12.7.1: Approach to polyuria and polydipsia

Question 1

Polyuria

Answer 1

• > 50ml/kg/day of urine

Question 2

Polydipsia

Answer 2

• > 100ml/kg/day intake (dogs)
• > 50ml/kg/day intake (cats)

Question 3

Differential diagnoses for primary polydipsia

Answer 3

• Difficult to prove and often diagnose as idiopathic.
• For some reason, there is altered thirst.

Centrally mediated disease
* Primary e.g. neoplasia
* Seconday e.g. changes to osmolarity or endocrine effects
* Compensating for losses other than urinary e.g. GI, third space

Physiological
* Salt toxicity e.g. seawater
* Exercise
* High environmental temperature

Question 4

Broad mechanisms for primary polyuria

Answer 4

An intrinsic renal problem or an extrinsic effect on the kidneys.
* Reduced ADH production/sensitivity
* Osmotic diuresis
* Medullary solute washout
* Reduction in interstitial tonicity
* Increased GFR

Question 5

What does ADH do?

Answer 5

ADH = anti-diuretic hormone
* Increases aquaporin density
* –> Increases reabsorption from the tubules

Question 6

Osmotic diuresis

Answer 6

if urine contains solutes above the normal values (e.g. glucose in DM), this draws water into the tubules, uncreasing urine output

Question 7

Medullary solute washout

Answer 7

loss of solutes from the medullam leading to concentration gradient that results in osmotic water loss
e.g. if you overdose the animal on fluids

Question 8

Reduction in interstitial tonicity

Answer 8

• Seen with protein-restricted diets
• There are reduced concentration gradients across the interstitium

Question 9

Explain how increased GFR lead to polyuria

Answer 9

• Increased GFR e.g. in hypertension will lead to increased filtraton in excess of the kidneys’ resorptive capacity
• Therefore there is increased urine output

Question 10

What might cause a patient to have no ADH?

Answer 10

• No ADH production (hypothalamus)
• No ADH release (pituitary)

Central diabetes insipidus

Question 11

Differential diagnoses for reduced ADH sensitivity/response

Answer 11

Primary nephrogenic diabetes insipidus

Secondary nephrogenic diabetes insipidus - variety of endocrine/inflammatory causes:
* Hyperadrenocorticism
* Hypoadrenocorticism
* Hyperthyroidism
* Hyperaldosteronism
* Liver disease
* Pyelonephritis
* Pyometra
* Hypokalaemia
* Hypercalcaemia (via hyperPTH, neoplasia)
* Erythrocytosis
* Lepto
* Acromegaly
* Neoplasia
* Drugs e.g. steroids

Question 12

Causes of osmotic diuresis

Answer 12

Glucose in urine
* Diabetes mellitus
* Primary renal glycosuria
* Fanconi’s syndrome

Sodium in urine
* Post-obstructive diuresis (e.g. blocked cats)
* High salt diet
* Addison’s (losing Na because not enough aldosterone)
* Diuretics

Question 13

Normal USG dogs

Answer 13

• Average USG throughout the day should be >1.020 in dogs.
• In dogs, often USG is >1.030 to 1.040 in samples of the first urine of the morning before consumption of food or water

Question 14

How do you judge if the USG is appropriate for the patient?

Answer 14

Does it make sense for the patient’s hydration status?

Question 15

Normal USG cats

Answer 15

1.035 to 1.060
A wide range of USGs can be encountered - 1.001 to >1.085 for cats – although values encountered typically for normally hydrated individuals are often closer to 1.015 to 1.045 for dogs, and 1.035 to 1.060 for cats.
>1.035 = often the figure for concentrated urine in cats

Question 16

Descrive how intrinsic renal disease could lead to primary polyuria

Answer 16

• Chronic renal failure - could be present in young animals with congenital defects e.g. renal dysplasia
• Acute kidney injury- e.g. phaeochromocytoma -> causes hypertension -> drives high GFR -> polyuria
• Often hard to know what is going on until renal biopsy (referral procedure)

Question 17

Initial approach to the animal with suspected primary polyuria

Answer 17

History and signalment
* Age (consider congenital defects if young)
* Breed e.g. Fanconi syndrome in younger breeds
* Species: e.g. hyperT4 and CKD in older cats
* Consider toxins/ drugs/ medication/ vaccine status/ diet

Clinical exam
* BCS
* Signs of dehydration would support primary polyuria
* Neuro disease would support central lesion
* Other signs associated with endocrinopathies e.g. dermatological, waxing and waning GI disease]
* Signs localised to other body systems e.g. jaundice, enlarged abdomen and third space loss

Question 18

You have a patient with USG <1.006. What do you think of this?

Answer 18

USG <1.006 = very dilute! The kidneys are actively diluting.
* Often seen in primary polydipsia - the animal is drinking so much!
* Seen in diabetes insipidus - there is no ADH / no response to ADH
* If unsure, reach for a textbook

Question 19

How should you get the ideal urine sample?

Answer 19

Sample from first thing in the morning (animal has been sleeping and hopefully not drinking -> urine should be concentrated)

Question 20

Your patient’s USG is <1.030. What does this tell you about the kidneys? What would it tell you if the animal showed clinical signs of dehydration?

