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competency 10/11 > ckd > Flashcards

ckd Flashcards

1
Q

CrCl =

A

[[140 - age(yr)]weight(kg)]/
[72serum Cr(mg/dL)]

1mg/dL = 88.4umol/L
x0.85 for women

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2
Q

ideal filtration markers are:

A
  • freely filtered by the kidney
  • not secreted, metabolised, or reabsorbed
  • does not modify renal function
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3
Q

gold standard for estimating GFR

A

inulin (fructose polysaccharide, not naturally occurring in the human body):
- freely filtered, not secreted, not metabolised, not reabsorbed, not protein bound

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4
Q

SCr is a product of

A

metabolism of creatinine, which is produced by the muscle
- endogenously produced at a relatively constant rate
- freely filtered, some secretion at the renal tubule, small amt or reabsorption

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5
Q

limitations of using SCr in eqn estimating renal function

A
  • variations in Cr production: vegetarian diet, creatinine supplements
  • reduction in muscle mass: amputation, malnutrition, fraility
  • when GFR is rapidly fluctuating eg. AKI, SCr takes some time to accumulate and reach a steady state
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6
Q

normal urine output >= 1200ml/day

A

non-oliguric: >500ml
oliguric: 50-500ml
anuric: <50ml

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7
Q

definition of AKI

A
  • incr in SCr by >= 0.3mg/dL (26.5umol/L) within 48hrs
  • incr in SCr to >= 1.5x baseline, which is known or presumed to have occurred within the prior 7 days
  • urine vol <0.5ml/kg/h for 6hrs
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8
Q

risk factors for AKI

A
  • advanced age
  • pre-existing kidney impairment
  • obstruction of urinary tract
  • sepsis/infections
  • rhabdomyolysis/ trauma/burns
  • dehydration/vol depletion: vomiting, diarrhea, poor fluid intake, fever, diuretic use, intravascular vol depletion (congestive cardiac failure, liver disease with ascites)
  • use of nephrotoxic agents/medications
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9
Q

causes of AKI

A
  • pre-renal/functional
  • intrinsic
  • post-renal
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10
Q

causes of AKI: pre-renal/functional

A

hypoperfusion or decr glomerular hydrostatic pressure
- hemorrhage, vol depletion, CHF, renal artery stenosis, emboli
- med: ACEi, ARB, NSAID

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11
Q

causes of AKI: intrinsic

A

structural damage to kidneys:
- acute tubular necrosis, acute interstitial nephritis, acute glomerulonephritis, infections
- med: aminoglycosides, vancomycn

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12
Q

causes of AKI: post-renal

A

obstruction of urinary flow
- trauma, BPH, tumours

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13
Q

under normal physiologic conditions, to maintain glomerular hydrostatic pressure for filtration:

A
  • afferent arterioles (PG): dilates, incr renal blood flow
  • efferent arteriole (ATII): constricts, incr GFR
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14
Q

NSAIDs on AKI

A

inhibit PG > constriction of afferent arterioles > decr renal perfusion

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15
Q

ACEi an ARBs on AKI

A

antagonise effects of ATII > decr glomerular filtration pressure > decr GFR

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16
Q

diuretics on AKI

A

deplete plasma vol > decr renal blood flow

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17
Q

Aminoglycosides on AKI

A

ATN
- uptake through receptor expressed on epithelial cells along proximal convoluted tubule
> concentrated > induce myeloid body formation, impair protein synthesis, degrade mitochondrial function, culminate in apoptosis and eventual necrosis of the renal tubular epithelial cells
- direct glomerular injury can also occur

neomycin>gentamicin=tobramycin>amikacin>streptomycin

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18
Q

strategies to minimise AKI with AO

A
  • in pt w pre-existing renal impairment or high risk of AKI, consider other abx choices
  • avoid other nephrotoxins, avoid dehydration
  • TDM
  • single daily dosing whenever possible: lower risk of AKI compared to multiple daily dosing, using PAE
  • use shortest duration possible
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19
Q

vancomycin on AKI

A
  • may alter mitochondrial function and induce dose-dependent proliferation of proximal tubular cells
  • oxidative stress may also be a potential mech of nephrotoxicity, esp involving the proximal tubule

