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Y4 SA - urinary & endocrine disease > Chronic kidney disease > Flashcards

Chronic kidney disease Flashcards

1
Q

Another term for CKD

A
  • Chronic Renal Failure (CRF)
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2
Q

What is CKD?

A
  • Long-standing, irreversible damage to the kidneys that impairs their function.
  • Self-perpetuating - Progressive over time at variable rate.
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3
Q

Is CKD common in cats & dogs?

A
  • Common in dogs
  • very common in cats (30-80% prevalence reported in geriatric cats)
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4
Q

Causes of CKD

A

Can have underlying cause e.g.
- Polycystic Kidney Disease
- pyelonephritis
- toxins
- glomerulonephritis
- neoplasia
- amyloidosis
- FIP

Often no cause identified
- age related degeneration

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5
Q

Common presenting signs

A
  • PU/PD
  • Anorexia
  • Weight loss
  • Vomiting and diarrhoea
  • Dehydration
  • Pallor
  • Mucosal ulcers
  • Uraemic breath
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6
Q

Breed predispositions

A
  • Dogs- Westie, Boxer, Shar Pei, Bull Terrier, Cocker Spaniel, CKCS
  • Cats-Persian, Abyssinian, Siamese, Ragdoll, Burmese, Russian Blue, Maine Coon
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7
Q

Age predispositions

A
  • Can be juvenile if underlying familial disease, e.g. Polycystic Kidney Disease
  • Older animals if not- age associated disease processes
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8
Q

Co-morbidities - Conditions likely to cause renal insult

A
  • e.g. Hyperthyroidism, hypercalcemia, heart diseases, periodontal disease, cystitis, urolithiasis, diabetes etc
  • Previous Acute Kidney Injury
  • Nephrotoxic Drugs- NSAID, aminoglycosides, sulphonamides, polymyxins, chemotherapeutics
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9
Q

CKD pathphysiology

A

Nephron damage progressive and irreversible
* Nephron loss > other nephrons GFRs increased to compensate> glomerular capillary wall damage and more plasma protein filtration > further glomerular and tubulointerstitial damage.
* Nephron loss > reduced total GFR> build-up of products normally excreted (e.g. urea)> uraemic crisis.
* Reduced renal function > reduced Erythropoietin (EPO) production > non-regenerative anaemia
* Reduced metabolism and excretion of parathyroid hormone > renal hyperparathyroidism (osteodystrophy)

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10
Q

What is uraemic crisis?

A
  • Build-up of urea and other toxins usually excreted in kidneys to intolerable levels
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11
Q

What does uraemic crisis occur due to?

A
  • End stage Chronic Kidney Disease
  • Acute Kidney Injury
  • Acute on Chronic –AKI (e.g. ischemic or toxic insult) exacerbating existing CKD
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12
Q

Uraemic crisis - CS

A
  • Vomiting/nausea
  • Anorexia
  • Lethargy
  • Depression
  • Oralulcers
  • Melena (GI ulcers)
  • Anaemia
  • Weakness
  • Hypothermia
  • Muscle tremors
  • Seizures
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13
Q

Uraemic crisis tx

A

Work out if AKI, CKD or acute on chronic and treat as needed but in addition:
* IVFT- Hartmann’s
– Replace dehydration + ongoing losses
– Care if AKI not to over perfuse- measure urine
* If can measure blood gases- assess for acidosis
– Bicarb if pH <7.2 or serum bicarb < 12
* Treat nausea/GI ulceration
– Omeprazole +/- H2 Blockers +/- sucralfate
– Antiemetics e.g. maropitant
– Pain relief – opioid
* Nutritional support- Important
– Appetite stimulants- Mirtazapine
– Feeding tubes (Nasogastric)
– Beware food aversion-DO NOT
introduce renal diet in hospital

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14
Q

Acute vs chronic (age, duration, hx, exam, harm/biochem, urine)

A

AKI & CKD can both present with uraemic crisis, but differentiation is very important as treatment and prognosis very different.

Age:
CKD - Often older
ARF - Any

Duration:
CKD - >3 months
ARF - <48 hours

Common history:
CKD - Weeks/ months of weight loss, reduced appetite PU/PD. Possible historic of renal insult
ARF - Sudden onset. Possible access to nephrotoxins (toxins or drugs) or evidence of urinary obstruction.

Exam:
CKD - BCS and coat quality reduced. Kidneys small and hard (enlarged possible dependant on cause e.g. PKD)
ARF - Good BCS, kidneys possibly enlarged and painful. Possibly v small bladder.

