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AKI and CKD Flashcards

1
Q

Compare CKD and AKI prognosis

A
  • AKI is reversible if treated early, sudden onset, can be rapidly fatal
  • CKD irreversible, manageable not curable, may live for some time
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2
Q

Describe the typical clinical pathology findings with AKI

A
  • PCV often normal or increased
  • HyperK
  • Azotaemia
  • HyperPhos
  • Metabolic acidosis (can be marked)
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3
Q

Describe the typical clinical pathology findings with CKD

A
  • Often non-regenerative mild anaemia
  • Often hypoK, sometimes hyperK
  • Hyperphos
  • Normal/mild acidosis
  • High creatinine (may be normal in early CKD or if poor muscle mass)
  • +/-Elevated SDMA
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4
Q

Which CKD dogs may be more at risk of becoming hyperkalaemic in late stage renal disease ?

A

Dogs fed renal diet and on ACE-I

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5
Q

Describe the signalment for CKD

A
  • Older animals, can be juveniles

- Some breed susceptibilities to: juvenile nephropathy (boxers), polycystic kidney disease, amyloidosisi

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6
Q

Give the normal water intake for dogs and cats

A
  • Dogs: 60-90ml/kg/day

- Cats: generally up to 45mls/kg/day

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7
Q

Describe the clinical signs that would be highly indicative of CKD

A
  • PUPD
  • Weight loss
  • V+
  • Lethargy
  • Dehydration
  • Halitosis
  • Low BCS
  • Small renal size, irregular
  • Oral ulceration
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8
Q

What USG would be indicative of CKD in dogs and cats?

A
  • Dog: 1.008-1.030

- Cat: 1.008-1.035

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9
Q

When might pre-renal azotaemia be challenging in the diagnosis of CKD?

A
  • Patient who is dehydrated (azotaemia will seem worse)
  • Azotaemic cat with relatively concentrate urine (SG 1.030) and vague clinical signs
  • Dog on furosemide with restricted access to water
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10
Q

What must be done in order to be able to accurately diagnose and stage an animal with CKD?

A

IVFT - resolve any pre-renal azotaemia and give better reflection of renal azotaemia

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11
Q

Outline the use of diagnostic imaging in the diagnosis of CKD in small animals

A
  • Cats: should nearly always be able to palpate the kidneys
  • Can palpate in some dogs, not all
  • If palpate small kidneys: radiography confirms size, margination, presence, secondary problems e.g. dystrophic calcification, loss of bone density. Ultrasonography may demonstrate changes in echogenictiy
  • Enlarged kidneys: imaging more useful than with small kidneys, radiography confirms size, ultrasonography shows changes in echogenicity that may be suggestive of specific conditions
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12
Q

Give the differentials for causes of an enlarged kidney in a cat

A
  • Polycystic kidney disease
  • FIP
  • Lymphoma
  • Perinephric pseudocyst
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13
Q

Discuss the prognosis for CKD in cats

A
  • Can have stable CKD for months - years

- May have CKD and die of another disease

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14
Q

Discuss the prognosis for CKD in dogs

A
  • Progressive, linear condition
  • More rapid deterioration in dogs vs. cats
  • More likely to die of CKD
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15
Q

List the markers of worsening CKD

A
  • Worsening azotaemia
  • Anaemia
  • High BP
  • Proteinuria
  • Soft tissue mineralisation
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16
Q

Outline the initial therapeutic plan for stabilisation of CKD

A
  • Fluid therapy e.g. Hartmann’s
  • Correct hypokalaemia if necessary (fluids likely enough)
  • Antiemetics e.g. maropitant, metoclopramide CRI
  • Gastroprotectants e.g. sucralfate, ranitidine, famotidine
  • Identify and resolve complicating factors e.g. UTI, hypertension
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17
Q

What group of drugs do ranitidine, cimetidine and famotidine belong to?

A

H2 receptor antagonists

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18
Q

What is the mechanism of action fo maropitant?