ATN, AIN

most ep developed btw 4-17 days after initiation of therapy

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20
Q

strategies to min AKI with vancomycin

A

TDM:
- aim AUC/MIC 400-600mg.h/L, assuming MIC 1mg/L
- incr risk of AKI if vanco trough levels are maintained >15-20mg/L or if AUC/MIC exceeds 650-1300mg.h/L
- AUC/MIC method not validated in pt on dialysis

minimise concurrent use of nephrotoxins: concurrent use of vanco and piper-tazo incr risk of AKI, closer monitoring of renal function is warranted
- monitoring of renal function via repeating blood tests and monitoring urine output

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21
Q

contrast-induced nephrotoxicity `

A
  1. renal ischemia: systemic hypotension, osmotic diuresis/dehydration, renal vasoconstriction caused by the release of adenosine, endothelin, and other vasoconstrictors
  2. direct tubular toxicity caused by oxidative stress

presentation: SCr rises within 12-24hrs and peaks 2-5 days after procedure

esp in pt with ckd+dm, chf, adv age, concurrent adm of nephrotoxic drugs

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22
Q

strategies to min AKI with radiocontrasts

A
  • use lowest possible dose of contrast medium in pt at risk
  • use either iso-osmolar or low-osmolar iodinated contrast media, rather than high-osmolar iodinated contrast media in pt with incr risk of CIN
  • iv vol expansion with either isotonic NaCl or sodium bicarbonate solutions 6-12hours before procedure
  • oral N-acetylcysteine pre- and post-procedure
  • discontinue current nephrotoxic agents and diuretics
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23
Q

clinical s/sx of ckd

A

fluid overload (SOB), HTN, uremic sx (nausea, anorexia, fatigue, LOA, itch, mental changes, uremic breath, asterixis, bleeding)

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24
Q

lab s/sx of ckd

A

azotemia, hyperP, hyperCa, hyperK, metabolic acidosis, anemia

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25
Q

stage 1 ckd

A

eGFR >=90, with risk factors

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26
Q

stage 2 ckd

A

60-89

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27
Q

stage 3 ckd

A

30-59

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28
Q

stage 4 ckd

A

15-29
- preparation for kidney replacement therapy

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29
Q

stage 5 ckd

A

<15, or dialysis

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30
Q

G3a

A

45-59

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31
Q

G3b

A

30-44

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32
Q

A1

A

<30mg/g
<3mg/mmol

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33
Q

A2

A

30-300mg/g
3-30mg/mmol

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34
Q

A3

A

> 300mg/g
30mg/mmol

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35
Q

causes of ckd

A
  • dm
  • htn
  • glomerulonephritis
  • autoimmune disease
  • genetic disorders: polycystic kidney disease
  • vascular diseases
  • drugs
  • infections
  • urinary obstructions: kidney stones
  • HIV-associated nephropathy
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36
Q

functions of kidney

A
  • regulates fluid balance
  • regulates electrolytes
  • regulates pH
  • removes waste/toxins
  • produces erythropoietin
  • activates vitD
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37
Q

complications of ckd

A
  • regulates fluid balance > fluid overload, htn
  • regulates electrolytes > electrolyte imbalance (K, P, Ca)
  • regulates pH > metabolic acidosis
  • removes waste/toxins > hyperuricemia, uraemia (contributes to LOA, anorexia, fatigue) > malnutrition
  • produces erythropoietin > anemia
  • activates vitD > secondary hyperparathyroidism, mineral bone disorders

PLUS ckd causes a systemic, chronic pro-inflammatory state contributing to vascular and myocardial remodeling processes > atherosclerotic lesions, vascular calcification > incr risk of cvd

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38
Q

s/sx of anemia

A

fatigue, sob, intolerance to cold weather, chest pain, tingling extremities, tachycardia, headaches, malaise

