12.7.1: Approach to polyuria and polydipsia Flashcards
Polyuria
- > 50ml/kg/day of urine
Polydipsia
- > 100ml/kg/day intake (dogs)
- > 50ml/kg/day intake (cats)
Differential diagnoses for primary polydipsia
- 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
Broad mechanisms for primary polyuria
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
What does ADH do?
ADH = anti-diuretic hormone
* Increases aquaporin density
* –> Increases reabsorption from the tubules
Osmotic diuresis
if urine contains solutes above the normal values (e.g. glucose in DM), this draws water into the tubules, uncreasing urine output
Medullary solute washout
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
Reduction in interstitial tonicity
- Seen with protein-restricted diets
- There are reduced concentration gradients across the interstitium
Explain how increased GFR lead to polyuria
- Increased GFR e.g. in hypertension will lead to increased filtraton in excess of the kidneys’ resorptive capacity
- Therefore there is increased urine output
What might cause a patient to have no ADH?
- No ADH production (hypothalamus)
- No ADH release (pituitary)
Central diabetes insipidus
Differential diagnoses for reduced ADH sensitivity/response
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
Causes of osmotic diuresis
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
Normal USG dogs
- 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
How do you judge if the USG is appropriate for the patient?
Does it make sense for the patient’s hydration status?
Normal USG cats
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
Descrive how intrinsic renal disease could lead to primary polyuria
- 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)
Initial approach to the animal with suspected primary polyuria
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
You have a patient with USG <1.006. What do you think of this?
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
How should you get the ideal urine sample?
Sample from first thing in the morning (animal has been sleeping and hopefully not drinking -> urine should be concentrated)
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?
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
You suspect primary polydipsia. What should you do? Consider the diagnostics in this case.
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
You suspect primary polyuria. What are your next steps to confirm your diagnosis?
- Dependent on the history: rule out major life-threatening diseasee.g. pyometra, Addison’s, AKI, DM becoming DKA, haemangiosarcoma
- Triage: POCUS, electrolytes, blood glucose, USG, urea/ creatinine/ potassium
- Consider intrinsic vs extrinsic renal disease: urinalysis and C&S, biochemistry, further imaging ± renal biopsy
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?
- Dog with polyuria and inappropriate hypertension -> phaeochromocytoma
- Cats - remember cats with CKD may be hypertensive
Azotaemia
Elevated urea and creatinine