A

NK1 receptor antagonist

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19
Q

Give the initial treatment of hypertension in CKD in dogs and cats

A
  • Cats: amlodipine (Ca Channel blocker)

- Dogs: ACE - I

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20
Q

What are the main aims of managing CKD?

A
  • Determine underlying cause
  • Control factors contributing to disease progression
  • Maintain quality of life
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21
Q

Discuss the determination of an underlying cause with CKD

A
  • Often not possible

- Treat specific disease where possible e.g. ureteral obstruction, pyelonephritis, renal lymphoma, PLN

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22
Q

Discuss the control of factors contributing to the progression of CKD

A
  • Renal hyperPTH (aka CKD -MBD): control occurs due to elevated phosphate, phosphate and PTH detrimental to nephrons, use phosphate, protein and sodium restricted diets
  • Consider adding phosphate binders only if using the renal diet
  • Bone demineralisation: care in high risk situations e.g. geriatric dental extractions
  • Glomerular hypertension and proteinuria: use ACE-Is (benazepril) in dogs
  • Benazepril or telmisartan (angiotensin II receptor antagonist) in cats for proteinuria (but no evidence for effect on survival)
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23
Q

List the aspects involved in the maintenance of quality of life in a CKD patient

A
  • Avoid dehydration
  • Use appetite stimulants e.g. mirtazepine (low dose q48hrs), maropitant (decrease vomiting, may improve appetite)
  • Manage hypokalaemia (consider supplementation with Kaminox, Tumil K)
  • Manage anaemia if causing clinical signs (darbepoietin + iron)
  • Manage/prevent constipation
  • NSAIDs if in pain
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24
Q

What signs may be seen with hypokalaemia?

A

Muscle weakness -> ileus -> reduced appetite

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25
Q

Describe the management of constipation in CKD

A
  • Encourage water intake
  • Laxatives e.g. lactulose, polyethylene glycol (Miralax)
  • Appropriate treatment for joint disease
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26
Q

Describe the steps involved in the IRIS CKD staging

A
  • Step 1: diagnose CKD
  • Step 2: Use fasting blood glucose checked at >2 time points and allocate stage I-IV
  • Step 3: allocate substage based on degree of proteinuria (UPCR), presence/absence of hypertension
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27
Q

What stage of CKD would the following creatinine results (umol/l) be indicative of?
Dogs: <125
Cats: <140

A

I, early CKD

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28
Q

What stage of CKD would the following creatinine results (umol/l) be indicative of?
Dogs: 125-180
Cats: 140-250

A

II, mild or absent clinical signs

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29
Q

What stage of CKD would the following creatinine results (umol/l) be indicative of?
Dogs: 181-440
Cats: 251-440

A

III, moderate renal azotaemia, onset of significant clinical signs

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30
Q

What stage of CKD would the following creatinine results (umol/l) be indicative of?
Dogs and cats: >440

A

IV, increased risk of uraemic crisis, significant clinical signs

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31
Q

What is SDMA and how is it used in CKD?

A

Symmetric dimethylarginine assay

- identifies early CKD, may identify when as little as 25% nephrons lost

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32
Q

Give the approximate SDMA values for the different IRIS CKD stages (ug/dl)

A

I: persistently >14 (adult) or 16 (if 1yr or younger)
II: >25 and low BCS (i.e. reduced muscle)
III: >46 and low BCS

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33
Q

In a borderline proteinuric patient where CKD is suspected, what action is appropriate?

A

Re-evaluate in 3-6 months

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34
Q

Indicate the level of risk of target organ damage depending on degree of hypertension

A
  • <150: minimal
  • 150-159: low
  • 160-179: moderate
  • > 180: high
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35
Q

List possible causes of chronic renal disease in cats

A
  • Chronic tubulointersittial nephritis
  • Lymphoma
  • FIP
  • Polycystic kidney disease
  • Pyelonephritis
  • toxins
  • Obstructive uropathy
  • Sequel to AKI
  • Amyloidosis (Abyssinians high risk)
  • Glomerulonephritis/PLN
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36
Q

