AKI and CKD Flashcards
(100 cards)
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
2
Q
Describe the typical clinical pathology findings with AKI
A
- PCV often normal or increased
- HyperK
- Azotaemia
- HyperPhos
- Metabolic acidosis (can be marked)
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
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
5
Q
Describe the signalment for CKD
A
- Older animals, can be juveniles
- Some breed susceptibilities to: juvenile nephropathy (boxers), polycystic kidney disease, amyloidosisi
6
Q
Give the normal water intake for dogs and cats
A
- Dogs: 60-90ml/kg/day
- Cats: generally up to 45mls/kg/day
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
8
Q
What USG would be indicative of CKD in dogs and cats?
A
- Dog: 1.008-1.030
- Cat: 1.008-1.035
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
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
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
12
Q
Give the differentials for causes of an enlarged kidney in a cat
A
- Polycystic kidney disease
- FIP
- Lymphoma
- Perinephric pseudocyst
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
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
15
Q
List the markers of worsening CKD
A
- Worsening azotaemia
- Anaemia
- High BP
- Proteinuria
- Soft tissue mineralisation
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
17
Q
What group of drugs do ranitidine, cimetidine and famotidine belong to?
A
H2 receptor antagonists
18
Q
What is the mechanism of action fo maropitant?
A
NK1 receptor antagonist
19
Q
Give the initial treatment of hypertension in CKD in dogs and cats
A
- Cats: amlodipine (Ca Channel blocker)
- Dogs: ACE - I
20
Q
What are the main aims of managing CKD?
A
- Determine underlying cause
- Control factors contributing to disease progression
- Maintain quality of life
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
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)
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
24
Q
What signs may be seen with hypokalaemia?
A
Muscle weakness -> ileus -> reduced appetite
25
Describe the management of constipation in CKD
- Encourage water intake
- Laxatives e.g. lactulose, polyethylene glycol (Miralax)
- Appropriate treatment for joint disease
26
Describe the steps involved in the IRIS CKD staging
- 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
27
What stage of CKD would the following creatinine results (umol/l) be indicative of?
Dogs: <125
Cats: <140
I, early CKD
28
What stage of CKD would the following creatinine results (umol/l) be indicative of?
Dogs: 125-180
Cats: 140-250
II, mild or absent clinical signs
29
What stage of CKD would the following creatinine results (umol/l) be indicative of?
Dogs: 181-440
Cats: 251-440
III, moderate renal azotaemia, onset of significant clinical signs
30
What stage of CKD would the following creatinine results (umol/l) be indicative of?
Dogs and cats: >440
IV, increased risk of uraemic crisis, significant clinical signs
31
What is SDMA and how is it used in CKD?
Symmetric dimethylarginine assay
| - identifies early CKD, may identify when as little as 25% nephrons lost
32
Give the approximate SDMA values for the different IRIS CKD stages (ug/dl)
I: persistently >14 (adult) or 16 (if 1yr or younger)
II: >25 and low BCS (i.e. reduced muscle)
III: >46 and low BCS
33
In a borderline proteinuric patient where CKD is suspected, what action is appropriate?
Re-evaluate in 3-6 months
34
Indicate the level of risk of target organ damage depending on degree of hypertension
- <150: minimal
- 150-159: low
- 160-179: moderate
- >180: high
35
List possible causes of chronic renal disease in cats
- Chronic tubulointersittial nephritis
- Lymphoma
- FIP
- Polycystic kidney disease
- Pyelonephritis
- toxins
- Obstructive uropathy
- Sequel to AKI
- Amyloidosis (Abyssinians high risk)
- Glomerulonephritis/PLN
36
Discuss polycystic kidney disease in cats
- 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
37
List causes of chronic kidney disease in dogs
- Tubulo interstitial nephritis
- Familial nephropathy esp. younger dogs
- PLN/glomerular disease
- Others: pyelonephritis, hypercalcaemia
- Sequel to AKI
38
Describe the clinical signs of protein losing nephropathy
- Weight loss and lethargy
- Peripheral oedema and ascites
- Progression to azotaemic CKD
- Hypertension
- Rarely may develop thromboemboic disease
39
Describe what is meant by nephrotic syndrome
- Hypoalbuminaemia (often <15g/l)
- Severe persistent proteinuria (>2weeks)
- Peripheral oedema +/- ascites
- Hypercholesterolaemia
40
List possible underlying causes of glomerular disease that may lead to PLN
- Intraglomerular immune complex deposition
- Infectious disease e.g. Leishmania
- Inflammatory disease e.g. pancreatitis, prostatitis, IBD, immune mediated diseases
- Neoplasia
41
Outline the treatment of PLN in small animals
- 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
Compare the pathologies the renal cortex and medulla are susceptible to
- 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
What are the 4 key phases in the pathophysiology of AKI?
