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Renal > Chronic renal failure > Flashcards

Chronic renal failure Flashcards

1
Q

Differentiate CRF and CKD

A
  • CHRONIC RENAL FAILURE: chronci azotaemia d/t intrisnic renal dz, >3/4 nephrons have to be lost
  • CHRONIC KIDNEY DISEASE: patients with chroncic disease +/- azotaemia
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2
Q

What is the IRIS staging system for kidney dz?

A
  • based on plasma [creatinine], proteinuria and BP
  • only applicable to patients with CKD (different system AKI)
  • without pre/post-renal causes of azotaemia
  • if not azotaemic, then some other abnormality myst be present to ID that the patient has CKD (e.g. ultrasound changes or marked proteinuria).
  • stages 1-4 (4 = most severe)
  • azotaemia must be stable for this staging
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3
Q

What is renal insufficiency?

A

avoid this term!

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4
Q

Features stage 1 IRIS kidney dz

A
  • some other renal abnormality present (renal structure, proteinuria)
  • non-azotaemic, normal or near-normal GR
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5
Q

Features stage 2 IRIS kidney dz

A
  • CS usually limited to PU/PD or may be absent

- non-azotaemic to mildly-azotaemic

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6
Q

Features stage 3 IRIS kidney dz

A
  • PU/PD usually
  • extrarenal CS (V, dehydration, wt loss) MAY be present
  • mild-moderately azotaemic
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7
Q

Features stage 4 IRIS kidney dz

A
  • PU/PD usually

- extrarenal CS (V, dehydration, wt loss) ARE LIKELY

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8
Q

What are the cut off values for UPC determining if animal is proteinuric or not?

A

NON-PROTEINURIC: 0.4 cats, >0.5 dogs

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9
Q

At what IRIS stage do you give renoprotective vs symptomatic tx?

A
  • RENOPROCTECTIVE: stage 2 and 3

- SYMPTOMATIC: stage 4

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10
Q

Causes - CKD in cats

A
  • lymphoma
  • polycystic kidney disease *
  • FIP
  • amyloidosis
  • primary glomerular disease
  • pyelonephritis
  • toxins
  • recovery from ARF/ AKI
  • obstructive nephropathy *
  • chronic tubulointerstitial nephritis*
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11
Q

Inheritance - polycystic kidney disease

A
  • persian and related breeds
  • autosomal dominant
  • DNA test
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12
Q

CS - polycystic kidney disease

A
  • palpably enlarged in azotaemic cats
  • azotaemia often doesn’t develop until middle-age
  • detected ultrasonographically before azotaemia (from 8m)
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13
Q

Another name - obstructive nephropathy

A

‘big kidney little kidney syndrome’

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14
Q

Outline obstructive nephropathy

A
  • calcium oxalate ureteroliths
  • obstruction of 1st kidney typically asymptomatic
  • CS when 2nd kidney obstructs
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15
Q

What is the most common diagnosis in cats with CKD?

A

tubulointerstitial nephritis

  • FREQUENCY: cats > dogs/humans
  • it is the end-stage of CKD, regardless of inciting cause
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16
Q

Causes - CKD in dogs

A
  • more mixed than cats
  • tubulointerstitial nephritis
  • familial/breed-related syndromes
  • primary glomerular dz
  • Others (pyelonephritis, post-ARF/AKI)
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17
Q

Indications - diagnostic imaging

A
  • young animals
  • dogs > cats
  • asymmetric kidneys
  • large kidneys
  • severe proteinuria
  • uncertain chronicity
  • ‘do everything’ owners
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18
Q

3 main management principles - CKD

A
  1. determine underlying cause
  2. control factors important in dz progression
  3. reduce patient morbidity
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19
Q

Progression - renal dz - dogs vs cats

A
  • many patients diagnosed with mild azotaemia eventially die of renal failure
  • more rapid in dogs vs cats
  • most dogs die within 1 year of diagnosis, cats live 2-3 years and may die of other things
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20
Q

Name putative mechanisms for renal dz progression

A
  • CKD-MBD (Mineral bone disorder, secondary renal hyperparathyroidism) (dietary therapy)
  • glomerular hypertension
  • direct proteinuria induced renal injury (ACEIs/ ARBs)
  • other mechanisms (acidosis/increased renal ammoniagenesis, hypokalaemia)
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21
Q

Describe CKD-MBD

A
  • abnormalities of Ca, phosphorous, PTH or vitamin D metabolism
  • abnormalities in bone turnover mineralisation, volume, linear growth or strength
  • vascular/other soft tissue calcification
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22
Q

What causes increased PTH release?

