Chronic kidney disease Flashcards

1
Q

chronic renal failure is the?

A

end result of chronic persistent renal disease

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2
Q

Define Acute kidney disease?

A
  • Reversible disease if detected early enough
  • there are enough surviving nephrons
  • treatment is started quickly
  • Prevention of acute kidney disease is better than any treatment
  • Sudden onset means there is no time for compensatory mechanisms
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3
Q

Every nephron is what?

A

Every nephron is precious …..”every little helps” in our mission to save the kidneys!

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4
Q

Define Chronic kidney disease?

A
  • Irreversible “end stage” kidney disease
  • manageable not curable
  • Gradual and progressive loss of nephrons
  • Clinical signs may have been present for weeks-months-years
  • polydipsia
  • polyuria
  • weight loss
  • lethargy
  • decrease in appetite
  • Above all typical signs of renal disease
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5
Q

Are there any useful clinical features to differentiate between AKI and CKD?

A

*There are exceptions to every rule: PKD, lymphoma, FIP. Kidneys become large in these

PKD= polycystic kidney disease, FIP= feline infectious peritonitis

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6
Q

Are there any useful laboratory features to distinguish CKI and AKI?

A

*There are exceptions to every rule: an underlying disease predisposing to AKI could also be causing anaemia; a patient with AKI could have GI bleeding and become anaemic.

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7
Q

CKD dogs fed a renal diet and on ACE-I for hypertension might be more at risk of?

A

Becoming hyperkalaemic in late stage renal disease. Sometimes these dogs need to have a specially formulated diet to counteract this but often it is not of any clinical significance in terms of the “big picture” of the dog’s problems.

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8
Q

CKD is a?

A

Polyuric state

  • urine output > 50 mls/kg /day (>2mls/kg/hr)
  • Kidneys cannot concentrate urine
  • Produce urine of a low USG
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9
Q

Normal water intake is between?

A
  • dogs can be up to 60-90mls/kg/day
  • cats probably up to 45 mls/kg/day
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10
Q

With regards to urine output AKI cases can be?

A
  • oliguric (urine output <0.5mls/kg/hour) Reduced renal ouput the kidney cannot concentrate or produce urine
  • anuric
  • polyuric (less likely)
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11
Q

Look at this schematic for chronic kidney disease?

A
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12
Q

Why is it important to record weight at every vet visit?

A

One of the reasons for recording weight in patients at every trip to the vets is to help clarify if a patient has lost weight because owners often don’t know when weight loss is slowly progressive.

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13
Q

Discuss diagnosis of CKD with regards to blood tests?

A

Azotaemia

•>75% functional loss of nephrons

creatinine can be normal in

  • early CKD
  • cases with poor muscle mass

SDMA

  • for early CKD?
  • <25% nephrons lost
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14
Q

Discuss diagnosis of CKD with regards to Urinalysis?

A
  • SG inappropriately dilute for the level of azotaemia*
  • dog <1.030
  • cat <1.035 (cats concentrate better even with CKD)
  • urine concentrating ability is affected with >66% functional loss of nephrons
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15
Q

Discuss exception to the rule with USG?

A

*Exceptions to every rule:

Producing hyposthenuric urine (SG <1.008) requires functional tubules. Such a low SG is therefore unlikely to be due to intrinsic kidney disease

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16
Q

What does SDMA stand for?

A

symmetric dimethylarginine assay

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17
Q

How do cats differ to dogs?

A

Note that cats are better at maintaining urine concentrating ability than dogs and therefore can still have renal azotaemia at a relatively higher urine concentration (Urine SG 1.033-1.035) compared with dogs. Dogs with CKD are usually unable to concentrate urine to an SG >1.030. If the kidneys are working, azotaemic patients should have very concentrated urine because the body is trying to conserve water ie they are dehydrated.

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18
Q

What should you never do?

A

Never (ever!) interpret raised­ creatinine +/or urea without urinalysis for urine SG

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19
Q

When might pre renal azotaemia be a challenge to our diagnosis of CKD?