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39
Q

causes of anemia in ckd

A
  • erythropoietin deficiency
  • iron deficiency
  • folate and b12 deficiency
  • increased blood loss during dialysis
  • reduced life span of erythrocytes
  • inflammation
  • infection
  • bone marrow fibrosis secondary to hyperPTH
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40
Q

anemia diagnosis

A

Hb <13 for males, <12 for females

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41
Q

lab parameters for investigation of anemia

A
  • Hb
  • reticulocyte counts
  • MCV, MCHC
  • serum ferritin, TSAT
  • serum b12 and folate levels
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42
Q

Hb target

A

10-11.5

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43
Q

give oral/IV iron if

A
  • TSAT =< 30%
    AND serum ferritin =< 500ng/mL
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44
Q

recommended daily dose of iron

A

200mg elemental iron

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45
Q

oral iron ddi

A
  • calcium supplements
  • tetracyclines
  • FQ: bind to Fe, decr absorption of FQ
  • thyroxine
  • antacids
  • H2RA, PPI: alters pH of gut, iron require acidic enough environment in gut for absorption, impaired absorption
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46
Q

ferrous sulphate Co Tab, contains ferrous sulphate anhydrous 200mg

A

32%, 65mg

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47
Q

ferrous gluconate Co cap (Sangobion), contains ferrous gloconate 250mg

A

12%, 30mg

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48
Q

iberet folate SR tab, contains ferrous sulphate 525mg

A

20%, 105mg

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49
Q

iron polymaltose drops 50mg/ml

A

50mg/ml (20 drops)

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50
Q

iron polymaltose 100mg tab/cap

A

100mg

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51
Q

ferrous fumarate, % elemental iron

A

33%

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52
Q

IV vs oral iron

A
  • IV fe improves responsiveness to ESA therapy
  • 100% bioavail
  • reduction of pill burden
  • reduction of ddi
  • can also be used in PD and pre-dialysis pts where oral iron is insufficient
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53
Q

adr of iv fe

A

*Allergic reactions, hypotension, dizziness, dyspnoea, headache, flushing, nausea, injection/infusion site reactions
*Rare but serious: anaphylaxis
*Iron overload
*Increased risk for infections
*Withhold during acute infections, restart after infection resolves (usually after the end of the abxcourse)
*May consider switching to oral iron

54
Q

evaluate iron status (TSAT and ferritin) at least every

A

3 months during ESA therapy, including decision to start or continue iron therapy
- but more frequently ie. monthly when: initiating or increasing ESA dose, blood loss, monitoring response after a course of IV iron

55
Q

short-acting ESA

A

Eprex, Recormon

56
Q

long-acting ESA

A

Darbepoietin alpha (Nesp), Methoxy polyethylene-glycol-epoietin beta (Mircera)

57
Q

moa of ESA

A

stimulate erythropoiesis either directly or indirectly by acting on the EPO receptor

58
Q

starting dose of eprex

A

IV 50-100u/kg, 3x/wk

59
Q

starting dose of recormon

A

SC 20u/kg 3x/wk
or IV 40u/kg 3x/wk

60
Q

starting dose of nesp

A

SC/IV 0.45mcg/kg once a week

61
Q

starting dose of MIrcera

A

SC/IV 0.6mcg/kg Q2weeks

62
Q

adr of ESA

A

generally well-tolerated:
- pure red cell aplasia
- HTN: not a c/i unless uncontrolled or urgency
- vascular access thrombosis
- seizuresL prior hx of seizure not a c/i
- flu-like sx
- use in caution in malignancy or hx of malignancy

63
Q

time to steady state of ESA

A

takes apporx 10 days for erythrocyte progenitor cells to mature and release into circulation

64
Q

finerenone

A

non-steroidal MRA
- shown to have potent anti-inflammatory and anti-fibrotic effects than steroidal MRA (spironolactone, eplerenone)
- used for HTN in CKD if ACEi/ARB does not achieve good control of BP