Haem/biochem:
CKD - K+ normal /decreased, relatively well for severity of azotaemia, non-regenerative anaemia
ARF - K+ increased, Metabolic acidosis, V unwell for severity of azotaemia, Haematology often normal

Urine:
CKD - USG <1.035 (inappropriately dilute), sediment usually not active though possible if UTI. Possible proteinuria.
ARF - USG usually 1.008-1.015 but can be any if bladder not emptied since onset. Urine casts/ proteinuria/ cell debris common. Possible glucosuria

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15
Q

Diagnosis - IRIS staging

A

Early stage (I or early II)- rarely picked up this soon:
* Abnormal renal imaging/ known insult OR
* Persistent elevation/ increasing Creatine/ SDMA OR
* Persistent renal proteinuria

Later stages (Late II- IV):
* Consistent clinical signs
* Azotaemia/ persistently elevated creatinine/ SDMA
AND
USG <1.035 (cats) or <1.030 (dogs) (this is important - doesn’t haven’t to be isosthenuric)

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16
Q

CKD - markers of GFR

A
  • Serum creatinine
  • SDMA (symmetric dimethylated arginine)

Current consensus: When staging- use either/both

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17
Q

Serum creatinine

A
  • Product of muscle metabolism
  • Produced at constant rate and excreted via kidney
  • Muscle atrophy/cachexia can decrease
  • Can increase after feeding- starved
    sample
  • only increase when >75% of nephrons already lost
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18
Q

SDMA

A
  • Produced by all nucleated cells at constant rate and cleared by kidneys
  • Not affected by muscle mass
  • Increases at 40% nephron loss
  • BUT more expensive, less available and possibly less sensitive?
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19
Q

CKD tx

A
  • Treat underlying cause if possible/known
  • Slow progression by managing risk factors.
  • Recommendations vary by stage/substage, but focus around monitoring/ controlling
    – Proteinuria
    – Hypertension and
    – Hyperphosphatemia
    As linked to progression and worse prognosis

Diet very important stage II onwards
Later stages - more emphasis on
* Treating 2ndary anaemia/acidosis/nausea
* Maintaining hydration
* Ensuring adequate nutrition

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20
Q

Why does hyperphosphataemia occur with CKD?

A
  • Phosphate- filtered by Kidneys so builds up in CKD
  • High phos > quicker progression of renal disease
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21
Q

What other condition can hyperphosphataemia cause?

A
  • hyperparathyroidism > Metabolic Bone Disease
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22
Q

Hyperphosphataemia tx

A

Aim to keep to low end of ref range via
* Dietaryrestriction(renaldiet)
* +/-enteric phosphate binders (e.g. Aluminium hydroxide)
Monitor serum Phos monthly until stable then 3 monthly.

FGF23- new biomarker;
- Increases in cats who have phos within target range but are still at increased risk of hyperparathyroidism
- Once phos stable consider measuring FGF23 – if elevated further restrict phos (care interpreting if anaemia/inflammatory dx or pre-existing hyperCa2+)

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23
Q

Primary causes of hypertension

A
  • Stress/environment
  • Idiopathic (prevalence >12% in healthy cats >10 yrs)
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24
Q

Secondary causes of hypertension

A
  • Iatrogenic (e.g. glucocorticoids)
  • Systemic disease including CRF, Cushing’s, hyperT4, hypoT4, DM,
    obesity, pheochromocytoma or primary hyperaldosteronism
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25
Q

Concern with hypertension

A
  • end organ damage if sustained
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26
Q

Hypertension diagnosis

A

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

  • Approx 20% of CKD patients have increased BP at diagnosis
  • A further 10-20% will develop increased BP over time- monitor

Treat if SBP reliably and consistently >160 mm Hg and evidence of EOD (CKD = evidence)

  • SBP <140mmHg = normotensive
  • SBP 140-159mmHg = pre-hypertensive
  • SBP 160-179mmHg = hypertensive
  • SBP >180mmHg = severely hypertensive
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27
Q

Effect of hypertension on kidneys

A
  • Faster decline of renal function
  • Increased proteinuria
  • More frequent
    uremic crises
  • Higher mortality
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28
Q

Tx of renal hypertension

A

ACE inhibitors (ACEi):
* e.g. Benazepril, Enalapril

Angiotensin receptor blockers (ARB)
* e.g. Telmisartan, Spironolactone

Calcium Channel Blocker (CCB)
* e.g. Amlodipine

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29
Q

Hypertension tx aim & specific for dogs + cats

A

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

Dogs – aim to interfere with RAAS activation . Should reduce BP and proteinuria
* Angiotensin receptor blockers (ARB) -1st choice
* ACE inhibitors (ACEi)
If needed can add in Calcium Channel Blocker (CCB)to ACEi or ARB

Cats- start with CCB as more effective at reducing BP unless also proteinuria
* Can add ARB or ACEi to CCB to increase effect if needed.
* If also proteinuria then start with an ARB (Telmisartan).

