CKD & AKI

Question 1

Complete the table

Answer 1

Question 2

• Hypoadrenocorticism in dogs can cause polydipsia, vomiting, diarrhoea, dehydration, azotaemia and hyperkalaemia. Urine SG is often in the range 1.008-1.025
• Why are dogs with hypoadrenocorticism unable to concentrate their urine?

Answer 2

–Hypoadrenocorticism ( → hyponatremia → hypovolemia → decreased renal perfusion)

Question 3

•What test would differentiate between a dog with hypoadrenocorticism and one with acute kidney failure?

Answer 3

–Basal cortisol level

Question 4

•What treatment would you give while waiting for this result?

Answer 4

–IV fluids and correct electrolyte levels (think about glucose and insulin or Ca borogluconate)

Question 5

What type of drug is benazepril?

Answer 5

ACE inhibitor

Question 6

•What is Semintra and how does it work?

Answer 6

–Aldosterone receptor antagonist, for proteinuria in cats

Question 7

Mojo: 7 mth old MN DSH

•Acute onset (24-48hrs)

–vomiting

–weakness/poor coordination

–tremors

• Indoor/outdoor cat
• Multi cat house

–one other cat seems quiet/off food

• He is usually a very well cat
• Heart/pulse rate 160 HIGH
• T 36.7°C LOW
• Poor pulse quality
• Dehydrated (7.5%)
• Twitching
• Bladder small
• Systolic blood pressure 80mmHg LOW

Haemtology - low WBC and lymphocytes

What do you do next?

Answer 7

URINALYSIS

Question 8

What type of crystals are these?

How can they be explained?

Answer 8

Calcium oxalate monohydrate

Renal azotaemia, inappropriately low SG for the level of dehydration, electrolyte imbalances. acute onset likely

•These are calcium oxalate monohydrate crystals which are generally seen in the very early stages of ethylene glycol toxicity. We should always look at a sediment exam of urine from cats if we suspect ethylene glycol toxicity as it can be a useful way to help support a suspected diagnosis. Sometimes we see calcium oxalate dihydrate crystals which form a little later in the disease (see next slide). Calcium oxalate dihydrate crystals are seen in cats that have not had exposure to ethylene glycol toxicity and therefore this is not a specific test. Seeing calcium monohydrate crystals is more specific.

Question 9

How can the biochemistry be interpreted?

Along with low WBC and lymphocytes?

Answer 9

• Results show severe renal azotaemia, hyperphosphataemia (consistent with reduced renal function/GFR), and hyperkalaemia (a marker of AKI). We also have hypocalcaemia (low total calcium) which is likely to be genuine because protein levels are normal- if you remember, most blood calcium is protein bound and if serum protein levels are low then calcium can also be low. In this case we have a low total calcium and normal protein suggesting this is a real concern. If we are unsure or are running additional tests then we would request an iCa (ionized calcium). Hypocalcaemia is also a marker for AKI associated with ethylene glycol toxicity.
• Haematology was not very helpful in this case.

Question 10

What does this show and how can we interpret in relation to ethylene glycol?

Answer 10

• These are calcium oxalate dihydrate crystals.
• NOT specific for ethylene glycol but could be indicative of eythlene glycol toxicity if other blood changes are consistent.

Question 11

How would you categorise the acid/base disturbance?

Answer 11

Metabolic acidosis, with compensatory respiratory alkalosis

metabolic acidosis (with a high anion gap)

hypocalcaemia occurs due to chelation of calcium by oxalate (one of the toxic metabolites of EG)

Question 12

Ethylene glycol poisoning:

What are the differentials?

Prognosis?

What would we do if any other cats in the house?

Answer 12

Differentials: pyelonephritis, lily toxicity or ureteric obstruction

• What is the prognosis for Mojo? bad
• Does the prognosis vary with your other differentials? better
• Do you have any concerns about the other cats in the house? What will you do? Treat with alcohol

Question 13

I have an animal in renal failure and suspect ethylene glycol toxicity. Can you test for that?

Answer 13

Ethylene glycol can be detected as a single agent or as part of the General Toxicology Panel (TO1).However, it takes several days for the increases in nitrogenous waste products to accumulate after the renal damage is caused by ethylene glycol, by which time the compound itself usually has been excreted. So often by the time the animal is presented the ethylene glycol has gone from blood and urine.