65
Q

preferred DM agents

A

SGLT2i
GLP-1 RA
DPP4-i

66
Q

absolute Fe deficiency

A

low TSAT, low ferritin

67
Q

functional Fe deficiency

A

low TSAT, high ferritin

68
Q

microcytic, hypochromic RBA

A

iron deficiency anemia

69
Q

macrocytic

A

b12 or folate deficiency

70
Q

normocytic, normochromic anemia

A

anemia of chronic disease

71
Q

iron panel for iron deficiency

A

MCV: microcytic
iron: low
ferritin: low
TIBC: high
transferrin: high
TSAT: low

72
Q

iron panel for inflammatory anemia

A

MCV: normal
iron: low
ferritin: high
TIBC: low
transferrin: low
TSAT: low

73
Q

iron panel for iron overload

A

MCV: normal
iron: high
ferritin: high
TIBC: low
transferrin: low
TSAT: high

74
Q

protein req

A

0.8g/kg/day, due to inability to excrete nitrogenous waste (urea)
- for dialysis pt: 1-1.2g/kg/day due to protein loss

75
Q

what adjust vit not recommended

A

vit A and E, risk for toxicity in ESRD pt
- vit C alos
- folic acid, L-carnitine, pentoxifylline not recommended as well

76
Q

metabolic acidosis

A
  • decr H+ excretion > drop in pH and serum bicarbonate levels
  • decr excretion of NH3 (mech to remove excess H+)
  • decr excretion of PO4 (mech to remove excess acid)

compensatory fall in pCO2 result in less decr in arterial pH

clinical presentation: anorexia, nausea, lethargy

77
Q

bicarbonate deficit formula

A

0.4 x weight (kg) x (24-bicarb level)

78
Q

serum bicarb goal

A

> 22mmol/L

79
Q

mgmt of metabolic acidosis

A

use of alkalinising salts to replenish bicarb stores:
- sodium bicarb
- citrate/citiric acid reparations (but re liver metabolism to bicarb, co2, water)

80
Q

dose of sodium bicarb

A

1g BD-TDS

81
Q

which is more selective: lokelma or resonium

A

lokelma (SZC)

82
Q

agents that reverse ECG effects (by hyperK)

A

calcium

83
Q

agents that allow urinary K loss

A

frusemide

84
Q

agents that redistributes K

A

insulin w glucose
sodium bicarb
b2 agonist

85
Q

agents that incr K elimination

A

SZC, SPS, patiromer (Veltessa), Hd

86
Q

corrected calc mg/dL

A

(0.8 * (Normal Albumin - Pt’s Albumin)) + Serum Ca

87
Q

goals of therapy for ckd-mbd

A

*Maintain normal levels of serum Calcium, Phosphate, PTH
*Prevent or reduce parathyroid gland hyperplasia
*Maintain normal skeletal function
*Prevent extra-skeletal and vascular calcification
*Reduce cardiovascular morbidity and mortality
77

88
Q

adr of sodium bicarb

A

sodium or fluid overload, gi intolerance eg stomach discomfort or bloatedness, nausea

89
Q

what is a classic feature of hyperphosphatemia

A

pruritis

90
Q

limit dietary phosphate intake

A

800-1000mg/day
- difficult since P found in most foods rich in protein, might compromise nutrition!

91
Q

phosphate binders: calcium salts

A

MOA: combines with dietary P to form insoluble calcium-phosphate - not absorbed systemically, cleared through feaces

92
Q

calcium carbonate

A

40% elemental Ca
1 tab TDS w meals
SE: n/v, constipation, hyperCa, LOA, urolithiasis

93
Q

calcium actate

A

25% elemental Ca, 667mg = 167mg elemental Ca

1-2 tabs TDS with meals
SE: n/v, constipation, hyperCa, LOA

94
Q

limit ____g of elemental Ca per day

A

2
- 1.5g from Ca-based binders: up to 3 tabs of calcium carbonate per day or 9 tabs of calcium acetate per day

95
Q

MOA of sevelamer

A

non-absorbable polymer that inhibits intestinal phosphate absorption

96
Q

dosing of sevelamer

A

800-1600mg TDS with meals

97
Q

SE of sevelamer

A

constipation, diarrhea, flatulence, indigestion, n/v, metabolic acidosis

98
Q

Renvela

A

sevelamer CO3

99
Q

Renagel

A

sevelamer HCl

100
Q

which sevelamer salt has lower risk of metabolic acidosis?

