CKD in Small Animals Flashcards

1
Q

definition of CKD

A

structural &/or fxnl abnormalities of 1+ kidneys continuously present for >3 mos

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2
Q

Renal dz is characterised by

A
  • permanent reduction in no. of fxn’ing nephrons
  • evidence of structural & fxnl derangements
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3
Q

CKD is an… dz

A

ireversible, progressive dz

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4
Q

What population of dogs is more commonly affected by CKD

A

older dogs

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5
Q

What breeds of cats are more prone to CKD

A

Maine coon, abyssinian, siamese, russian blue, burmese

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6
Q

Causes of CKD in dogs

A
  • familial & congenital conditions
    1. chronic tubulointerstitial nephritis
    2. glomerulonephropathy
    3. amyloidosis
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7
Q

Causes of CKD in cats

A
  1. tubulointerstitial nephritis
  2. glomerulonephropathy
  3. lymphoma
  4. amyloidosis
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8
Q

CKD is a syndrome secondary to…

A

loss of kidney fxn

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9
Q

impaired glomerular, tubular, endocrine fxns leads to

A

retention of toxic metabolites & body fluid imbalances

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10
Q

Clinical presentation of CKD

A
  • PU/PD
  • anorexia, nausea, V
  • oral ulceration, stomatitis, necrosis, halitosis
  • D/melena, haematochezia
  • wt loss/cachexia
  • lethargy/depression
  • urinary incontinence
  • anaemia
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11
Q

primary fxn of kidneys

A

maintain water & electrolyte balance

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12
Q

decline in GFR means there is an increase in…

A

excretion of water & electrolytes per nephron

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13
Q

80% reduction of GFR does NOT impair

A

Na, K, water balance

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14
Q

disturbed excretion of electrolytes & water have limited compensatory mechanisms meaning…

A

failure towards end stage

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15
Q

clinical manifestation of disturbed excretion of electrolytes & water

A
  • oedema
  • hypertension
  • hyponatraemia
  • hyperkalaemia
  • hyperphosphataemia
  • metabolic acidosis
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16
Q

CKD has a what main clinical consequences?

A
  • disturbed excretion of electrolytes & water
  • reduced excretion of organic solutes
  • impaired renal hormone synthesis
  • arterial hypertension & CV consequences
  • renal secondary hyperparathyroidism
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17
Q

glomerular filtration of solutes is done by

A

tubular reabsorption

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18
Q

abnormalities due to reduced excretion of organic solutes

A
  • inhibition of Na-K-ATPase
  • inhibition of platelet fxn
  • leukocyte dysfxn
  • insulin resistance
  • loss of RBC membrane lipid asymmetry
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19
Q

Renal hormone synthesis normal includes secretion of…

A

EPO, calcitriol, prostaglandins, renin, kinins

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20
Q

Calcitriol is the most metabolically active form of…

A

Vit D

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21
Q

Vit D def leads to

A

renal secondary hyperparathyroidism

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22
Q

PTH has been id’d as a

A

uraemic toxin leading to renal osteodystrophy

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23
Q

EPO def leads to

A

chronic non-regen anaemia

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24
Q

CKD is the most common cause of secondary…

A

hypertension in dogs/cats

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25
Q

secondary hypertension causes

A
  • target organ damage - eyes, kidney, heart, brain
  • proteinuria
  • cardiac remodelling
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26
Q

fluid retention is the main cause of

A

hypertension in humans w/ CKD causing haemodialysis

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27
Q

diuretics are used to manage…

A

fluid overload to control hypertension

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28
Q

what are arterial hypertension & CV consequences of CKD?

A
  • secondary hypertension
  • fluid retention
  • activation of RAAS
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29
Q

ischaemia/vascular lesions cause the enhancement of

A

renin secretion

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30
Q

activation of RAAS causes what in cats

A

retention of salt (elevated aldosterone, low renin)

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31
Q

ACEi are ineffective in…

A

cats

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32
Q

Pathogenesis of secondary renal hyperparathyroidism

A
  • PO4 retention secondary to GFR decline -> elevation in FGF-23
  • limits PO4 retention, inhibits 1-alphaH activity -> decreased calcitriol
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33
Q

Clinical consequences of renal secondary hyperparathyroidism

A
  • renal osteodystrophy - uncommon cats/dogs –> bones of skull/mandible mostly -> demineralise & fibrous tissues (rubber jaw)
  • cystic bone lesion, bone pain
  • nephrocalcinosis - loss of renal fxn
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34
Q

diagnostic eval of CKD

A
  • confirm presence of kidney dz
  • differentiate btw acute vs chronic
  • ID biochem & haemotological complications
  • determine type &/or cause of CKD
  • ID presence of comorbidities
  • Stage
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35
Q

What biochemical values should you use to determine CKD?

