CKD & AKI Flashcards
Complete the table
- 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?
–Hypoadrenocorticism ( → hyponatremia → hypovolemia → decreased renal perfusion)
•What test would differentiate between a dog with hypoadrenocorticism and one with acute kidney failure?
–Basal cortisol level
•What treatment would you give while waiting for this result?
–IV fluids and correct electrolyte levels (think about glucose and insulin or Ca borogluconate)
What type of drug is benazepril?
ACE inhibitor
•What is Semintra and how does it work?
–Aldosterone receptor antagonist, for proteinuria in cats
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?
URINALYSIS
What type of crystals are these?
How can they be explained?
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.
How can the biochemistry be interpreted?
Along with low WBC and lymphocytes?
- 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.
What does this show and how can we interpret in relation to ethylene glycol?
- 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.
How would you categorise the acid/base disturbance?
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)
Ethylene glycol poisoning:
What are the differentials?
Prognosis?
What would we do if any other cats in the house?
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
I have an animal in renal failure and suspect ethylene glycol toxicity. Can you test for that?
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.
Is fomepizole a magic antidote for ethylene glycol toxicity?
Would you ever really give vodka?
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.
What does this hsitopath show?
Renal tubules containing calcium oxalate deposits