A
  • a CKD patient who is dehydrated
  • the azotaemia might seem worse due to dehydration
  • IRIS staging is only appropriate in a stable patient
  • an azotaemic cat with relatively concentrated urine (SG 1.030) and vague clinical signs
  • a dog who is on furosemide with restricted access to water

To rule out any influence of pre renal azotaemia give fluid therapy and assess the response to treatment

•pre renal azotaemia resolves quickly with IVFT

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20
Q

Dogs on furosemide should never have what restricted?

A

have water restriction but sometimes this happens (despite what we say!) because owners think it’s an appropriate thing to do if they are struggling with a dog who is polyuric. In fact what will happen is the dog will continue to produce excessive urine volume due to the furosemide and can become dehydrated. Renal perfusion then reduces and they can become azotaemic. The combination of azotaemia and low urine SG could be misdiagnosed as intrinsic kidney disease if we fail to take in to account the medication the dog is on. As a clinical example: think about a geriatric dog in heart failure

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21
Q

Diagnostic imaging & CKD: is it worthwhile for small or normal kidneys?

A

Radiography:

  • confirms renal size
  • margination
  • are there 2 kidneys?
  • any 2ry problems
  • dystrophic calcification
  • loss of bone density

Ultrasound:

  • normal?
  • change in echogenicity?
  • loss of corticomedullary border

Diagnostic imaging is often unhelpful if both kidneys are already small

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22
Q

Diagnostic imaging & CKD: is it worthwhile for Enlarged kidney(s)?

A

Radiography:

•confirms renal size

Ultrasound:

  • normal?
  • change in echogenicity?
  • polycystic kidney disease
  • FIP
  • lymphoma
  • perinephric pseudocyst
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23
Q

Can we palpate cats kidneys?

A

we should nearly always be able to palpate a cat’s kidneys unless they are really obese or the kidneys are especially small

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24
Q

Can we palpate dog kidneys?

A

We can palpate the kidneys in some but definitely not all dogs…it isn’t just you! Think about the body shape, where the kidneys are and then work out how likely it is you will feel them. If the kidneys are enlarged then that might be easier. Think about the need for diagnostic imaging to assess renal size and shape in dogs.

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25
Q

What are the indications fo Renal biopsy & CKD?

A
  • Suspected neoplasia
  • Familial nephropathy where results might have an impact on other animals. Biopsy may change situation for siblings or breed in general
  • Non azotaemic protein losing nephropathy
  • ie kidney disease not failure

Biopsying a small fibrotic “end stage” kidney will not contribute to management of the case but will contribute to risks and costs. Need to be confident it will change your treatment. Not relevant for CKD but maybe indicated for lymphoma.

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26
Q

What is the prognosis for CKD in cats?

A
  • approx. 30-50% of cats >15 yrs old have CKD
  • can have stable CKD for months to years
  • can have CKD and die of another disease
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27
Q

What is the prognosis for CKD in dogs?

A
  • approx. 10% of geriatric dogs have CKD
  • progressive, linear, more rapid deterioration common in dogs than cats
  • are more likely to die of CKD if they have CKD
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28
Q

What are the Markers associated with progression of CKD:

A

worsening azotaemia, anaemia, high blood pressure, proteinuria, soft

tissue mineralisation

The markers associated with progression of CKD signify consequences of CKD but also contribute to further deterioration

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29
Q

Think about something that might have destabilised the patient with CKD e.g?

A

GI upset, 2ry UTI, respiratory infection, stress of some kind, restricted access to water, a cat that goes off its food or has not been fed

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30
Q

What does the sick patient with CKD suffer from?

A
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31
Q

Discuss a stabilisation plan for CKD?

A

Fluid therapy to restore deficit, provide maintenance and cover any on-going losses

  • crystalloid eg Hartmann’s
  • addresses any pre renal component to azotaemia
  • remember your patient is polyuric
  • what impact does that have on ongoing losses?

Correct hypokalaemia if necessary (cats with renal failure pee more of it out)

  • with iv fluids?
  • oral?

Anti emetics: also help with nausea in cats

  • NK-1 receptor antagonist (maropitant)
  • metoclopramide CRI (less effective?)

