Chronic kidney disease Flashcards

1
Q

what is chronic kidney disease

A

Long-standing, irreversible damage to the kidneys that impairs their function

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2
Q

List 8 common presenting signs of CKD

A

PU/PD
Anorexia
Weight loss
Vomiting and diarrhoea
Dehydration
Pallor
Mucosal ulcers
Uraemic breath

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3
Q

describe how nephron damage gets worse and therefore irreversible

A

Nephron loss > other nephrons GFRs increased to compensate> more damage

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4
Q

how can reduced renal function lead to non-regenerative anaemais

A

reduced EPO production

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5
Q

what is a uraemic crisis

A

Build-up of urea and other toxins usually excreted in kidneys to intolerable levels.

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6
Q

list 3 conditions that can lead to uraemic crisis

A

End stage Chronic Kidney Disease
Acute Kidney Injury
Acute on Chronic Kidney disease

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7
Q

List 11 clinical signs of a uraemic crisis

A

VERY SICK
* Vomiting/nausea
* Anorexia
* Lethargy
* Depression
* Oral ulcers
* Melena (GI ulcers)
* Anaemia
* Weakness
* Hypothermia
* Muscle tremors
* Seizures

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8
Q

why should you not introdue a renal diet to a cat in hospital for renal disease

A

food aversion
offer when at home

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9
Q

describe the difference in duration of signs between CKD and AKI

A

CKD > 3 months
AKI <48 hours

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10
Q

what do we tend to find on clinical exam with CKD

A

BCS and coat quality reduced. Kidneys small and hard (enlarged possible dependant on cause e.g. PKD)

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11
Q

Describe stage 1 and 2 of IRIS STAGING

A

rarely picked up this soon
Abnormal renal imaging/ known insult OR
Persistent elevation/ increasing Creatine/ SDMA OR
Persistent renal proteinuria

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12
Q

Describe late 2 -4 stages of IRIS staging

A

consitent clinical signs
Azotaemia / persistently elevated creatinine/ SDMA
AND
USG <1.035 (cats) or <1.030 (dogs)

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13
Q

what is stage 1-4 of Iris staging based on

A

cratinine OR SDMA

consistent elevation in hydrated patient

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14
Q

what is substage of iris staging based on

A

proteinuria
systolic blood pressure

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15
Q

when does serum creatinine increase

A

when 75% of nephrons have been lost

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16
Q

when does SDMA increase

A

at 40% nephron loss

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17
Q

Describe how to treat CKD

A

treat underlying cause
mange risk factors to slow progression
renal diet

changes as it progresses

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18
Q

what is the problem with hyperphosphataemia with CKD

A

causes quicker progression of renal disease
can also lead to hyperparathyroidism –> Metabolic Bone Disease

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19
Q

Why do we get hyperphosphataemia in CKD

A

Phosphate –> filtered by kidneys so builds up in CKD

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20
Q

why is hypertension a concern

A

can cause end organ damage if susteined

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21
Q

describe how to diagnose hypertension

A

Based on repeated measurements of systolic blood pressure (SBP) - consistent technique and equipment

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22
Q

at what point do we treat hypertension

A

Treat if Systolic BP reliably and consistently >160 mm Hg

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23
Q

List 3 ways to treat renal hypertension

A

ACE inhibitor - e.g. Benazepril, Enalapril
Angiotensin receptor blockers (ARB) - e.g. Telmisartan, Spironolactone
Calcium Channel Blocker (CCB) - e.g. Amlodipine

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24
Q

how quick do you aim to reduce hypertension

A

Aim to reduce to <150mmhg over a few weeks – quicker (hours) if severe ocular / CNS signs

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25
Q

How do we treat CKD in dogs

A

aim to interfere with RAAS activation .
1st choice= Angiotensin receptor blockers (ARB) OR
ACE inhibitors (ACEi)

If needed can add in calcium channel blocker

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26
Q

How do we treat CKD in cats

A

start with Calcium Channel Blocker as more effective at reducing BP unless also proteinuria

can add angiotensin receptor blockers or ACEi to increase effect if needed

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27
Q

what should you do if urine dipstick +ve for protein

A

Urine Protein Creatinine Ratio

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28
Q

How do we treat proteinuria

A

RAAS inhibitor (ACEI or Angiotensin Receptor Blocker ) and feed a clinical renal diet

29
Q

define pyelonephritis

A

bacterial infection of the renal pelvis and parenchyma

30
Q

describe how to diagnose pyelonephritis

A

Very sick
haem- neutrophilia with left shift
U ltrasound - renal pelvis dilatation with hyperechoic mucosa, altered cortex/ medulla echogenicity.
NOT pyelocentesis as high risk- culture urine sample

31
Q

Describe how to treat UTIs/ pyelonephritis

A

choose renally excreted drugs e.g. amoxycillin / amoxyclav

32
Q

why should we avoid aminoglycosides in patients with CKD

A

can cause acute tubular necrosis

e.g. gentamycin

33
Q

why should we avoid Enrofloxacin in patients with CKD

A

can cause renal damage in cats with reduced renal function at high

34
Q

why do renal neoplasia generally not show signs of CKD

A

usually unilateral so other kidney compensates

35
Q

Describe Polycystic Kidney Disease (PKD)

A

congenital disease
seen more in cats
Fluid filled cysts present from birth in the kidney–> Size and number gradually increase with age —> CKD

36
Q

what do you find on clinical exam with
Polycystic Kidney Disease (PKD)

A

as CKD but large irregular kidneys

37
Q

describe how to diagnose Polycystic Kidney Disease (PKD)

A

-ultrasound -hypo/anechoic spherical cavities
there is genetic testing- PCR for mutated gene (helps find animals we should not be breeding from)

38
Q

describe Fanconi’s syndrome

A

Disease of proximal tubule > reduced resorption of solutes
Dogs

39
Q

List the clinical signs of Fanconis syndrome

A

PU/PD
weight loss
signs or uraemia

40
Q

describe how to diagnose Fanconi’s syndrome

A

Increased urinary fractional excretion of glucose, , Na+, K+, phosphorus & bicarbonate in urine despite normal plasma concs.