A

renvela, co3

101
Q

adv of sevelamer

A
  • does not contain Ca or Al; does not contribute to Ca load, no risk for hyperCa or Al-induced toxicities, allowing higher doses of vit D
  • lipid lowering effects
102
Q

disadv of sevelamer

A
  • pill burden: swallow whole, cannot chew
  • expensive
103
Q

MOA of lanthanum

A

rare earth element, inhibits absorption of dietary phosphate by forming highly insoluble lanthanum phosphate complexes in gut

104
Q

Fosrenol

A

lanthanum carboante

105
Q

lanthanum dosing

A

500-1000mg TDS w meals, chewed

106
Q

Al-based P binder: MOA

A

binds with phosphorus in GIT
- al hydroxide 600mg tab, mixture

107
Q

SE of al-based P binder

A

GI: constipation, diarrhoea, gi obstruction
phosphate depletion: weakness, mental status changes
al toxicity: dementia, encephalopathy, worsening anemia, osteomalacia, adynamic bone disease (esp w concurrent use of citrate salts)

108
Q

when are al-based P binders used?

A

severe hyperP (>2.2mmol/L) uncontrolled by other binders
- not for lt use, due to risk of toxicity
- not recommended for use > 4 weeks

109
Q

Velphoro

A

sucroferric oxyhydroxide
- novel polynuclear iron(II)-oxyhydroxide P binder

110
Q

sucroferric oxyhydroxide dose

A

2.5g chewable tablet = 500mg elemental Fe
- 500mg TDS, incr to 1g TDS based on response
- minimal iron absorption

111
Q

velphoro vs sevelamer

A

as effective, but loewr pill count
3 vs 9 tabs per day

112
Q

velphoro SE

A

high incidence of GI se: nausea, diarrhea, abnormal stool colour (black)

113
Q

phosphate binder ddi

A

quinolones, thyroxine, digoxin, warfarin, antiepileptics

114
Q

native/nutritional vit D

A

ergocalciferol (D2) - less effective, 50000IU

cholecalciferol (D3) - 1000IU

115
Q

when is vit D and its analogues used?

A

reserved for ckd stage 4-5 pt with severe and progressive hyperPTH

116
Q

vit D analogues

A

active form
- alfacalcidol
- paricalcitol

117
Q

MOA of vit D and its analogues

A
  • incr absorption of Ca and P
  • decr PTH secretion and synthesis
118
Q

PO dose of calcitriol and alfacalcidol

A

0.25mcg, 3x/wk

119
Q

IV dose of calcitriol and alfacalcidol

A

1mcg/wk

120
Q

limitations of of calcitriol and alfacalcidol

A

incr GI absorption of Ca and P > resulting in hyperCa and hyperP (dose-limiting SE)

121
Q

alfacalcidol requires

A

hepatic function for conversion to active form

122
Q

paricalcitol adv over calcitriol and alfacalcidol

A

less hyperCa or hyperP
- selective actiation of vit D receptors in PTH glands inhibiting PTH synthesis and secretion

123
Q

MOA of calcimimetics

A

binds and modifies calcium sensing receptors on parathyroid glands, causing incr sensitivity to extracellular ca hence reducing pth levels

124
Q

Regpara

A

PO cinacalcet 25mg tab
- 25mg 3x/wk, uptitrated to 100mg OD at 3-wk intervals

125
Q

what to monitor for with hypoCa

A

seizures

126
Q

Parsabiv

A

IV etelcalcitide
2.5-15mg 3x/wk, with dose adj every 4 weeks

127
Q

switching from cinacalcet to etelcalcitide

A

discont cinacalcet for at least 7 days prior to starting etelcalcitide

128
Q

switching from etelcacitide to cinacalcet

A

discont etelcalcitide for at least 4 days prior to starting cinacalcet

129
Q

acoid fleet enemas in renal failure due to

A

high phosphate content

130
Q

PD peritonitis should be diagnosed when at least 2 of the following are resent

A

1.Clinical features consistent with peritonitis, that is, abdominal pain and/or cloudy dialysis effluent;
2.Dialysis effluent white cell count > 100/μL or > 0.1 ×109/L (after a dwell time of at least 2 h), with > 50% polymorphonuclearleukocytes (PMN);
3.Positive dialysis effluent culture

131
Q
A

competency 10/11 (31 decks)

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