However, urine cytology can be helpful in that it will identify both acute renal tubular injury and the presence of calcium oxalate monohydrate crystals which very commonly accompany this specific toxicity.

Question 14

Is fomepizole a magic antidote for ethylene glycol toxicity?

Would you ever really give vodka?

Answer 14

You might have found discussion of fomepizole as a treatment/antidote for ethylene glycol toxicity but sadly it’s not available in time for most cases. Vodka has however been used as a treatment (see resources) and can be effective in some cases. The prognosis is grim but this does not mean that occasional “miracle stories” don’t occur.

Question 15

What does this hsitopath show?

Answer 15

Renal tubules containing calcium oxalate deposits

Question 16

How does ethylene glycol toxicity come about and what is seen?

Answer 16

• minimum toxic dose of just 1.4 ml/kg
• The toxic products of the metabolism of ethylene glycol cause metabolic acidosis and renal tubular damage resulting in acute renal failure (ARF). EG is metabolised by the enzyme alcohol dehydrogenase (AD) to glycoaldehyde and further metabolised to acidic products and oxalate. Formation of calcium oxalate crystals occurs resulting in hypocalcaemia and crystalluria.
• Initial clinical signs ( less than 12 hours post intoxication) are gastrointestinal (vomiting) and neurological (ataxia, depression, ‘drunken’ appearance) representing intoxication due to the EG and glycoaldehyde.
• 12 to 24 hours after EG ingestion further depression is observed along with anorexia, tachycardia and the start of ARF.
• After 24 hours clinical signs reflect ARF and include oliguria or anuria and vomiting. If the cat is hyperkalaemic bradycardia may be noted. Unfortunately it is unusual to identify a cat in the earlier stages and most have ARF at presentation. With ingestion of large volumes of EG severe signs including ARF can occur sooner ( less than 12 hours).

Question 17

How do we diagnose and treat ethylene glycol poisoning?

Answer 17

• Diagnosis - Azotaemia is present if ARF has developed, along with hyperphosphataemia. Hypocalcaemia (total and ionised) may be noted. Hyperkalaemia may be present with oliguric or anuric renal failure. An increased anion gap acidosis is commonly observed. Urinalysis will reveal isosthenuria and calcium oxalate monohydrate crystals, which vary in appearance from rounded to more pointed (see figure). Renal ultrasound may demonstrate hyperechoic cortices. The bladder may be small, reflecting reduced urine production. Ethylene glycol blood levels are rarely measured due to the delay receiving results and low toxic dose in cats.
• Treatment
• If cats are observed ingesting EG and examined rapidly ( less than one hour) then gastric decontamination with induction of emesis can be attempted. This is contraindicated if consciousness is reduced due to the risk of aspiration. Metabolism of EG can be inhibited by ethanol, which acts as a preferred substrate for AD.
• After 12 hours or once ARF has developed treatment with ethanol is unlikely to be effective and may complicate management of ARF. However, prior to the development of ARF then 20% medical ethanol can be administered IV at a dose of 5 ml/kg intravenously over 15 minutes and repeated every 6 hours for five treatments then every 8 hours for four treatments.

Question 18

Lily toxicity:

When is it seen?

Clinical signs?

Treatment?

Prognosis?

Answer 18

• Cats have been shown to be extremely sensitive to the toxic effects of lilies. As little as 2 leaves or part of a single flower have resulted in deaths. It should be pointed out that the whole plant—petals, stamen, leaves, and pollen are toxic.
• The quick onset of clinical signs suggests a rapid absorption rate of the toxin. The renal tubular epithelium appears to be the target of the toxin
• clinical signs of lily intoxication include salivation, vomiting, anorexia, and depression. Polyuric renal failure leads to dehydration and anuric renal failure and death results
• Successful treatment includes initiation of fluid diuresis before the onset of anuric renal failure. Once anuria develops, peritoneal dialysis or hemodialysis is the only potential treatment
• Prognosis is excellent if fluid diuresis is started before anuric renal failure has developed

Question 19

Alfie:

Clinical history

•Vague…. lethargy?

–“not quite right”

• Appetite used to be good, now variable
• Less keen to go for walks
• Mild weight loss

Physical examination

• No abnormal findings
• BCS 6/9
• Alfie’s owner is worried he has “Cocker Spaniel Kidney Disease”

What is she referring to?

What investigations would you suggest for Alfie to see if her concerns are valid?

What treatment options might there be?