Consider low salt diet- increased effects of ACEis and ARBs in dogs and cats.

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30
Q

Monitoring hypertension

A

Wait 3-4 weeks between changes (unless emergency) but recheck sooner (after 1-2 weeks if CRF stable or 3-4 days if unstable/ late stage)

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

Antihypertensives should reduce proteinuria if present
* Aim for >50% reduction in UPCR

Once stable and BP <150mmHg can check BP Q4 months

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31
Q

Why does CKD cause proteinuria?

A

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

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32
Q

Proteinuria diagnosis

A

If urine dipstick positive assess via Urine Protein Creatinine Ratio (UPCR)
– UPCR >0.5 (dog) or >0.4 (cat) –Likely caused by glomerular leakage, IF no inflammation/haematuria
(UPCR >3.5 = more likely primary glomerular disease)

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33
Q

Proteinuria tx

A
  • RAAS inhibitor (ACEI or ARB) and feed a clinical renal diet
34
Q

Other causes of chronic renal disease

A

While CKD can occur as a result of aging changes and fibrosis there are conditions which can predispose CKD development.

Renal examples:
- Glomerular disease
- Fanconi’s syndrome
- Polycystic Kidney Disease
- Pyelonephritis
- Nephrotoxin exposure
- Neoplasia

Extrarenal examples:
-Hypertension
-Cardiac disease
- Hyperthyroidism
-Diabetes
- Urolithiasis/ obstruction Cystitis
- Neoplasia
- Hypercalcaemia

35
Q

What is pyelonephritis?

A
  • bacterial infection of the renal pelvis and parenchyma
36
Q

Pyelonephritis prevalence

A

Uncommon in cats and dogs with normal urinary tracts but
* 5-8% prevalence if CKD
* Increased prevalence in other conditions e.g. AKI/ urolithiasis/ obstruction

37
Q

Can pyelonephritis worsen/cause underlying kidney dz?

A
  • yes
38
Q

Pyelonephritis diagnosis

A
  • Compatible clinical signs (fever, abdo pain, pu/pd)
  • Haematology - neutrophilia with left shift
  • Ultrasound - renal pelvis dilatation with hyperechoic mucosa, altered cortex/ medulla echogenicity.
  • NOT pyelocentesis as high risk- culture urine sample
39
Q

Antibiotics and CRF

A

Up to 33% dogs and 25% cats with CKD +ive urine culture – subclinical

Only treat if clinical signs of cystitis/ pyelonephritis (point of debate)

40
Q

Treatment of UTIs/ pyelonephritis with antibiotics

A

Choose renally excreted drugs e.g. amoxycillin/ amoxyclav -higher conc in urine
* E.coli can be resistant so culture if recurrence/ pyelonephritis

Other options
* TMPS- beware many adverse effects
* Fluoroquinolones?- NOT Enrofloxacin in cats
* 3rd Gen Cephalosporins (e.g. cefotaxime)?

Note - fluoroquinolone & 3rd Gen cephalosporins are protected, so only use if confirmed pyelonephritis

41
Q

Nephrotoxic antibiotics

A
  • avoid when treating any infection in patient with CKD
  • Aminoglycosides – can cause acute tubular necrosis
  • Enrofloxacin- can cause renal damage in cats with reduced renal function at high
    doses
42
Q

Benign primary neoplasia of the kidneys

A

Adenomas, lipomas, fibromas, and papillomas- usually incidental

43
Q

Malignant primary neoplasia of the kidneys

A
  • usually unilateral so rarely signs of CKD
44
Q

Is primary renal neoplasia common?

A
  • no
45
Q

Are the kidneys a common site of metastatic spread?

A
  • yes
  • consider CKD signs if bilateral or underlying issue
46
Q

Renal carcinoma

A
  • Usually at one pole and well demarcated
  • Mets early to other kidney/ lungs/ liver/ adrenals
  • Less common- Transitional cell carcinomas, renal sarcomas

Multicentric- Can result in CKD

47
Q

Renal lymphoma

A
  • renal lesions found in up to 50% of dogs and cats with lymphoma
  • Can be found only in kidneys (particularly in cats)
  • Usually multifocal or diffuse, interstitial, and bilateral > large, irregular kidneys
48
Q

What is polycystic kidney disease (PKD)?