- Initiation phase
- Extension phase
- Maintenance phase
- Recovery phase
44
Outline the initiation phase of AKI
- 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
Describe the extension phase of AKI
- 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
Describe the maintenance phase of AKI
- 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
Describe the recovery phase of AKI
- 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
Describe the clinical signs of AKI
- 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
Describe the clinical pathology abnormalities that may be seen with AKI
- 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
When might glucosuria be seen in AKI?
If proximal tubular injury
51
What might be found on urinalysis in a dog with AKI?
- Evidence of underlying cause e.g. pyuria, bacteriuria, casts, crystalluria (rarely signficiant unless calcium oxalate)
- SG inappropriate (isosthenuric)
- Protein
52
Outline a diagnostic plan for a patient you suspect of having AKI
- 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
What conditions that may be an underlying cause of AKI might be ruled in or out by diagnostic imaging?
- Urinary tract rupture
- Ureteric calculi
- Urolithiasis
- Evidence of pyelonephritis
54
Discuss the overall prognosis for AKI in both cats and dogs
May be treatable if underlying cause is found and treatment is rapid, may have ongoing CKD after
55
What is the prognosis for leptospirosis causing AKI in dogs?
83% survival overall
56
List the negative prognostic indicators in AKI in dogs
- Creatinine >885umol/l
- Anaemia (PCV < 33%)
- Proteinuria
- Hypocalcaemia
- Concurrent disease e.g. sepsis, pancreatitis
- Toxic cause
57
List the negative prognostic indicators for AKI in cats
- Hypoalbuminaemia
- Hyperkalaemia
- Toxic cause e.g. ehthylene glycol - grave
58
Outline the steps in the initial therapeutic plan for stabilisation of an AKI patient
- 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
Outline the management of hyperkalaemia in an AKI patient
- 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
Outline the management of acidosis in an AKI patient
- 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
Outline the signs of fluid overload
- Unexpected/excessive weight gain
- Tachypnoea/dyspnoea
- Pulmonary crackles
- Nasal discharge
- Chemosis
- Peripheral oedema
- Ascites
- Jugular venous distension/jugular pulse
62
What are the indications for renal replacement therapy?
- Persistent oliguria/anuria (6-12 hours)
- Life threatening electrolyte or acid base imbalance
- Exposure to dialysable toxins
- Fluid overload
63
List the options for renal replacement therapy
- Peritoneal dialysis
- Continuous renal replacement therapy (CRRT)
- Intermittent haemodialysis
64
Discuss the nutrition of an AKI patient
- 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
List causes of poor renal perfusion
- Hypovolaemic shock
- Severe trauma
- Anaesthesia and surgery
- Severe hypothermia
- Heat stroke
- Severe dehydration
66
List causes of severe hypoxia
- Near drowning
- Pneumonia
- GA related
67
List the potential causes of AKI
- Poor renal perfusion
- Severe hypoxia
- Nephrotoxins
- Cardiovascular cause
- Urinary tract obstruction
- Urinary tract rupture
- Intrinsic renal disease
68
List the common causes of AKI in cats
- Pyelonephritis
- Ethylene glycol toxicity
- Lily toxicity
- Ureteric obstruction
69
List the cardiovascular causes of AKI
- Reduced cardiac output (CHF, dysrhythmia, tamponade)
- Hypertension
- Thrombosis
- Coagulopathy
70
List the common causes of AKI in dogs
- Lepto
- Grapes/raisins
- Ischaemic events (pancreatitis, DIC, sepsis, hypovolaemia, liver failure, hypotensive shock)
71
Briefly outline cutaneous and renal glomerular vasculopathy in dogs
- 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
What are the 5 main iatrogenic causes of AKI in small animals?