Gastroprotectants:

  • sucralfate
  • H2 receptor antagonist
  • ranitidine, cimetidine, famotidine
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32
Q

Discuss what fluid therapy does in CKD stabilisation?

A

Fluid therapy corrects the pre renal azotaemia and protects the kidneys from further damage. It cannot repair irreversible renal damage or restore function where intrinsic renal failure is present.

What does this mean? There is NO POINT continuing on fluid therapy for days in CKD cases unless you are managing another aspect of the patient’s condition in a more successful way and just need to support the patient for a while longer.

33
Q

Discuss stabilising and Identifying and resolving any complicating factors in CKD?

hypertension

A

Is your patient hypertensive?

  • systolic BP >180 mmHg?
  • risks of target organ damage ­ ­
  • are there any fundic changes to support this?
  • how likely is the “white coat effect”?
  • 1st line treatment of choice:
  • amlodipine for cats (Ca channel blocker)
  • ACE-I for dogs
34
Q

Target organs for damage secondary to systemic hypertension include the?

A

Eyes, kidneys (exacerbating an already bad situation) and central nervous system. The heart can also be adversely affected by hypertension but this is more of a theoretical list.

35
Q

Young healthy cats are quite resistant to?

A

UTI (partly due to their concentrated urine) but this changes in CKD, DM and hyperthyroidism.

36
Q

Identify and resolve any complicating factors:

Does your patient have a UTI?

A
  • Clinical signs are not always evident (“occult UTI”)
  • Young dogs: if congenital renal disease often have UTI at diagnosis
  • urinalysis (cysto sample)
    • sediment exam
  • white cells?
  • bacteria?
    • culture
  • cats 80-85% are E.coli
  • dogs more variable pathogens (E.Coli, Proteus, Staphs)
37
Q

Do we always need to treat occult UTI in cats with CKD?

A
  • likely to have abnormalities which could predispose to pyelonephritis
  • lower UTI –> ascending infection
  • less able to cope with even minimal damage to remaining nephrons
  • “every nephron is precious”
  • Our justification to treat
  • The approach to managing occult UTI is evolving
38
Q

What are the aims managing CKD?

A
  1. Determine the underlying cause (stand a better chance of treatment if we can find this but very often we cannot find this problem)
  2. Control factors contributing to disease progression
  3. Maintain quality of life
39
Q

Discuss determining the underlying cause in managing CKD?

A
  • often not possible
  • treat specific disease appropriately if you can
  • ureteral obstruction
  • Pyelonephritis (infection in kidney)
  • renal lymphoma (can do well if put on chemo)
  • protein losing nephropathy (needs to have management regime focussing on managing the proteinuria)
40
Q

Discuss controlling factors contributing to disease progression in managing CKD?

renal hyperPTH

A

Renal hyperparathyroidism (­increase in PTH)

  • now referred to as CKD-MBD (mineral bone disorder)
  • Ca, phosphorus, PTH &/or vit D metabolism changes
  • abnormal bone turnover
  • soft tissue and/or vascular mineralisation
  • Cats: 50% with mild stable CKD have increased­ PTH
  • Increase in serum phosphate is a good indicator of PTH and easier to measure than PTH
  • ie routine biochemistry rather than dedicated hormonal assay requiring specific methods for sample collection, processing and transport
  • Increase­ phosphate and ­ PTH are detrimental to nephrons so if we can reduce them it will help
  • “every nephron is precious” *if red it is what we need to know
41
Q

Managing CKD?

A

We need to control hyperphosphataemia and hyperparathyroidism

42
Q

The whole topic of CKD-MBD is complex and evolving- don’t get bogged down in the details just try to understand the broad concepts. Which are?

A

Beneficial effects of increased PTH are to encourage loss of phosphate when excretion becomes compromised. BUT with progressive deterioration increased PTH becomes counterproductive leading to soft tissue mineralisation and demineralisation of bone.

43
Q

Discuss phosphate restricted diets?

