD, Constipation, Abdominal pain

MONITOR: Ca, PO4, PTH

47
Q

Alu/Ca Free Phosphate binder:

Sevelamer Carbonate (Ren-vela)
Sevelamer Hydrochloride (Ren-agel)
  • No Hypercalcemia; No Aluminum
  • Not systemically Absorbed
A

Sevelamer Carbonate (Renvela)

Sevelamer Hydrochloride (Renagel)

CONTRAINDICATIONS: Bowel obstruction

WARNING: reduce dietary absorption of vit DEK and folic acid; give with vit supplement

SE: *NVD (GREATER THAN 20%), Dyspepsia, Constipation, Abdominal Pain, Flatulence

MONITOR: Ca, PO4, HCO3,Cl, PTH

Note: * lower CHOLESTEROL and LDL by 15-30%.

Sevelamer Carbonate maintain bicarbonate concentration.

48
Q

Phosphate binder interactions

A

*Separate administration from levothyroxine and antibiotics that chelate (quinolones, tetracycline)

49
Q

Key Anti-infectives drugs that require lower dose or increase interval in CKD

A

Aminoglycosides (increase dosing interval primarily)

Beta-lactam antibiotics (most)

Fluconazole

Quinolones (except Moxifloxacin)

Vancomycin

50
Q

Key Cardiovascular drugs that require lower dose or increase interval in CKD

A

LMWHs (enoxaparin)

Rivaroxaban (for AFib)

51
Q

Key Gastrointestinal drugs that require lower dose or increase interval in CKD

A

H2RAs (famotidine, ranitidine)

Metoclopramide

52
Q

Key Other drugs that require lower dose or increase interval in CKD

A

Bisphosphonates

Lithium

53
Q

Other Anti-infectives drugs that require lower dose or increase interval in CKD

A

Amphotericin B

Anti-tuberculosis meds ( ethambutol, pyrazinamide)

Antivirals ( Acyclovir, Valacyclovir, Ganciclovir, Valganciclovir, Oseltamivir)

Aztreonam

NRTIs, including tenofovir

Polymyxins

Sulfamethoxazole / Trimethoprim

54
Q

Other cardiovascular drugs that require lower dose or increase interval in CKD

A

Antiarrhythmics (digoxin, disopyramide, dofetilide, procainamide, sotalol)

Apixaban ( for Afib)

Dabigatran (for Afib)

Statins (most)

55
Q

Other Pain/Gout drugs that require lower dose or increase interval in CKD

A

Allopurinol

Colchicine

Gabapentin, Pregabalin

Morphine and Codeine

Tramadol ER

56
Q

Other drugs that require lower dose or increase interval in CKD

A

Cyclosporine

Tacrolimus

Topiramate

57
Q

Select drugs that are contraindicated in CKD

CrCl less than 60 mL/min

A

Nitrofurantoin

58
Q

Select drugs that are contraindicated in CKD

CrCl less than 50 mL/min

A

Tenofovir Disoproxil Fumarate containing products (Ex. Stribild, Complera, Atripla, Symfi, Symfi Lo)

Voriconazole IV ( due to the vehicle)

59
Q

Select drugs that are contraindicated in CKD

CrCl less than 30 mL/min

A

Tenofovir Alafenamide containing products ( ex. Genvoya, Biktarvy, Descovy, Odefsey, Symtuza)

NSAIDs

Dabigatran *(DVT/PE)

Rivaroxaban* (DVT/PE)

60
Q

Select drugs that are contraindicated in CKD

GFR less than 30 mL/min/1.73m3

A

SGLT2 Inhibitor (Canagliflozin, Dapagliflozin, Empagliflozin)

Metformin

Other:

Meperidine. ***Not specific

61
Q

Other drugs that are contraindicated in CKD

CrCl less than 30 mL/min

A

Avanafil

Bisphosphonates

Duloxetine

Fondaparinux

Potassium Sparing Diuretics

Tadalafil*

Tramadol ER

Others not specific recommendations:

Dofetilide

Edoxaban

Glyburide

Sotalol (Betapace AF)

*indication specific

62
Q

After controlling hyperphosphatemia, ELEVATED PTH are treated primarily with….

A

Vitamin D

63
Q

What cause Vit D deficiency in CKD?

A

Kidney is unable to Hydroxylate Vit D to its final ACTIVE FORM ;

1,25 - Dihydroxy Vit D

64
Q

Vitamin D deficiency can lead to ?

A

Worsen Bones Disease

Impair Immunity

Increased ris of CARDIOVASCULAR Disease

65
Q

What are the 2 forms of Vitamin D?