- Sepsis (e.g. pyo)
- Major surgery
- Low cardiac output
- Hypovolaemia e.g. bleeding bitch spay
- Medications
73
Explain the role of hypercalcaemia in AKI
- 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
Describe the normal radiographic appearance of the canine kidney
- 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
Describe the normal radiographic appearance of the feline kidney
- Oval shape
- 2-3xL2 length (smaller in neutered cats)
- More often get superimposition
76
What are the contraindications for an IVU radiograph?
- Dehydration/hypovolaemia
| - Severe renal failure/anuria
77
Briefly describe the patient preparation for an IVU
- Starve 24(-36) hours
- Thoroughly cleans with enema
- GA
78
Briefly outline the normal appearance of an IVU radiograph over time
- 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
What is contrast radiography of the baldder particularly useful for?
- Identification of bladder location
- Investigation of possible rupture
- Detection of radiolucent calculi
- Evaluation of bladder wall
80
Briefly outline the technique for a retrograde cystogram
- Catheterise/empty bladder
| - Inject contrast medium (6-12ml/kg), feel until bladder just turgid
81
Compare the different contrast cystograms that can be performed
- 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
Give examples of potential pitfalls of retrograde cystograms
- 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
Briefly outline the technique for a retrograde vaginourethrogram
- 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
Briefly outline the technique for a retrograde urethrogram
- 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
Describe the ultrasonographic appearance of the renal cortex
- Evenly granular
- Hypoechoic (occasionally isoechoic) vs liver in dogs
- Often more echogenic in cats
86
Describe the ultrasonographic appearance of the renal medulla
- Hypoechoic vs. cortex
| - Should have good corticomedullary definition
87
Describe the ultrasonographic appearance of the renal pelvis
Echogenic peripelvic fat (more echogenic vs. medulla)
88
Describe the ultrasonographic appearance of the renal crest
Hyperechoic
89
Give the normal kidney:aorta size ratio as seen on ultrasonography
5.5-9.1
90
Describe the ultrasonographic appearance of the bladder wall
- 3 layers
- Inner mucosal surface hyperechoic
- Muscle layer hypoechoic
- Outer serosal layer hyperechoic
- Wall thickness depends on distension
91
Explain why hypoadrenocorticism leads to isosthenuria and PUPD
Low aldosterone = less retention of sodium = loss of water
92
Describe benazepril with regards to its mode of action, function, and the species it is licensed for
- 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
List the potential causes of increased corticomedullary definition on ultrasonography
- Non-specific change
- Early nephritis
- Lymphoma
- Incidental fat accumulation in cats
94
List the possible causes of decreased corticomedullary definition on ultrasonography
- Non-specific change in many renal diseases
- Progressive chronic renal disease
- Lymphoma
- FIP
95
Describe the appearance and significance of the medullary rim sing on ultrasonography
- 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
What might lead to the bladder not being seen on radiography?
- Very small bladder e.g. just urinated, bilateral ectopic ureters with bladder hypoplasia, ureteral rupture
- Bladder rupture
- Bladder displacement
- Peritoneal disease shadow
97
Give examples of causes of radiographic contrast filling defects in the bladder
- Calculi
- Polyps
- Blood clots
- Air bubbles
98
Describe the location, shape and margination of calculi in the bladder
- Centre of contrast puddle usually
- Round or slightly irregular
- Distinct margination
99
Describe the location, shape and margination of polyps in the bladder
- Adjacent to bladder wall
- Smooth and elongated or larger and irregular
- Usually distinct
100
Describe the location, shape and margination of blood clots in the bladder
- In contrast puddle (roll down most dependent part of bladder0 or adjacent to wall
- Irregular shape (relatively amorphous)
- Indistinct margination