41
Q

describe how to treat Fanconis syndrome

A

remove cause if possible
supplement electrolytes lost

42
Q

List the indications of renal biopsy

A

Only if will alter patient management (generally not CKD) e.g.
- Protein Losing Nephropathy – unexpected/doesn’t respond to treatment
- AKI- cause and prognosis
- Mass lesions

43
Q

List 6 contraindications of renal biopsy

A

Late stage CKD
Severe anaemia/ azotaemia
Uncontrolled hypertension/ coagulopathy
Severe hydronephrosis/ many large cysts
Pyelonephritis/ perirenal abscesses
NSAIDs in last 5 days

44
Q

what is nephrotic syndrome

A

Lost so much protein from blood–> no longer keep water in the blood so oedema formed

45
Q

what is seen with nephrotic syndrome

A

Pitting oedema /ascites/ pleural effusion
Hypoalbuminaemia
Hyperlipidaemia (TGs and cholesterol)

46
Q

Describe how to treat nephrotic syndrome

A

Antiproteinurics- ACE inhibitors
Anticoagulants - Aspirin or Clopidogrel- minimize spontaneous platelet aggregation
Fluid removal - if QOL decreasing as result

47
Q

describe how to treat glomerular disease

A

If a cause of immune complex disease present – treat
Manage Nephrotic syndrome if present
Limit proteinuria - with ACE inhibitors
Monitor and manage CKD as per IRIS staging

48
Q

List 5 things that decrease prognosis of CKD

A

Uncontrolled hypertension
Persistent ↑ Serum Phosphorus
Persistent Proteinuria
Unable to medicate/ switch to renal diet.
Can’t control underlying issue.

49
Q

Describe how to treat CKD in cats

A

Treat underlying causes if possible
Discontinue nephrotoxic drugs- NSAIDS
Treatment as dogs/cats BUT dietary management different
2ndary hypertension common- diagnose as dogs/cats and treat with ACEi

50
Q

List 7 potential underlying causes of CKD

A

Polycystic kidney disease
pyelonephritis
toxins
glomerulonephritis
neoplasia
amyloidosis
FIP

51
Q

List 5 examples of nephrotoxic drugs that can cause CKD

A

NSAIDs
aminoglycosides
sulphonamides
polymyxins
chemotherapeutics

52
Q

Why do we get renal hyperparathyroidism secondary to CKD

A

reduced metabolism and excretion of parathyroid hormone

53
Q

How do we treat a uraemic crisis

A

IVFT- Hartmanns
Assess acidosis (blood gas analysis)
Treat nausea and GI ulceration (Maropitant, pain relief, omeprazole )
Nutritional support

54
Q

Describe how we reduce phosphate levels

A

renal diet- low in phosphate
phosphate binders e.g. Aluminium hydroxide

55
Q

What is a biomarker for cats at risk of hyperphosphataemia

A

FGF23

56
Q

How can hypertension effect the kidneys

A

Faster decline of renal function
Increased proteinuria
More frequent uremic crisis
Higher mortality

57
Q

How does CKD lead to proteinuria

A

Nephron loss => other nephrons GFRs increased to compensate => glomerular capillary wall damage and more plasma protein filtration => further glomerular and tubulointerstitial damage.

58
Q

How do we monitor patients being treated for hypertension

A

Evidence of worsening EOD on exam
Marked increase in azotaemia
Evidence syncope/hypotension (SBP <120mmHg)

59
Q

Describe how we treat pyelonephritis

A

Only if clinical signs
Choose renally excreted drugs e.g. amoxycillin/ amoxyclav - higher conc in urine
TMPS
Fluoroquinolones (not enroflocacin) - protected

60
Q

List some nephrotoxin antibiotics

A

Aminoglycosides - can cause acute tubular necrosis
Enrofloxacin- can cause renal damage in cats with reduced renal function at high doses

61
Q

what type of cancer can result in CKD

A

Lymphoma- multi centric

62
Q

What testing can we do for polycystic KD before disease develops

A

Genetic testing - PCR for mutated PKD1 gene

63
Q

List the clinical signs of glomerular disease

A

Signs consistent with CKD/ uraemia or can be non-specific weigh loss/ lethargy.

64
Q

Describe how to diagnose glomerular disease

A

Haematology/ Biochem
- Likely as for CRF but may not be azotaemia
- Likely hypoproteinaemia

Urinalysis
- Proteinuria => always
- May still be able to concentrate urine
- Hyaline casts common as protein lines tubules

Renal biopsy - definitive diagnosis

65
Q

Which part of the kidney would you biopsy for glomerular disease diagnosis

A

cortex only

66
Q

which diuretic is potassium sparing

A

spironolactone

67
Q

How do we diagnose CKD in rabbits

A

urinalysis
biochemistry

68
Q

How do we get a urine sample in rabbits

A

Don’t cysto if possible
Free catch/express best option

69
Q

Describe how to treat CKD in rabbits

A

Treat underlying causes if possible
Discontinue nephrotoxic drugs
Treatment as dogs/cats BUT dietary management different (see endocrine)
2ndary hypertension common- diagnose as dogs/cats and treat with ACEi