Answer 19

• What is she referring to? Familial nephropathy
• What investigations would you suggest for Alfie to see if her concerns are valid? DNA test
• What treatment options might there be? None to treat, but can slow the rate damage

–Specialised diets for dogs with renal failure - low protein, phosphate, salt and potassium (to reduce the work of the kidneys)

–angiotensin converting enzyme (ACE) inhibitor (reduces blood pressure and reduce the rate of blood proteins passing into the urine).

–Dependent on electrolyte levels, blood pressure and dehydration

Question 20

Lola:

Long term history:

•“Weak bladder”

–since she was a puppy stress/excitement has often made Lola urinate

• Urinary incontinence sometimes when she is asleep
• Occasionally urinates by the kitchen door overnight

Recent history:

• Polydipsia 3-4 mths
• Increasingly lethargic compared with her usual “mad Boxer” approach to life
• T, R: normal
• BCS (3/5)
• Bright & alert (very)
• Cardiovascular:

–heart/pulse rate 116 HIGH

–good peripheral pulses

–systolic grade I/VI murmur

• Pale pink mm, CRT good
• Abdominal palpation is normal
• No urine scalding seen

How worried are you about Lola’s heart murmur?

• What are 2 possible reasons for Lola’s incontinence?
• Give 3 likely differentials for Lola’s polydipsia
• What is your initial diagnostic plan?

Answer 20

• How worried are you about Lola’s heart murmur? Low grade, but high HR. Compensating? But not in heart failure
• What are 2 possible reasons for Lola’s incontinence?

–Polyuria

–Poor urethral sphincter

•Give 3 likely differentials for Lola’s polydipsia

–Juvenile nephritis

–pyometra

–Addison’s

•What is your initial diagnostic plan?

–Urinalyisis – SG, protein/glucouria

–Biochemistry - electrolytes

Question 21

Mild normochromic normocytic anaemia, renal azotaemia – with proteinuria and heamtouria

What else do we need to know?

Answer 21

Is she entire? Ever had kidney investigations before? Family history

UTI?

Question 22

Thinking about all the information we have so far, what reasons could there be for Lola’s infection?

Answer 22

UTI

Question 23

•148mmHg

–Doppler method

–Systolic reading

Lola was quite excitable for her blood pressure measurement….

is this reading normal?

Can we believe it?

Do we need to repeat it?

Answer 23

• is this reading normal? Yes
• can we believe it? Not entirely
• do we need to repeat it? Ideally, but not hypertensive

Question 24

Both kidneys

• were small
• had irregular margins
• showed loss of the normal corticomedullary definition

Both ureters seemed to enter the bladder normally.

The bladder was normal. No calculi were seen.

• Lola has renal azotaemia- you can IRIS stage her if you assume this is stable azotaemia. She has proteinuric renal disease. She has mild anaemia likely 2ry to CKD- revise the mechanisms for anaemia in dogs with renal disease.
• Is her UTI 2ry to CKD/incontinence or does she have pyelonephritis which has resulted in CKD…sometimes we don’t know what the initial problem was and we just need to manage what we can.

•

• Diagnostic imaging changes were probably more consistent with CKD associated with juvenile renal disease rather than pyelonephritis causing CKD…but again this is not an easy decision. Often with pyelonephritis all we will see is a mildly dilated renal pelvis on ultrasound– imagine how easy that is to miss!
• Ultrasound seemed to rule out ectopic ureters…if you were not confident with ultrasound you might need to do an IVU or a positive contrast retrograde urethrogram to check this.
• What treatment would you like to give Lola?
• What is your follow up plan for her?

Answer 24

•What treatment would you like to give Lola?

–Antibiotics for UTI

–Renal diet

–ACE inhibitors

–Fluids if needed

•What is your follow up plan for her?

–Repeat bloods in a month of renal diet?

Question 25

What is the prognosis of boxer nephropathy?

Answer 25

“Survival times varied from zero to \>5 years post diagnosis”

Question 26

* Presented with decompensated CKD after an episode of gastroenteritis * After 48 hours of fluid therapy & anti-emetics he is stable & starting to eat * Bob has IRIS stage 3 CKD –He is not hypertensive –His UPC is 0.3 * He is hyperphosphotaemic * You suggest this diet for Bob * List all the advantages of a renal care diet over a standard commercial diet * His owner is worried he won’t eat this food- what will you do if he doesn’t like it?

Answer 26

–Are highly palatable –Consider a different one/water/adding things