A
  • Vitamin D3 (CHOLECALCIFEROL) ; synthesize in skin after exposure to ultraviolet light from the sun
  • Vitamin D2 (ERGOCALCIFEROL); produce from plant steriod; dietary source of Vit D

Oral supplements of both may be necessary for pt with early CKD (stage 3&4)

66
Q

What are Vitamin D analog used for?

A

Use in later stage of CKD or ESRD to
INCREASE Ca Absorption from the gut;

Raise Ca concentration ; and

Inhibit PTH Secretion

67
Q

What’s Vitamin D Analog MOA?

A

Increased intestinal absorption of Ca which provides negative feedback to the parathyroid gland

68
Q

Vitamin D Analog

Treatment of Secondary Hyperthyroidism

Pari and Doxer cause less hypercalcemia

A

Calci-triol (ROCAL-TROL) : active form of Vit D3; take with food

Calci-fediol (RAYAL-DEE) : prodrug of calcitriol; 25 hydrox toxicity

Doxer-calci-ferol (HECTO-ROL)

Pari-calci-tol (ZEM-PLAR)

CONTRAINDICATIONS: Hypercalcemia; Vit D Toxicity

WARNING: Digitalis toxicity by hypercalcemia

SE: *Hypercalcemia, Hyperphosphatemia, NVD ( GREATER THAN 10%)

MONITOR: *Ca, PO4, 25 hyroxy vit D (Calcifediol)

69
Q

What are CALCIMIMETIC Used for?

A

Mimic the action of Calcium on the parathyroid gland and reduce PTH

It is only used in dialysis patients

70
Q

What the MOA of CALCIMIMETIC?

A

INCREASED SENSITIVITY of the calcium-sensing receptors on the parathyroid gland, which causes DECREASE PTH, Ca , PO4.

71
Q

CALCIMIMETIC Drugs

Treatment of Secondary Hyperthyroidism

A

-Cina-calcet (SENSI-PAR)

CONTRAINDICATIONS: Hypocalcemia

WARNING: caution in pt with hx of seizures

SE: *Hypocalcemia, NVD, Paresthesia, HA, Fatigue, Depression, Constipation, UTI, muscle pain and weakness, fracture

MONITOR: Ca, PTH, PO4

-Etel-calce-tide (PAR- SABIV)

WARNING: *Hypocalcemia, worsening HF, GI bleeding, decreased bone turnover

SE: *Muscle Spasms, Paresthesia, NVD

MONITOR: Ca, PTH, PO4

72
Q

What is hemoglobin level is consider Anemia?

A

Hemoglobin less than 13 g/dL

73
Q

Why is Anemia common in CKD?

A

One of the causes of Anemia is LACK OF ERYTHROPOIETIN(EPO), which is normally PRODUCED by the KIDNEY.

EPO goes to the bone marrow to Stimulate the production of red blood cells (RBCs).

RBCs (contains hemoglobin) and they transport oxygen to the blood.

74
Q

Anemia in CKD is treated with what?

A
  • Erythropoiesis Stimulating Agents (ESAs)

- Iron

75
Q

Erythropoiesis Stimulating Agents (ESAs)

A

INDICATION: Anemia in CKD to prevent the need of blood transfusion.

EFFECTIVE: If adequate IRON is Available. Check ferritin and Tstat.

WHEN TO USE: hemoglobin less than 10 g/dL

WHEN TO D/C: Hemoglobin greater than 11 g/dL due to risk of thromboembolic disease (DVT, PE, MI, STROKE)

Risk: Elevated Blood Pressure and Thrombosis

TYPES:
E-poetin Alfa (PROCRIT, EPOGEN, RETACRIT)

Darbe-poetin Alfa (ARANESP) : long lasting formulation

76
Q

Why is iron levels low in ESRD and what is the solution?

A

Low level can be due reduce GI absorption and blood loss from dialysis treatment.

Solution: IV IRON is given at dialysis center.

77
Q

What is Hyperkalemia?

A

Normal Potassium: 3.5 to 5

Potassium Levels greater than 5.3 or 5.5

Clinical Concerns: levels greater than 5

Most Common Cause: DECREASED RENAL EXCRETION due to KIDNEY FAILURE.

SYMPTOMS:

Muscle Weakness

Bradycardia (monitor with ECG)

Fatal Arrhythmias ( (monitor with ECG))

78
Q

What is potassium?

A

Most abundant INTRACELLULAR CATION essential for life.

Normal daily intake: 1mEq/kg/day

Food: meats, beans and fruits

79
Q

How is potassium Eliminated?

A

via KIDNEY and partially by GUT

Renal potassium excretion is increased by:

Aldosterone hormone

Diuretics ( loops is greater than thiazides)

High urine flow ( osmotic diuresis)

Negatively charge ion in the distal tubule (bicarbonate)

80
Q

Potassium in normal kidney function?