A

•Evidence based medicine:

•CKD cats and dogs successfully fed a PO4 restricted diet live longer than those fed a normal diet

  • Start as soon as CKD is diagnosed?
  • if phosphate is normal, PTH can still be ­
  • Introduce new diets sensibly
  • educate your client
  • palatability?
  • food aversion in hospital situations?
  • trial and error with different brands?
44
Q

What do renal care diets diets also aim to do: is it just about phosphate restriction?

A
45
Q

Discuss Phosphate binders?

A

As renal disease progresses and renal function declines, phosphate restriction alone is not enough

Intestinal phosphate binding drugs make sense but

  • only worthwhile with a renal care diet
  • must mix with food
  • can cause constipation +/- other side effects
  • constipation is already a risk in CKD cats due to borderline dehydration
  • availability of different products varies
46
Q

What can we use as phosphate binders?

A

Aluminium hydroxide

  • powder more palatable but not always available
  • dose very variable (60-150mg/kg/day)
  • very high doses –>microcytosis, encephalopathy, weakness as well as constipation

Calcium carbonate or acetate

  • Ipakitine® marketed for cats and has a fishy smell
  • Tums ® (human product)
  • beware, can cause hypercalcaemia and­ increase risk of calcium oxalate uroliths

Lanthanum carbonate

  • still available on human market
  • expensive
  • (discontinued for vet market as Renlazin® )
47
Q

Is there a role for calcitriol in managing hyperparathyroidism?

A

Calcitriol is not a substitute for renal care diet or phosphate binders

48
Q

IF see evidence of demineralisation of bone it is more likely in young animals with congenital renal disease but it might be associated with older patients.

Possible risky situations:

A

1. geriatric dogs undergoing significant dental extractions….why is the dog off its food? Is it “just” bad teeth or could this dog have CKD?

2. restraining a difficult geriatric cat for blood samples….never struggle with a cat but especially not if there could be demineralised bone –> pathological tibial fractures have been reported.

49
Q

Discuss controlling factors contributing to disease progression in managing CKD?

hypertension and proteinuria

A

Glomerular hypertension and proteinuria

  • loss of functional nephrons leads to adaptive hyperfiltration of the remaining nephrons
  • with progressive disease –> counterproductive
  • inflammation –> further nephron loss
  • interstitial fibrosis
  • The pathophysiological mechanism for hyperfiltration is glomerular capillary hypertension linked to local activation of RAAS
  • proteinuria is a marker for this process
50
Q

Proteinuria and CKD: what do we know?

A
  • We need to rule out pre and post renal causes of proteinuria before assuming proteinuria is renal in origin
  • UTI or lower urinary tract inflammation?
  • Proteinuria (defined as UPC >0.5) is associated with shorter survival times in cats with renal disease
  • ACE-Is (to manage proteinuria) prolong survival in dogs with
  • biopsy proven glomerulonephritis
  • Samoyed familial nephropathy
51
Q

There is currently no evidence to show that controlling proteinuria has a beneficial effect on survival in cats with CKD?

A

Proteinuria might just be a marker of disease progression rather than a key factor we need to control

Just because cats with proteinuria have shorter survival times than cats without proteinuria doesn’t mean we can necessarily make them live longer if we control the proteinuria. More research is ongoing!

52
Q

Illustrate the exacerbating cycle of proteinuria?

A
53
Q

How can we Control proteinuria: if we want/need to?

A

•ACE-I

  • benazepril is licensed for use in CKD cats with persistent proteinuria (ie not all CKD cats)
  • potential adverse effects include hypotension, azotaemia and hyperkalaemia

Aldosterone receptor antagonists

•telmisartan is licensed for management of proteinuria associated with CKD in cats

These drugs have similar results in reducing proteinuria but we still need evidence to say this has a positive impact on survival.

The objective of using treatment to control proteinuria is only to delay progression of disease rather than improve the current situation. Only use these treatments if your patient is stable and well hydrated.

54
Q

How can you control factors contributing to disease progression?11111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111 (sorry just saw hanny and got excited and lent on my keyboard)

A

Monitor blood pressure and treat hypertension

Anti hypertensive drugs:

  • Amlodipine (cats)
  • Benazepril (dogs)
  • Telmisartan
55
Q

Discuss maintaining quality of life in the CKD patient?