Discuss polycystic kidney disease in cats

A
  • Persian and related breeds, exotic and British short hair
  • Autosomal dominant inheritance
  • Cysts seen from 8mo
  • Azotaemia may not develop for years
  • DNA test available
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37
Q

List causes of chronic kidney disease in dogs

A
  • Tubulo interstitial nephritis
  • Familial nephropathy esp. younger dogs
  • PLN/glomerular disease
  • Others: pyelonephritis, hypercalcaemia
  • Sequel to AKI
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38
Q

Describe the clinical signs of protein losing nephropathy

A
  • Weight loss and lethargy
  • Peripheral oedema and ascites
  • Progression to azotaemic CKD
  • Hypertension
  • Rarely may develop thromboemboic disease
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39
Q

Describe what is meant by nephrotic syndrome

A
  • Hypoalbuminaemia (often <15g/l)
  • Severe persistent proteinuria (>2weeks)
  • Peripheral oedema +/- ascites
  • Hypercholesterolaemia
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40
Q

List possible underlying causes of glomerular disease that may lead to PLN

A
  • Intraglomerular immune complex deposition
  • Infectious disease e.g. Leishmania
  • Inflammatory disease e.g. pancreatitis, prostatitis, IBD, immune mediated diseases
  • Neoplasia
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41
Q

Outline the treatment of PLN in small animals

A
  • Identify and manage underlying disease where possible
  • Non-specific treatment: renal care diet with low protein, omega 3 FA supplements, ACE-Is
  • Manage hypertension
  • Anti-thrombotic agents e.g. aspirin, clopidogrel
42
Q

Compare the pathologies the renal cortex and medulla are susceptible to

A
  • Cortex: more at risk from blood borne toxins (receives 90% renal blood flow)
  • Medulla: more at risk from ischaemia (receives 10% of renal blood flow)
43
Q

What are the 4 key phases in the pathophysiology of AKI?

A
  • Initiation phase
  • Extension phase
  • Maintenance phase
  • Recovery phase
44
Q

Outline the initiation phase of AKI

A
  • Exposure to renal insult
  • Duration: hours to days
  • GFR reduced (e.g. reduced renal blood flow, tubule obstruction)
  • Fluid back leak (increased pressure from renal tubules/ureter)
  • Hypoxia and cell swelling compromising blood flow more
  • Initially clinically silent
45
Q

Describe the extension phase of AKI

A
  • Amplification of renal insult by ongoing hypoxia
  • Ischaemia, inflammation, cell injury leads to apoptosis (if milder injury)/necrosis (if severe injury), which leads to renal casts, free radicals, neutrophil activation (worsens ischaemia etc)
  • Duration 1-2 days
  • Non-specific signs: lethargy, inappetance, abdominal pain
  • Early intervention required
46
Q

Describe the maintenance phase of AKI

A
  • Duration 1-2 weeks
  • Constriction of afferent arterioles worsens ischaemia
  • Reduces GFR
  • Clinical signs relate to worsening azotaemia and possible anuria
  • Damage consolidates, signs become more evident (may be acute onset of signs)
47
Q

Describe the recovery phase of AKI

A
  • Duration weeks to months
  • Renal tubules repair and heal (if basement membrane intact) or scarring and fibrosis
  • GFR either fully recovers or permanently reduced
  • Kidneys remain vulnerable, may decompensate
  • May be indicated by significant PU
48
Q

Describe the clinical signs of AKI

A
  • Anorexia
  • V+, D+
  • (PUPD)
  • Oliguria progressing to anuria
  • Ataxia
  • Dyspnoea
  • Seizures
  • Can be vague
  • Dehydration
  • Tachycardia (pain, hypovolaemia) or bradycardia (hyperK)
  • Renomegaly/assymetry/pain
  • Pyrexia
  • Evidence of platelet dysfunction
49
Q

Describe the clinical pathology abnormalities that may be seen with AKI

A
  • PCV and total solids may be high (dehydration) or low (non-regenerative anaemia in CKD with acute decompensation, OR regenerative anaemia with gastric ulceration)
  • Creatinine dependent on GFR, may be normal in early stages
  • K: hyper or hypo
  • Elevated BUN
  • May find evidence of cause for decompensation e.g. liver disease
50
Q

When might glucosuria be seen in AKI?