A

High level potassium DOESNOT cause HYPERKALEMIA in normal kidney.

High level are offset by release of INSULIN,
which causes potassium to shift into the cells.

80
Q

Why are Diabetic patients at high risk of hyperkalemia?

A

Insulin deficiency reduce the ability to shift potassium into the cell.

Many patients with diabetes take ACE inhibitors or ARBs.

81
Q

Key Drugs that Raise Potassium Levels?

A

ACE Inhibitors

ARBs

Aldosterone Receptor Antagonists

Aliskiren

Canagliflozin

Drospirenone containing COCs

Sulfamethoxazole/ Trimethoprim

Transplant Drugs (Cyclosporine, Everolimus, Tacrolimus)

Other Drugs:

Glycopyrrolate

Heparin

NSAIDs

Potassium containing IV fluids (parenteral nutrition)

Potassium Supplements

Pentamidine

82
Q

Treatment of Severe Hyperkalemia?

A

D/C potassium source

Stabilize the Heart: Stabilize myocardial cells ( prevent arrhythmias)

Move it: rapidly shift potassium intracellularly

Remove it: induce elimination from the body.

84
Q

Drugs use to treat HYPERKALEMIA?

A

They work quickly but DONOT LOWER total body potassium

See Chart on pg 299 & 300

85
Q

Drugs use to Stabilize the Heart in severe Hyperkalemia?

A

Calcium Gluconate

Route : IV

Onset: 1 to 2 mins

Indication: Stabilize myocardial cell and prevent arrhythmias.

86
Q

Drugs use to SHIFT EXCESS K INTRACELLULAR LY severe Hyperkalemia?

A

Regular Insulin: IV, 30 min; with glucose&dext

Dextrose: IV, 30 stimulate insulin; not alone

Sodium Bicarbonate: IV, 30; use when metabolic acidosis is present

Albuterol: neb, 30 min; monitor tachy and chest pain

87
Q

Drugs use to REMOVE K in severe Hyperkalemia?

A

Furosemide: IV, 5 min; K in Urine

Sodium Polystyrene: Oral & Rectal, 1 hr; bind K in GI; use rectal in acute

Patiromer: Oral; 7 hr; bind K in GI; notfor acute/ emergency

Sodium Ziconium Cyclosilicate: oral,1hr; bind K in GI ; not for acute/ emergency

Hemodialysis: Remove K from Blood; too long to set up/ complete

88
Q

Drugs for Treatment of Hyperkalemia?

A

Sodium Polystyrene Sulfonate (Kayexalate, Kionex): Rectal dose use in Emergency

Patiromer (Vel-tassa):* Not for Emergency; refrigerate powder and used 3 month at room temp

Sodium Zirconium Cyclosilicate (Lo-kel-ma): *Not for Emergency; store at room

SE: N/D, *Constipation ,Vomiting (Kionex), peripheral Edema (Lokelma)

WARNING: *bind to other oral medication (Separate by 3 for Veltassa and 2 hrs for Lokelma)

Can worsen GI motility (Veltassa and Lokelma)

Electrolyte Disturbances

Hyper-Na, Hypo-Mg,K,Ca, fecal impaction and GI necrosis: increase risk with sorbitol not to be use together (Kionex)

*Hypo-Mg( Veltassa)

MONITOR: K, Mg ( Na, Ca for Kionex)

89
Q

Metabolic Acidosis in CKD

A

CAUSE: KIDNEYS ability to reabsorb bicarbonate DECREASE as CKD Progress.

90
Q

Metabolic Acidosis in CKD Treatment

A

INITIATED: Serum Bicarbonate less than 22 mEq/L

TREATMENT: Replace Bicarb

  • Sodium Bicarbonate (Neut)
  • Sodium Citrate/Citric acid solution (Cytra-2, Oracit, Shohl Solution); metabolized in the liver; may not be effective in liver failure.

MONITOR: *sodium level; caution in HTN and Cardiovascular disease.

91
Q

When is Dialysis required?

A

If CKD progress to Failure ( STAGE 5) and pt who did not receive KIDNEY TRANSPLANT.

92
Q

Primary TYPE of Dialysis ?

A

Hemodialysis Dialysis (HD); Dialysis Machine 3 to 4 hrs/3 time per week

Peritoneal Dialysis (PD); Dialysis solutions pump into peritoneal cavity repeated though out the day, everyday

93
Q

Factors that affect drug removal during Dialysis

A

DRUG CHARACTERISTIC:

Molecular weight/size: smaller

VD: small vd

Protein-Binding: low protein bound

DIALYSIS FACTORS:

Membrane; high( large pore)

Blood Flow Rate; high flow rate

CKD (1 decks)

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