A

Avoid dehydration

  • encourage water intake at home
  • water fountains
  • wet food
  • administration of s/c fluids at home?
  • s/c indwelling ports?
  • feeding tubes?
  • think about IVFT for patients in hospital but (please!) don’t believe you can “flush out” the kidneys
56
Q

Discuss maintaing quality of life with appetite stimulants?

A

Mirtazapine

  • beneficial effects
  • increased appetite
  • decreased vomiting
  • weight gain
  • beware of adverse effects
  • low dose every 48 hours

Maropitant

  • decreased vomiting
  • might improve appetite
57
Q

Discuss maintain quality of life in CKD by managing hypokalaemia?

A

Manage hypokalaemia

  • risks for decrease K include poor appetite and polyuria
  • 20-30% of cats with CKD are hypokalaemic
  • consequences:
  • muscle weakness –> ileus –> drop in appetite
  • possible worsening of renal function?
  • theoretical risk only?

What can we do?

  • supplements often unpalatable but might make cats brighter and stronger
  • Kaminox®, Tumil K®
58
Q

How can we Maintain quality of life in CKD by managing anaemia if this seems to be causing clinical signs?

A

Causes of anaemia in CKD (multifactorial)

  • erythropoietin deficiency
  • blood loss: GI and/or frequent blood samples, surgery
  • reduction in red cell life span
  • uraemic inhibition of erythropoiesis
  • iron deficiency

Treatment:

  • darbepoietin + iron
  • protocols are available but vary
59
Q

How can we maintain quality of life in CKD by managing or prevent constipation?

A

Contributing factors:

  • immobility
  • dehydration (often borderline)

Management:

  • encourage water intake
  • laxatives
  • lactulose
  • polyethylene glycol (Miralax®)
  • appropriate treatment for joint disease
60
Q

CKD and NSAIDs: how careful should we be?

A
  • Nephrotoxicity is reported but is less common than GI signs
  • Risks associated with administration to dehydrated or hypovolaemic patients
  • We must keep pain under control
  • ISFM and AAFP Consensus Guidelines “….NSAIDs can be used safely in cats with stable CKD at judicious doses, and this should not be a reason for withholding analgesic therapy…” Sparkes (2010) JFM&S 12 521-538
61
Q

Staging CKD helps us plan appropriate treatment and monitoring for our patients. Outline the IRIS staging protocol?

A

Step 1: diagnose CKD

IRIS staging is only appropriate for patients with CKD

Rule out pre renal azotaemia with IVFT if in doubt or any signs of dehydration

Step 2: use a fasting blood creatinine checked at > 2 time points and allocate the stage (I-IV)

Step 3: allocate a substage based on

Degree of proteinuria (UPCR)

Presence (or absence) of hypertension

62
Q

UPCR= urine protein creatinine ratio. Referred to as UP/C on the IRIS website. Best checked on a cystocentesis sample. Levels can vary from day to day so beware of overinterpreting small fluctuations. We often suggest?

A

Checking a pooled 3 day sample to minimise the effect of day to day variation.

If you are staging a patient with CKD be aware that dehydration might lead to a higher stage than appropriate. You need to use fasting creatinine checked at >2 time points ie your patient should be stable…which means well hydrated. CKD cats can be borderline dehydrated and staging will still work if creatinine is stable but don’t try to stage a sick dehydrated CKD cat. Stabilise and then review.

63
Q

Look at this IRIS staging chart?

A

It is likely that modification of IRIS staging will occur at some point as SDMA becomes more accepted as a marker for early renal disease. Keep referring to the website as a useful resource now and in the future!

* Early CKD may be detected by palpation of small or abnormal kidneys, PU/PD with no other cause found, proteinuria consistent with renal origin (ie you have ruled out other causes of proteinuria such as UTI).

64
Q
A
65
Q

IRIS staging: what is the current role of SDMA?

A
66
Q

Discuss Functional reserve of the kidneys?

A
67
Q

Compare functional reserve to IRIS staging?