A

If proximal tubular injury

51
Q

What might be found on urinalysis in a dog with AKI?

A
  • Evidence of underlying cause e.g. pyuria, bacteriuria, casts, crystalluria (rarely signficiant unless calcium oxalate)
  • SG inappropriate (isosthenuric)
  • Protein
52
Q

Outline a diagnostic plan for a patient you suspect of having AKI

A
  • History and clinical signs, anything suggestive of cause/toxins?
  • Identify predisposing problems e.g. hypovolaemia, dehydration
  • Rule out causes of post-renal azotaemia e.g. urethral/ureteric obstruction
  • Blood biochem, CBC, urinalysis
  • Diagnostic imaging
  • Disease specific testing e.g. PCR for lepto -
53
Q

What conditions that may be an underlying cause of AKI might be ruled in or out by diagnostic imaging?

A
  • Urinary tract rupture
  • Ureteric calculi
  • Urolithiasis
  • Evidence of pyelonephritis
54
Q

Discuss the overall prognosis for AKI in both cats and dogs

A

May be treatable if underlying cause is found and treatment is rapid, may have ongoing CKD after

55
Q

What is the prognosis for leptospirosis causing AKI in dogs?

A

83% survival overall

56
Q

List the negative prognostic indicators in AKI in dogs

A
  • Creatinine >885umol/l
  • Anaemia (PCV < 33%)
  • Proteinuria
  • Hypocalcaemia
  • Concurrent disease e.g. sepsis, pancreatitis
  • Toxic cause
57
Q

List the negative prognostic indicators for AKI in cats

A
  • Hypoalbuminaemia
  • Hyperkalaemia
  • Toxic cause e.g. ehthylene glycol - grave
58
Q

Outline the steps in the initial therapeutic plan for stabilisation of an AKI patient

A
  • Test for the testable (e.g. IMHA, lepto)
  • Treat the treatable (i.e. correct hydration, correct any obstruction)
  • Support kidneys (alleviate obstructions or cysto)
  • IVFT (correct deficit then manage maintenance)
  • +/- Diuretics e.g. furosemide or mannitol (no mannitol if olig/anuric): no effect on renal flow so need to ensure perfusion is adequate first
  • Manage hyperkalaemia
  • Manage acidosis (rarely)
59
Q

Outline the management of hyperkalaemia in an AKI patient

A
  • ECG monitoring
  • Manage olig/anuria (fluid theray to restore GFR and allow excretion of K+)
  • Protect heart using calcium gluconate slow IV
  • Increase K+ uptake by cells using glucose (50% soln, 1-2mls/kg) given IV +/- soluble insulin CRI
60
Q

Outline the management of acidosis in an AKI patient

A
  • Generally not needed
  • Correct dehydration and let kidneys deal with acidosis
  • May be necessary in some cases e.g. ethylene glycol toxicity
  • Consider NaHCO3 in saline: monitoring of serum bicarb crucial if do this
61
Q

Outline the signs of fluid overload

A
  • Unexpected/excessive weight gain
  • Tachypnoea/dyspnoea
  • Pulmonary crackles
  • Nasal discharge
  • Chemosis
  • Peripheral oedema
  • Ascites
  • Jugular venous distension/jugular pulse
62
Q

What are the indications for renal replacement therapy?