A
  • decreased ionised Ca2+

- calcitriol

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23
Q

PTH -effects

A
  • KIDNEY: increase Ca retention, decrease NaPi transporter insertion, increase phosphorous excretion
  • BONE: increase osteoclastic/osteoblastic activity, release Ca2+ and phosphorous
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24
Q

What happens to phosphate clearance in mild CKD?

A

decreased nephron mass –> decreased phosphate clearance –> increase FGF-23 –> increase phosphate clearance

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25
Q

What happens to phosphate clearance in severe CKD?

A

decreased nephron mass –> decreased phosphate clearance –> increase phosphate –> 3 things:

  1. decreased active vitamin D3
  2. increased PTH
  3. decreased ionised Ca –> increased PTH
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26
Q

Does CKD-MBD cause progressive renal injury?

A
  • dietary phosphate restriction effectively reduces PTH and FGF-23
  • phosphate restriction reduce histological evidence of injury (experiments)
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27
Q

How does dietary management help kidney dz?

A
  • decreased protein = decreased signs of uraemia
  • decreased phosphorous = decreased secondary renal hyper-PTH
  • decreased Na = decreased arterial hypertension
  • increased vitamin B = water-soluble vitamins lost
  • increased caloric density = counteract decreased appetite
  • less acidifying = risk of acidosis
  • increased K = cats predisposed to hypokalaemia
  • increased ration omega 3:omega6 PUFA = decreased glomerular pressure
  • increased soluble fibre = binds urea
28
Q

Define PUFA

A

Polyunsaturated fatty acids

29
Q

What are the targets for phosphorous management?

A
  • stage 2 CKD: keep [phosphate] in lower half of reference range
  • more advanced dz = have to compromise
  • staged approach: initially diet, addition of phosphate binders if required.
30
Q

Name 4 phosphate binders

A
  • aluminium hydroxide
  • lanthanum carbonate (Renalzin)
  • calcium carbonate/acetate/ citrate
  • Ipakitin/ Epakitin
31
Q

Outline aluminium hydroxide as a phosphate binder

A
  • cheap, effective
  • causes constipation
  • poor palatability
  • rare side effects at high doses
32
Q

Outline lanthanum carbonate as a phosphate binder

A
  • reasonable cost, effective

- being discontinued

33
Q

Outline calcium carbonate/acetate/ citrate as a calcium bindiner

A

may cause hypercalcaemia

34
Q

What is ipakitin/epakitin?

A

chitosan/calcium carbonate

35
Q

Is proteinuria of prognostic signficance?

A

yes (proteinuria –> excessive tubular reabsorption of protein –> renal injury. Proteinuria is also a disease marker)

36
Q

Does glomerular capillary hypertension cause proteinuria?

A

Yes

37
Q

What type of drug is benazepril?

A

ACE-i

38
Q

What is the effect of ACEI in cats with CKD?

A
  • significant reduction in proteinuria (effect greatest in most proteinuric cats)
  • no difference if survival cf. placebo tablet
39
Q

Outline use of ACEi in dogs with CKD

A
  • no ACEI/ARB licensed for tx of CKD dogs

- definite indication in management of primary glomerular disease (paradoxically more common in dogs vs cats)

40
Q

Outline rational use of ACE-i in CKD

A
  • animals with higher UPCs
  • animals likely to live long enough to reap benefits
  • must not expect ‘biochemical improvement’
  • aim is to slow disease
41
Q

Effects on blocking Ang 2 action on AT1-R

A
  • vasoconstriction
  • aldosterone secretion
  • tubular Na reabsorption
  • thirst
  • vasopressin secretion
  • cellular hypertrophy
  • calcium transport
42
Q

Effects on blocking Ang 2 action on AT2-R

A
  • vasodilation
  • decreased cell growth
  • antioxidant actions
  • apoptosis?
43
Q

What is telmisartan?

