PUPD SA

History

·    Is it actually PUPD? - >50ml/kg/day urine, >100ml/kg/day intake (dogs), >50 (cats)

·    Signalment – age, breed, species? – e.g. younger animal = congenital, small breed dogs = Fanconi syndrome, older cats = hyperT4 + CKD

·    On any medications? Access to toxins?

·    Vaccination status?

·    Diet?

Clinical examination

·    BCS – differentiate chronic vs acute

·    Assess hydration status – dehydrated = primary polyuria (® compensatory PD)

·    Any neurological signs? – indicate central lesion

·    Signs associated with endocrinopathies? – dermatological disease = cushings, waxing/waning GI disease – Addison’s

·    Signs associated with other body systems? – jaundice = hepatopathy, D+ causing dehydration

·     

Investigations

·    Urinalysis

o  USG – is urine appropriately concentrate for hydration status?

§ Dehydrated patient should have concentrated urine

§ Hyposthenuria – actively diluting urine = kidneys working

§ Isosthenuria = 1.008 – 1.012 – kidneys not doing anything

·    If suspect primary polydipsia (therefore secondary PU) – usually diagnose by ruling stuff out

o  Consider history – physiological? Toxin exposure? GI losses?

o  POCUS – rule out third space losses (fluid pooling into abdomen ® increased thirst)

o  Endocrine or osmolarity changes

§ Haematology and biochemistry – polycythaemia, electrolyte disturbances

§ Calculate osmolality – if low = primary PD

o  Central disease – neurological assessment +/- MRI

·    If suspect primary polyuria (therefore secondary PD)

o  Rule out life threatening diseases, e.g. pyometra, Addison’s, AKI, DM/DKA

o  Triage – POCUS, blood gas, USG, electrolyte levels

o  If suspect intrinsic renal disease:

§ Further urinalysis – UPCR (check protein levels), urine sediment exam (casts = tubular disease), C+S (e.g. pyelonephritis)

§ Biochemistry – urea and creatinine, SDMA

§ Renal U/S

o  If suspect extrinsic renal disease:

§ Further urinalysis – urine glucose level, C+S (ascending infections common in DM, hyperT4, HAC)

§ Haematology and biochemistry

§ Further U/S +/- biopsy/FNA

§ Physiological assessment – is high BP just due to stress?

Management

·    Confirm primary polydipsia and no physiological explanation – referral for neurological assessment +/- MRI

Causes of PUPD

Primary polydipsia: altered thirst (rare)

·    Centrally mediated disease: primary (e.g. neoplasia), secondary (e.g. changes to osmolarity or endocrine effects), compensating for non-urinary losses (e.g. GI, third space)

·    Physiological: salt toxicity (e.g. drinking sea water), exercise, high environmental temperature

Primary polyuria:

·    Intrinsic renal problem:

o  Chronic renal failure

o  AKI

·    Extrinsic effect on kidney:

o  Reduced ADH sensitivity/response

§ Primary nephrogenic diabetes insipidus = rare

§ Secondary NDI: cushings, Addison’s, hyperthyroidism, pyometra, hypercalcaemia, drug-induced (steroids)

o  Osmotic diuresis:

§ Increased glucose: diabetes mellitus, Fanconi’s syndrome

§ Increased sodium: post-obstructive diuresis, Addison’s, diuretics

o  Reduced medullary/interstitial tonicity: low protein diet, medullary washout