A
  • Persistent oliguria/anuria (6-12 hours)
  • Life threatening electrolyte or acid base imbalance
  • Exposure to dialysable toxins
  • Fluid overload
63
Q

List the options for renal replacement therapy

A
  • Peritoneal dialysis
  • Continuous renal replacement therapy (CRRT)
  • Intermittent haemodialysis
64
Q

Discuss the nutrition of an AKI patient

A
  • Manage nausea: maropitant, metoclopramide, analgesia
  • Address uraemic gastritis (sucralfate, famotidine, ranitidine)
  • Need to avoid catabolic state caused by anorexia
  • If still not eating, use NG tube for enteral feeding
65
Q

List causes of poor renal perfusion

A
  • Hypovolaemic shock
  • Severe trauma
  • Anaesthesia and surgery
  • Severe hypothermia
  • Heat stroke
  • Severe dehydration
66
Q

List causes of severe hypoxia

A
  • Near drowning
  • Pneumonia
  • GA related
67
Q

List the potential causes of AKI

A
  • Poor renal perfusion
  • Severe hypoxia
  • Nephrotoxins
  • Cardiovascular cause
  • Urinary tract obstruction
  • Urinary tract rupture
  • Intrinsic renal disease
68
Q

List the common causes of AKI in cats

A
  • Pyelonephritis
  • Ethylene glycol toxicity
  • Lily toxicity
  • Ureteric obstruction
69
Q

List the cardiovascular causes of AKI

A
  • Reduced cardiac output (CHF, dysrhythmia, tamponade)
  • Hypertension
  • Thrombosis
  • Coagulopathy
70
Q

List the common causes of AKI in dogs

A
  • Lepto
  • Grapes/raisins
  • Ischaemic events (pancreatitis, DIC, sepsis, hypovolaemia, liver failure, hypotensive shock)
71
Q

Briefly outline cutaneous and renal glomerular vasculopathy in dogs

A
  • Aka Alabama rot
  • Initially presents as distal extremity skin lesions
  • Systemic signs ~4 days later: progressive non-responsive AKI, anaemia, thrombocytopaenia, increased bilirubin
  • Hopeless prognosis
  • Histo shows renal thrombocytic microangiopathhy
72
Q

What are the 5 main iatrogenic causes of AKI in small animals?

A
  • Sepsis (e.g. pyo)
  • Major surgery
  • Low cardiac output
  • Hypovolaemia e.g. bleeding bitch spay
  • Medications
73
Q

Explain the role of hypercalcaemia in AKI

A
  • HyperCa leads to PU, leads to PD
  • Dehydration leads to pre-renal effects and reduced perfusion of kidney
  • Calcification of renal tubules exacerbates damage
  • Need to diagnose cause, manage the hyperCa and protect kidneys
74
Q

Describe the normal radiographic appearance of the canine kidney

A
  • 2.5-3.5x length of L2 in VD view
  • Right kidney at level of T13-L1/2
  • Left kidney slightly further caudal
  • Bean shape
75
Q

Describe the normal radiographic appearance of the feline kidney

A
  • Oval shape
  • 2-3xL2 length (smaller in neutered cats)
  • More often get superimposition
76
Q

What are the contraindications for an IVU radiograph?

A
  • Dehydration/hypovolaemia

- Severe renal failure/anuria

77
Q

Briefly describe the patient preparation for an IVU

A
  • Starve 24(-36) hours
  • Thoroughly cleans with enema
  • GA
78
Q

Briefly outline the normal appearance of an IVU radiograph over time

A
  • 0 mins = angiogram
  • 0-1mins = nephrogram (see uniform opacification of renal parenchyma in both kidneys)
  • 5 mins VD = pyelogram (see renal pelvises and ureters, normal pelvic width no more than 2-3mm, ureteral width approx 2-3mm)
  • 10-15mins: both ureters should run into retroperitoneal space to terminate at bladder trigone
79
Q

What is contrast radiography of the baldder particularly useful for?

A
  • Identification of bladder location
  • Investigation of possible rupture
  • Detection of radiolucent calculi
  • Evaluation of bladder wall
80
Q

Briefly outline the technique for a retrograde cystogram

A
  • Catheterise/empty bladder

- Inject contrast medium (6-12ml/kg), feel until bladder just turgid

81
Q

Compare the different contrast cystograms that can be performed

A
  • Pneumo: cheap, readily available, good for identifying bladder and wall thickness, but poor mucosal detail and may miss small tears
  • Positive: expensive, mainly for suspected bladder rupture
  • Double: excellent mucosal detail, good for radiolucent calculi
82
Q