A

= semintra (liquid formulation)

  • randomised comparison to benazepril
  • primary endpoint = reduced proteinuria, not increased survival
44
Q

Factors contributing to CKD morbidity

A
  • UTIs
  • anaemia
  • dehydration
  • hypokalaemia
  • acidosis
  • systemic hypertensions
45
Q

Describe UTIs in CKD patients

A
  • common
  • often asymptomatic
  • pyelonephritis as an inciting cause of CKD is more common in the dog than in the cat: highly concentrated urine resistant to infection
  • cats: stage 2-4
  • dogs: all stages
46
Q

Describe hypopkalaemiain CKD patients

A
  • CAUSE: decreased appetite, increased urinary loss, hyperaldosteronism
  • RESULTS IN: mm weakness, worsens renal function?
  • SUPPLEMENT: palatability issue
  • CATS&raquo_space;» dogs (more common with hypertension)
47
Q

Outline dehydration in CKD patients

A
  • variable
  • may result in pre-renal component to azotaemia
  • anticipate in hospitalised patients
  • selected patients benefit from SQ fluids at home
48
Q

For a well-hydrated cat with stable, mild CKD that you place on fluids at 3x maintenance?

A
  • increased urine output
  • unchanged GFR
  • decreased [creatinine]
49
Q

How do fluids help in CKD?

A 
FACT:
- correct pre-renal azotaemia
- treat dehydration
- expand plasma volume
FICTION:
- improve renal function (but have temporary dilutional effect)
- don't flush out kidneys
50
Q

Outline SC fluids in CKD

A
  • valuable for cats that repeatedly get dehydrated
  • more advanced dz
  • 60-100ml
  • hartmann’s/LRS/CSL
  • can teach owners
51
Q

Outline constipation in CKD

A
  • cats > dogs

- increases with stage

52
Q

Tx - constipation in CKD

A
  • hydration, mobility
  • lactulose
  • miralax (polyethylene glycol, 1/4 tsp/meal, titrate to effect)
53
Q

What appetite stimulants are given in CKD?

A
  • traditionally given antacids (sucralfate, H2-blockers) but actually GI ulceration is uncommon and efficacy of these tx is unknown
  • MAROPITANT
  • MIRTAZAPINE
  • required for cats and dogs, stages 3+4
54
Q

Outline maropitant in CKD

A
  • selective NK1-R antagonist
  • decreases V in cats with CKD
  • didn’t improve appetite, no wt gain
55
Q

Outline mirtazapine in CKD

A
  • appetite stimulant (unlicensed)
  • increases appetite
  • decreases vomiting
  • wt gain
56
Q

Describe anaemia in CKD

A
  • cats and dogs, stage 4 (usually)
  • multifactorial cause but lack of EPO most important
  • recombinant human EPO (moderate/severe anaemia, tupocally when PCV
57
Q

What is darbopoeitin?

A
  • modified EPO molecule
  • increase half-life and greater in vitro potency
  • decreased immunogenicity
  • initial dose tapered
  • very expensive
58
Q

Describe acidosis in CKD

A
  • cats and dogs, stage 4 usually
  • not usually until advanced dz or patient is dehydrated/ hypovolaemic
  • correct with IVFT usually
  • renal diets tend to be more alkalinising than maintenance pet foods
59
Q

What is the prevalence of hypertension in CKD?

A
  • 3/4 cats presenting with hypertensive retinopathy/ choroidpathy will have azotaemic CKD
  • azotaemia usually mild at diagnosis of hypertension
  • about 30% cats with CKD will be hypertensive
  • prevalence in dogs is probably similar, although few develop ocular changes
60
Q

What neuro signs might occur with CKD?

A
  • depression
  • seizures
  • head tilt
  • vestibular signs
  • ataxia
  • death
61
Q

What cardiac signs might occur with CKD?

A
  • overt heart failure uncommon
  • may exacerbate pre-existing conditions
  • murmurs are common but not specific
  • mild LV hypertrophy
62
Q

Normal cat/dog BP

A
  • systolic 125mmHg
  • mean 100mmHg
  • diastolic 90mmHg
63
Q

What constitutes hypertension in terms of tx?

A
  • systolic BP >170mmHg repeatedly

- systolic BP >160mmHg and consistent CS present

64
Q

Tx - feline hypertension with CKD

A 
GENERALLY INEFFECTIVE
- beta blockers
- spironolactone
- diuretics
- ACEI
EFFECTICE:
- calcium channel blocker (amlodipine)
- tx saves vision but doesn't slow CKD progression
65
Q

Tx - canine hypertension with CKD

A

ACEI generally 1st line tx, response often poor, multimodal tx often required. Then add amlodipine (response often still poor). Consider alternatives (but risk of side-effects without high risk of end-organ damage (i.e. consider risk/benefit ratio and keep low).

Renal (30 decks)

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