A
  • Autosomal dominant hereditary condition
  • Fluid filled cysts present from birth in the kidney and possibly other organs (e.g. liver and pancreas)
  • Size and number gradually increase with age > CRF.
49
Q

PKD signalment

A
  • Breeds- Persians (34%), Exotic Shorthair, Himalayan, British/American Shorthair, Burmilla, Ragdoll, Maine Coon
  • Average age clinical signs 7 yrs
50
Q

PKD exam & diagnosis

A
  • Exam- as CRF but large irregular kidneys
  • Diagnosis -ultrasound -hypo/anechoic spherical cavities
51
Q

Advise for PKD

A

Advise all Persians / exotic short haired screened before breeding even if parents ultrasound negative.
* Ultrasound (from 10 months)
* Genetic testing preferred (any age)- PCR for mutated PKD1 gene

52
Q

What is Fanconi’s syndrome?

A

Disease of proximal tubule > reduced resorption of solutes -> loss of glucose, Na+, K+, phosphorus, bicarbonate, albumin, and amino acids

53
Q

Causes of Fanconi’s syndrome

A
  • Idiopathic
  • Hereditary- gradual onset- mostly Basenjis (genetic marker)
  • Gentamycin nephrotoxicosis (discontinue)
  • Chicken Jerky treats(discontinue)
54
Q

Signs of Fanconi’s syndrome

A
  • PU/PD and wt loss +/- signs of uraemia
55
Q

Fanconi’s syndrome diagnosis

A
  • Increased urinary fractional excretion of glucose, Na+, K+, phosphorus & bicarbonate in urine despite normal plasma concs.
56
Q

Fanconi’s syndrome tx

A
  • remove cause if possible
  • Supplement oral NaCl (5–10 mg/kg/day, PO), K+ (potassium citrate 10–30 mg/kg/day, PO), and bicarb (sodium bicarbonate 10–30 mg/kg/day, PO) if serum concentration is low
57
Q

Glomerular disease

A
  • Can be secondary to advanced CKD or primary and cause/worsen CKD - Glomerular damage > low-molecular-weight proteins (notably Albumin and antithrombin) pass into urine = Protein Losing Nephropathy (PLN)
58
Q

Glomerular disease - signs

A
  • consistent with CKD/ uraemia or can be non-specific weigh loss/ lethargy
59
Q

Glomerular disease diagnosis

A

Haematology/ Biochem
* likely as for CRF but may not be azotaemia
* likely hypoproteinaemia

Urinalysis
* Proteinuria
* May still be able to concentrate urine
* Hyaline casts common as protein lines tubules

60
Q

Primary glomerular disease signalment

A

CATS- less common than in dogs

DOGS- A leading from of renal disease, Most common in middle age

61
Q

Primary glomerular disease - common causes in cats

A
  • neoplasia
  • systemic inflammatory diseases
  • chronic FeLV/ FIV/ FIP
62
Q

Primary glomerular disease - common primary forms in dogs

A

Immune complex glomerulonephritis
* immune complexes in the glomerular capillary wall, > inflammatory change
* Idiopathic (most) or associated with neoplasia, rickettsial diseases , SLE, heartworm, pyometra, chronic septicaemia or adenovirus.

Familial glomerulopathies
* in several breeds including Bernese Mountain Dogs, English
Cocker Spaniels, English Springer Spaniels, Doberman, Greyhounds and more

Amyloidosis (non-familial form)
*Chronic inflammation results in protein deposition in glomerulus

Glomerulosclerosis
* Currently poorly characterised but IDed at histology

63
Q

Glomerular disease- investigations

A

Proteinuria is a hallmark of glomerular disease
- Assess proteinuria via Urine Protein Creatinine Ratio (UPCR)
– UPCR >0.5 (dog) or >0.4 (cat) –Likely caused by glomerular leakage, IF no inflammation/haematuria
– Higher UPCR = more likely primary glomerular disease- >3.5 investigate for Glomerular disease

Imaging findings may be non-specific, possible:
* Small kidneys
* Increased cortex echogenicity
* Loss of corticomedullary definition

Renal biopsy- definitive diagnosis

64
Q

Indications for renal biopsy

A

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

65
Q

Contraindications for 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

Requires GA & operator skill

66
Q

Renal biopsy technique

A
  • Ultrasound guided- preferred
  • Laparoscopic/keyhole
  • Surgical wedge biopsy- avoid specific areas * Blind/palpation?-care - cats only

Only sample CORTEX or bleeds/ infarctions/ fibrosis
Ideally cranial or caudal pole for best sample of glomeruli
Ask lab what to fix samples with for histo/ electron microscopy/ immunofluorescence

67
Q

Renal biopsy after care

A

Severe haemorrhage post procedure possible
* IVFT 24 hours post to reduce chance renal pelvis clots
* Rest patient for 72 hrs and monitor PCV

68
Q

What is nephrotic syndrome?