Give examples of potential pitfalls of retrograde cystograms

A
  • Inadeqate distension of bladder/urethra
  • Air bubbles in residual urine in bladder causing honeycomb appearance
  • Faeces pressing on bladder distorting shape
  • Insertion of urinary catheter too far (iatrogenic damage to mucosa, may also form knot)
83
Q

Briefly outline the technique for a retrograde vaginourethrogram

A
  • Prepare as for IVU
  • Use Foley catheter or urinary catheter + clamp
  • Insert catheter into urethra and clamp around urethral opening
  • Inject dilute iodine contrast medium, test for leaks, avoid vaginal rupture (inject 1/2 dose first)
84
Q

Briefly outline the technique for a retrograde urethrogram

A
  • catheterise urethra
  • Position tip distal to area under investigation
  • Clap sheath tightly around catheter
  • Inject diluted iodine contrast medium (mix with sterile aqueous gel 1:1 if needed)
  • Take radiograph immediately after end of injection
85
Q

Describe the ultrasonographic appearance of the renal cortex

A
  • Evenly granular
  • Hypoechoic (occasionally isoechoic) vs liver in dogs
  • Often more echogenic in cats
86
Q

Describe the ultrasonographic appearance of the renal medulla

A
  • Hypoechoic vs. cortex

- Should have good corticomedullary definition

87
Q

Describe the ultrasonographic appearance of the renal pelvis

A

Echogenic peripelvic fat (more echogenic vs. medulla)

88
Q

Describe the ultrasonographic appearance of the renal crest

A

Hyperechoic

89
Q

Give the normal kidney:aorta size ratio as seen on ultrasonography

90
Q

Describe the ultrasonographic appearance of the bladder wall

A
  • 3 layers
  • Inner mucosal surface hyperechoic
  • Muscle layer hypoechoic
  • Outer serosal layer hyperechoic
  • Wall thickness depends on distension
91
Q

Explain why hypoadrenocorticism leads to isosthenuria and PUPD

A

Low aldosterone = less retention of sodium = loss of water

92
Q

Describe benazepril with regards to its mode of action, function, and the species it is licensed for

A
  • ACE inhibitor, prevents conversion from Ang I to Ang II
  • Stimulates release of aldosterone and AH to increase water retention
  • Direct potent vasoconstrition
  • Increases BP
  • Licensed for dogs (CHF) and cats (reduce proteinuria in CKD)
93
Q

List the potential causes of increased corticomedullary definition on ultrasonography

A
  • Non-specific change
  • Early nephritis
  • Lymphoma
  • Incidental fat accumulation in cats
94
Q

List the possible causes of decreased corticomedullary definition on ultrasonography

A
  • Non-specific change in many renal diseases
  • Progressive chronic renal disease
  • Lymphoma
  • FIP
95
Q

Describe the appearance and significance of the medullary rim sing on ultrasonography

A
  • Hyperechoic band in outer medulla
  • May be due to: hypercalcaemia, acute tubular necrosis, chronic renal disease, FIP
  • Questionable significance as many animals have no other signs of renal disease
96
Q

What might lead to the bladder not being seen on radiography?

A
  • Very small bladder e.g. just urinated, bilateral ectopic ureters with bladder hypoplasia, ureteral rupture
  • Bladder rupture
  • Bladder displacement
  • Peritoneal disease shadow
97
Q

Give examples of causes of radiographic contrast filling defects in the bladder

A
  • Calculi
  • Polyps
  • Blood clots
  • Air bubbles
98
Q

Describe the location, shape and margination of calculi in the bladder

A
  • Centre of contrast puddle usually
  • Round or slightly irregular
  • Distinct margination
99
Q

Describe the location, shape and margination of polyps in the bladder

A
  • Adjacent to bladder wall
  • Smooth and elongated or larger and irregular
  • Usually distinct
100
Q

Describe the location, shape and margination of blood clots in the bladder

A
  • In contrast puddle (roll down most dependent part of bladder0 or adjacent to wall
  • Irregular shape (relatively amorphous)
  • Indistinct margination

URI2 (9 decks)

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