A
  • creatinine
  • BUN
  • SDMA
  • USG
  • UA & culture
  • electrolytes - P, K, Ca
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36
Q

serum creatinine conc is a surrogate for…

A

GFR - minimum reabsorption

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37
Q

serum creatinine conc is insensitive in estimating…

A

GFR

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38
Q

every time GFR decreases by half, the S-creat…

A

doubles

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39
Q

S-creat conc is influenced by…

A

muscle mass

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40
Q

BUN is a surrogate for

A

GFR but is less specific/sensitive than Creatinine

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41
Q

BUN is a surrogate for all…

A

uraemic toxins

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42
Q

What is the goal of a low protein diet?

A

to limit uraemic toxin prod’n

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43
Q

BUN can increase w/

A

GI ulcers/bleeding
enhanced protein catabolism
dehydration/pre-renal azotaemia
drugs

44
Q

BUN low can be assoc’d w/

A

starvation

45
Q

decreases in BUN can be impacted by which organ impairment/failure?

A

liver (hepatic failure, PSS)

46
Q

SDMA is a produce to

A

protein degradation (methylation of arginine)

47
Q

What % of SDMA is eliminated by glomerular filtration?

48
Q

SDMA is an ideal

49
Q

SDMA concentration correlates w/ what in dogs/cats?

50
Q

SDMA is minimally impaired by…

A

muscle mass

51
Q

USG should be obtained…

A

at the same time as blood

52
Q

USG is essential to differentiate

A

pre-renal from primary renal

53
Q

Dogs have primary renal azotaemia if USG is

54
Q

Cats have primary renal azotaemia if USG is

55
Q

Adv’d CKD causes USG to be…

A

isosthenuric b/c kidneys no longer modifying urine conc from plasma conc

56
Q

complete UA & culture is mandatory for…

A

staging of CKD

57
Q

Why does hyperphosphataemia occur in CKD

A
  • decline in GFR = retention of phosphate = hyperphosphataemia as compensatory mechanism initially
58
Q

Serum PO4 conc is directly linked to…

A

mortality in cats/dogs/humans w/ CKD

59
Q

Higher PO4 conc in cats predicts…

A

progression to Stage III

60
Q

reduced intake of PO4 is the only way to control & limit

A

PO4 retention

61
Q

metabolic acidosis promotes…

A

anorexia, V, lethargy, muscle wasting, & wt loss

62
Q

how do kidneys normally maintain acid-base balance?

A

tubular excretion of H via ammonium or PO4 & reabsorption of bicarb to maintain balance

63
Q

when excretion of ammonium decreases w/ GFR it leads to

64
Q

Acidosis leads to

A

decreased PO4 & sulfate compound excretions + impaired tubular proton secretion

65
Q

What is not typical of k9/fel CKD?

A

reduced reabsorption of bicarb

66
Q

metabolic acidosis is commonly associated w/

A

Fanconi syndrome

67
Q

how does iCa respond in CKD

A

increased or decreased
but lower in cats w/ CKD than healthy cats but tCa may be hypercalcaemic

68
Q

HypoK is common in

A

cats w/ CKD
NOT IN DOGS

69
Q

HypoK can induce

A
  • a decline in GFR -> Na restriction -> activation of RAAS -> enhanced kaliuresis (+ hypertension), reduced food intake, dehydration
  • DDX: Primary hyperaldosteronism in geriatric cats
70
Q

how do you differentiate primary hyperaldosteronism from CKD

A

Aldosterone:renin ratio (elevated) + imaging

71
Q

haematology of CKD may show

A

non-regen anaemia

72
Q

testing required for CKD

A
  • haematology
  • serum biochem
  • UA/culture
  • Blood gas & electrolytes
  • BP
  • UPC
  • rads, U/S
  • infectious dz screening: UTI +/- pyelonephritis; lepto; borrelia; fip
  • any specialised tests PRN
73
Q

AKI vs CKD

A

AKI: potentially reversible once injury corrected due to adaptive/compensatory mechanisms
CKD: irreverisble & progressive loss of kidney fxn for 3+ mos