A
68
Q

Outline IRIS sub-staging: proteinuria?

A

Ideally based on 2 separate urine samples collected at least 2 weeks apart

Rule out post renal proteinuria ie UTI and lower urinary tract inflammation and/or haemorrhage before trying to interpret the UPCR

  • Borderline proteinuric patients can be re-evaluated in 3-6 months
  • You can consider pooled samples to check UPCR to avoid issues with day to day variability eg samples from 3 days all pooled together to run through the lab as one sample (reducing costs)
69
Q

Discuss IRIS sub-staging: of arterial systolic blood pressure (Doppler)?

A

TOD= target organ damage

70
Q

Discuss Causes of CKD in cats?

A
  • chronic tubulointerstitial nephritis
  • histological description, cause unknown, common
  • lymphoma
  • FIP
  • PKD
  • pyelonephritis
  • toxins (see AKI)
  • obstructive uropathy
  • sequel to AKI
  • amyloidosis
  • glomerulonephritis / PLN
71
Q

What are Abyssinian cats more at risk from?

A

The picture is an Abyssinian and these cats are more at risk of a relatively rare problem- amyloidosis.

72
Q

Discuss Polycystic Kidney Disease (PKD) in cats?

A
  • Persian & related breeds, exotic and British short hair
  • Autosomal dominant inheritance
  • Cysts often seen from 8 mths of age with ultrasound
  • Azotaemia may not develop for years
  • DNA test now available so may help with control through selective breeding
73
Q

Discuss Causes of CKD in dogs?

A

This is not a complete list but we should consider:

  • chronic tubulointerstitial nephritis
  • histological description, cause unknown, common
  • familial nephropathy especially in young dogs
  • Boxers (juvenile nephropathy)
  • Shih Tzu, Lhasa Apso, Golden Retriever: renal dysplasia
  • Sharpei: amyloidosis
  • PLN/glomerular disease
  • others eg pyelonephritis, hypercalcaemia
  • sequel to AKI
  • There are many juvenile renal diseases in dogs which occur sporadically. These are just a few examples.
74
Q

Discuss Protein losing nephropathies?

A
  • Characterised by severe proteinuria indicating presence of glomerular disease
  • Dogs>>cats
  • Clinical signs vary with severity:
  • weight loss and lethargy
  • peripheral oedema and ascites
  • progression to azotaemic CKD –> polyuria, anorexia, vomiting, weight loss
  • hypertension
  • rarely may develop thromboembolic disease
  • aortic thrombus
  • in cats more likely to be cardiac disease
  • in dogs more likely to be PLN
  • pulmonary thromboembolism
75
Q

What is “Nephrotic Syndrome”?

A
  • hypoalbuminaemia
  • often <15g/l
  • differentials for PLN include PLE….
  • severe persistent (>2 weeks) proteinuria
  • peripheral oedema +/- ascites
  • “weight gain” but drop in BCS
  • hypercholesterolaemia
76
Q

How can you differentiate between:

PLN protein losing nephropathy

PLE protein losing enteropathy

A

A urine sample will differentiate these immediately: significant protein = PLN.

Bloods: PLN usually has low albumin only but PLE can have low albumin and globulin.

77
Q

Protein losing nephropathy

Discuss Underlying cause of glomerular disease?

A
  • intra-glomerular immune complexes
  • developed in situ
  • filtered out from circulation
  • think about ruling out
  • infection/infectious disease
  • pyoderma, pyometra
  • think about travel history for exotic disease such as Leishmania
  • inflammatory disease
  • pancreatitis, prostatitis
  • IBD
  • immune mediated diseases
  • neoplasia
78
Q

Discuss PLN: treatment?

A

Identify and manage the underlying disease

  • easier said than done
  • think about breed related disease
  • English Cockers http://www.antagene.com/sites/default/files/familial_nephropathy_-_english_cocker_spaniel.pdf

Non specific treatment:

  • renal care diet with moderately lowered protein
  • omega-3 FA supplements
  • ACE-I
  • manage hypertension
  • anti thrombotic eg aspirin, clopidogrel
79
Q
A