Answer 20

USG <1.030 = poorly concentrated urine; the kidneys are not working.
* If the animal is dehydrated, they should be concentrating their urine, but for some reason they can’t :(
* Consider primary polyuria, intrinsic renal disease, or extrinsic disease impairing renal function

Question 21

You suspect primary polydipsia. What should you do? Consider the diagnostics in this case.

Answer 21

This is difficult to prove; make sure you rule out other diseases.
* History: could this just be physiological? Consider toxin exposure, GI losses, etc.
* Rule out third space loss -> POCUS
* Analyse endocrine / osmolarity changes, haematology and biochem to work out if the animal is definitely actively diluting the urine to be more dilute than blood
* Check for central disease -> neuro exam ± MRI

Question 22

You suspect primary polyuria. What are your next steps to confirm your diagnosis?

Answer 22

1. Dependent on the history: rule out major life-threatening diseasee.g. pyometra, Addison’s, AKI, DM becoming DKA, haemangiosarcoma
2. Triage: POCUS, electrolytes, blood glucose, USG, urea/ creatinine/ potassium
3. Consider intrinsic vs extrinsic renal disease: urinalysis and C&S, biochemistry, further imaging ± renal biopsy

Question 23

You have a patient with hypertension, but it is inappropriate and you cannot think of a reason why it would be hypertensive. What might you be suspicous of?

Answer 23

• Dog with polyuria and inappropriate hypertension -> phaeochromocytoma
• Cats - remember cats with CKD may be hypertensive

Question 24

Azotaemia

Answer 24

Elevated urea and creatinine

Question 25

Pre-renal azotaemia

Answer 25

• Azotaemia originated from a pre-renal cause - this is fluid loss that results in reduced renal blood flow. This will eventually become renal azotaemia too once the kidneys have been hypoxic for long enough.
• These animals are rapidly fluid-responsive

Question 26

True/false: pre-renal azotaemia occurs in any dehydrated animal.

Answer 26

False
* Pre-renal azotaemia is not just dehydration!
* Dehydration = interstitial fluid loss (hence the animal feels a bit crispy)
* To get pre-renal azotaemia, we must also have hypovolaemia -> we will see haemoconcentration (i.e. we have loss fluid from circulation as well as the interstitial space)

Question 27

You have an animal with pre-renal azotaemia. You don’t think an AKI is the cause. What might you be suspicious of and what test will you do?

Answer 27

• Suspicious of Addison’s - this can produce a marked pre-renal azotaemia that looks similar to an AKI.
• Test: basal cortisol

Question 28

True/false: a patient could have pre-renal + renal + post-renal azotaemia all at the same time.

Answer 28

True

Question 29

You have an animal with renal azotaemia. What would you expect their USG to be?

Answer 29

• The USG will be hyposthenuric
• Urine will be poorly concentrated because the kidneys are shot
• Urine will not be dilute because the kidneys cannot actively dilute because they are shot

Question 30

What causes renal azotaemia?

Answer 30

Acute kidney injury or chronic renal failure
* To get intrinsic renal disease, we have to lose 2/3 of functional tissue

Question 31

What would you expect blood phosphorus levels to be in a pre-renal azotaemia?

Answer 31

Likely to be high but this is GFR dependent

Question 32

What would you expect blood phosphorus levels to be in a renal azotaemia? How would this differ between an AKI vs CKD?

Answer 32

• Phosphorus is likely to be high (GFR dependent)
• AKI: marked phosphorus increase
• CKD: more moderate phosphorus elevation which is consistent with creatinine elevation
• Therefore we can use phosphorus to differentiate AKI vs CKD but remember there are acute on chronic presentations where the patient with CKD gets an AKI!

Question 33

Which electrolyte derangement can happen in the oliguric or anuric AKI patient and how could this be fatal?

Answer 33

Can get hyperkalaemia -> leads to potentially fatal bradycardia/ bradyarrhythmias

Question 34

What type of anaemia might you see in the patient with CKD and why is this?

Answer 34

Non-regenerative anaemia
Due to reduced EPO production from the damaged kidneys

Question 35

True/false: PUPD is a common feature of post-renal azotaemia at the time of presentation.

Answer 35

False
PUPD is not typically a feature until after the obstruction has been removed

Question 36

Which electrolyte derangement can occur with patients with post-renal azotaemia and why is this the most dangerous?

Answer 36

• These patients can rapidly get hyperkalaemia.
• This can kill by causing bradydysrhythmias.

Question 37

What diseases is the water deprivation test designed to differentiate between? Describe how.

Answer 37

• Primary polydipsia
  If you are denied water, your USG will become more concentrated.
• Central diabetes insipidus
  You have no ADH. When you are given ADH analogue (vasopressin), your USG improves.
• Nephrogenic diabetes insipidus
  You do not response to anything we do in this test. If we keep restricting water, you keep urinating with no ability to concentrate, and you die.

Question 38

Describe how the water deprivation test is carried out

Answer 38

• Restrict water gradually over 3-5 days
• Then completely remove water until 5% dehydration
• Then provide vasopressin (this is an ADH analogue)
• Monitor USG throughout
• Dangerous - rarely done and should only be done under close observation in hospital

Question 39

You do not want to do the water deprivation test but you want to differentiate between primary polydipsia and central diabetes insipidus. What could you do?

Answer 39

Trial vasopressin therapy -> will see a positive and consistent response if central diabetes insipidus (i.e. the USG becomes more concentrated)