74
Q

staging of CKD is based on…

A

P’s creatinine or SDMA

75
Q

Stage 1/2 CKD

A

non-azotaemic (1)/ mild azotaemia (2)
no clin signs or mild (PU/PD, wt loss, selective appetite)
clin signs assoc’d w/ underlying cause (pyelonephritis, nephrolithiasis)
clin signs secondary to complications (proteinuria, hypertension)

76
Q

proteinuria & hypertension can be detected at

77
Q

mgmt of CKD

A

Supportive conservative medical mgmt
- ameliorate clin signs
- improve fluid deficits/excesses
- electrolyte, acid-base, nutritional balance

78
Q

Diet therapy of CKD

A
  • renal diets have the greatest benefit
  • Omega 3’s/antioxidants - dogs
  • protein restriction?
79
Q

commercial renal diets limit

A

phosphate intake - indicated for Stage 2 p’s to slow progression & reduce mortality

80
Q

it is best to initiate the conversion to a renal diet prior to the onset of…

81
Q

phosphorous mgmt in CKD

A
  • intake must be reduced as GFR decreased to avoid retention
  • diet PO4 restrictions
  • intestinal binding agent to trap PO4 in intestines & prevent absorption (Aluminum hydroxide)
82
Q

What is a caution w/ Al-containing products for PO4 management?

A
  • Decreased palatability & cause constipation
  • toxicosis in adv’d CKD in dogs
83
Q

Lanthanum is used as a

A

PO4 binder

84
Q

Why is Al hydroxide sometimes used over Lanthanum?

85
Q

Ca-based chelating agent used for PO4 mgmt

A

Calcium carbonate

86
Q

Calcitriol is used in PO4 mgmt to…

A

reduce PTH lvls

87
Q

how does dehydration occur in CKD

A

if PU is not compensated by PD & water intake

88
Q

dehydration can promote…

A

poor appetite, lethargy, constipation, pre-renal azotaemia/AKI (dz progression)

89
Q

dehydration can be worsened by…

90
Q

SQF can be admin’d in

A

chronically dehydrated P’s (cats»dogs)

91
Q

Why are SQF good for CKD?

A

balanced electrolyte sln

92
Q

how often should SQF be given?

A

q 1-3 days

93
Q

What is the dose of SQF for cats?

A

75-125 ml/dose; can be increased but caution w/ fluid overload

94
Q

GI mgmt in CKD

A
  • anti-emetics
  • appetite stimulation
  • O-tube or gastrostomy feeding tube
95
Q

what class of anti-emetic therapy is ideal?

A

proton pump inhibitors

96
Q

the chemoreceptor trigger zone is stimulated by

A

uraemic toxins causing Nausea & V

97
Q

What drugs act on the CTZ (chemoreceptor trigger zone)

A

maropitant
ondansetron

98
Q

What is an appetite stimulant commonly used in CKD?

A

mirtazepine

99
Q

adverse effects of mirtazepine

A

hyperexcitability, tremors, vocalisation

100
Q

signs of hypertension

A

lethargy, blindness, retinal haemorrhage, retinal detachment, seizures, stupor, cardiac remodeling (ventricular hypertrophy)

101
Q

hypertension is assoc’d w/

A

proteinuria - promoting progression of CKD

102
Q

indications for therapy of hypertension

A
  • treat &/or prevent target organ damages
  • 180 mmHg > BP >160 mmHg - rechecked 3x over 2 mos to confirm persistence
  • BP > 180 mmHg - recheck w/i 1-2 wks & if confirmed = severe hypertension
  • stages I-IV w/ confirmed or severe hypertension
103
Q

guideline for txt of hypertension

A
  • reducing BP <180 mmHg except in p’s w/ severe acute ocular or neuro lesions
104
Q

drugs used in a stable dog for hypertension

A
  1. ACEi - Benazepril/enalapril
  2. Add Ca channel blocker - Amlodipine
  3. Add Angiotensin receptor blocker (ARB) - Sartan
    Note: may discontinue ACEi prior to Sartan or monitor closely for HyperK, Hypotension, azotaemia
105
Q

Drugs used in stable cat for hypertension

A
  1. Ca channel blocker - Amlodipine
  2. ARB - Sartan
106
Q

mgmt of anaemia in CKD

A
  • erythrocyte stimulating agents (Darbopoetin)
107
Q

Managing progression of CKD

A
  • diet + increasing Rx PRN
  • control BP
  • control proteinuria
  • control phosphorus lvl
  • monitor QOL
  • restage when uraemic crisis & azotaemia worsens