A

Uncommon result of Protein Losing Nephropathies (PLNs)
Pathognomonic for glomerular disease

69
Q

Clinical findings of nephrotic syndrome

A

in addition to usual signs of renal disease)
* Pitting oedema /ascites/ pleural effusion
* Hypoalbuminaemia
* Hyperlipidaemia (TGs and cholesterol)

70
Q

Why does PLN/nephrotic syndrome cause hyperlipidaemia, ascites/oedema & hypoalbuminaemia?

A
  • Excessive protein loss via kidneys -> hypoalbuminaemia
  • Hypoalbuminaemia -> Upregulation of cholesterol and triglyceride production & reduced plasma oncotic pressure
  • Upregulation of cholesterol and triglyceride production -> hyperlipidaemia
  • reduced plasma oncotic pressure + increased vascular permeability + altered renal tubule Na+ retention -> 3rd spacing of fluid (ascites/oedema)
71
Q

Nephrotic syndrome tx

A
  • Antiproteinurics
  • Anticoagulants
  • Fluid removal
72
Q

Use of antiproteinurics for tx of nephrotic syndrome

A
  • Slow nephron damage and increase plasma oncotic pressure
  • ACE-inhibitors- e.g. Benazepril/ Enalapril
73
Q

Use of anticoagulants for tx of nephrotic syndrome

A
  • Risk of thromboembolism - as regulatory proteins (e.g.
    antithrombin and protein S) lost along side albumin
  • Aspirin or Clopidogrel- minimize spontaneous platelet
    aggregation.
74
Q

Use of fluid removal for tx of nephrotic syndrome

A
  • Only if severe impairment of resp/ heart/QoL as result
  • Will reform as RAS upregulates and worsens hypovolaemia
  • Abdominal/ pleural tap
  • Diuretics- frusemide? Spironolactone (K+ sparing)
75
Q

Glomerular disease- treatment

A
  • If a cause of immune complex disease present – treat
  • Manage Nephrotic syndrome if present
  • Limit proteinuria
    – ACEi (or ARBs) – reduce further interstitial fibrosis
  • If glomerular inflammation at biopsy and no known primary antigenic stimulus consider Immunosuppressives
    – e.g. mycophenolate, azathioprine, cyclophosphamide, cyclosporine
    – NB-Corticosteroids only beneficial in mild glomerulopathy and can worsen
    proteinuria.
  • Monitor and manage CKD as per IRIS staging
76
Q

CRF prognosis - dependent on

A
  • Complications (e.g. high BP, glomerulonephritis)
  • Patient age
  • Duration and severity of signs
  • Serum phosphorus
  • Severity of proteinuria
  • IRIS stage
  • Primary disease process
  • Owner commitment
  • Ability to medicate/ feed
    as required
77
Q

CRF prognosis in cats

A

Mean days survival from diagnosis:
- Stage II =1151 days
- Stage III =679 days
- Stage IV =35 days

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

78
Q

CRF prognosis in dogs

A

Median survival from diagnosis:
- Stage II = 200-400 days
- Stage III = 110 to 200 days
- Stage IV = 14 to 80 days

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

79
Q

Rabbits and CKD

A
  • Same underlying disease processes as dogs and cats (but also can be due to E. Cuniculi)
80
Q

Rabbits and CKD - CS

A
  • PU/PD, weight loss (hide signs well)
  • occasional haematuria (renal infarctions / 2ndary to hypercalciuria > uroliths)
81
Q

Rabbits and CKD - diagnosis

A

Urinalysis
- (Don’t cysto if possible -free catch/ express)
- Inappropriate urine concentration (ref 1.003-1.035- should be >1.035 if dehydrated). - Proteinuria common in CRF
–possible in healthy animals/ inflammatory disease/contaminants
– interpret with USG and sediment and consider UPCR

Biochem
- hypercalcaemia and azotaemia (use lab reference ranges for rabbits).
- If severe also ^K+ and Phos.

82
Q

Rabbits and CKD - tx

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

Y4 SA - urinary & endocrine disease (17 decks)

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