PUPD

• Whats the definition of polyuria?

  More than 50ml/kg/day of urine.
• What’s the definition of polydipsia?

  More than 100ml/kg/ day if water in dogs.

  More than 50ml/kg/day of water in cats.
• Primary polyuria vs primary polydipsia

  Both are often present, but one can drive the other - i.e. if you drink a lot, as a consequence you will urinate a lot, if you urinate a lot you will need to drink a lot to keep up.
• Primary polydipsia - altered thirst

  Centrally mediated disease

  • Primary e.g. neoplasia
  • Secondary e.g. changes to osmolarity or endocrine effects
  • Compensating for losses other than urinary e.g. GI, third space (ascites, big effusions).

  Physiological

  • Salt toxicity e.g. saltwater
  • Exercise
  • High environmental temperature.
• Causes of primary polyuria - intrinsic vs extrinsic

  Intrinsic renal problem:

  • Not concentrating the urine and conserving the water

  Extrinsic renal problem:

  • Either they kidneys themselves or something outside the kidneys.
• Causes of primary polyuria - ADH (anti diuretic hormone)

  Increases aquaporin density and increase reabsorption from tubules. ADH or its receptors are often affected to cause polyuria.
• Causes of primary polyuria - osmotic duiresis

  If urine contains solutes above normal values (e.g. glucose in diabetes mellitus) this draws water into the tubules increasing output.
• Causes of primary polyuria - medullary solute washout

  i.e. loss of solutes from the medulla, also leads to a concentration gradient and osmotic water loss (not common).
• Causes of primary polyuria - interstitial tonicity reduction

  Protein restricted diets; reduced concentration gradients across the interstitium.
• Causes of primary polyuria - increased GFR

  E.g. hypertension will lead to increased infiltration (due to the increased blood pressure) In excess of the kidneys resorptive capability. (Seen in older cats)
• Primary polyuria due to no ADH production - causes

  Reduced ADH sensitivity/ response

  • Primary Nephrogenic Diabetes Insipidus (rare) - affects the sensitivity of the ADH receptors.
  • Secondary NDI - primarily endocrine/inflammatory but can be other poorly known interactions.
  • Hyperadrenocorticism (Cushing’s)> hypo (Addison’s)
  • Hyperthyroidism
  • Pyometra
  • Hypercalcaemia
  • Drugs i.e. Steroids
• Primary polyuria due to osmotic diuresis - causes

  Glucose:

  • Diabetes mellitus
  • Primary renal glycosuria
  • Fanconi’s syndrome - proximal tubular disease)

  Sodium:

  • Post-obstructive diuresis (booked cats - multifactorial, glomerular/ renal damage)
  • High salt diet
  • Addison’s
  • Diuretics - Spironolactone, Furosemide
• Primary polyuria due to reduced medullary/ interstitial tonicity

  Low protein diet (uncommon as not prescribed by vets, could be an inappropriate diet due to the client)

  Medullary washout - e.g. prolonged PUPD, prolonged fluid therapy.
• Diagnostic approach to PUPD - history and signalment

  Age e.g. congenital in young, neoplastic in older patient.

  Breed e.g. Fanconi syndrome in small breeds

  Species e.g. Hyper T4 and CKD in older cats

  Toxin/ drugs/ medications

  Vaccination status - lepto?

  Diet!
• Diagnostic approach to PUPD - clinical exam

  Body condition - chronic vs acute disease missed by the owners

  Signs of dehydration - primary polyuria

  Neurological disease - central lesions

  Other signs associated with endocrinopathies - e.g. dermatological disease (Cushing’s) or waxing/waning GI disease (Addison’s).

  Clinical signs of other body systems e.g. jaundice in hepatopathy, increased GI loss in diarrhoea driving thirst, enlarged abdomen and third space loss.
• Diagnostic approach to PUPD - specific gravity overview

  Not thinking about normal patients, thinking about patients with PUPD so are thinking is this USG appropriate for the patients hydration status.
• Diagnostic approach to PUPD - specific gravity >1.030 with normal hydration

  Either normal (i.e. the owner is wrong) or primary polydipsia driving intermittent polyuria (not present at time of sampling) e.g. primary polydipsia, variable hypothalamic or pituitary disease e.g. inflammatory/infectious (look for CNS signs) or physiological.
• Diagnostic approach to PUPD - specific gravity >1.030 with dehydration

  (most likely primary polydipsia) - check for glucosuria, consistent with diabetes meillitus, Fanconi’s and renal tubular glycosuria.
• Diagnostic approach to PUPD - specific gravity <1.030 with normal hydration

  (more likely to be primary polyuria) consider primary polydipsia again, but consistently present.
• Diagnostic approach to PUPD - specific gravity <1.030 with dehydration

  Consider primary polyuria and intrinsic renal disease or extrinsic disease affecting renal function.
• Diagnostic approach to PUPD - specific gravity <1.006

  Hyposthenuria - diabetes insipidus (no ADH), primary polydipsia (extreme), hypercalcaemia (due to extreme duiresis), hyperadrenocorticism, the kidneys will be working very hard to actively excrete the water.
• What if polydipsia is suspected?

  It is difficult to fully prove sometimes; and may be wrong so don’t rule out polyuria to the detriment of avoiding other tests - can sometimes end up testing for everything else until you rule them out.

  History:

  • Could this just be physiological
  • Toxin exposure
  • GI losses.

  Rule out third space loss
• Diagnosing primary polyuria - intrinsic renal disease

  Further urinalysis including PCR, urine sediment exam (e.g. cats in tubular disease), culture and sensitivity (e.g. pyelonephritis).

  Biochemistry - urea, creatinine, symmetric dimethylarginine (SDMA)

  Further imaging +/- renal biopsy (don’t normally biopsy the kidney as it doesn’t usually change the treatment, and has quite a bit of risk due to its level of vascularisation).
• Diagnosing primary polyuria - extrinsic renal disease

  Further urinalysis including urine glucose and culture and sensitivity (ascending infectious common in diabetes mellitus, hyperadrenocorticism and hyperthyroidism)

  Haemotology and biochemistry (see differentials list)

  • Ideally ionised calcium for Hypercalcaemia

  Further imaging +/- FNA/biopsy

  Physiological assessment e.g. inappropriate hypertension on phaeochromocytoma.
• What is azotaemia?

  Elevated urea and creatinine
• Causes of azotaemia in PUPD - pre-renal

  Fluid loss i.e. haemoconcentration and reduced renal blood flow (eventually becomes renal also due to renal hypoxia).

  • Addison’s can cause a marked pre-renal azotaemia similar to renal disease.
  • Phosphorous is likely to be high (GFR dependant)
  • PUPD may be present depending on the case, so USG may can vary.
  • Rapidly fluid responsive.
• Causes of azotaemia in PUPD - post-renal


  Obstruction or Uroabdomen - first thing that will kill a blocked animal is they hypokalameia.

  • PUPD not really a feature - until after removing the obstruction.
  • POCUS!
  • Hyperkalaemia can develop rapidly.
• Causes of azotaemia in PUPD - renal


  AKI or chronic renal chronic renal failure (intrinsic disease) (2/3rd renal mass loss).

  • USG will be poorly concentrated (functional loss) but not dilute (hyposthenuric) which indicates active dilution from kidneys (proximal tubules and loop of Henle).
  • Cats can develop glomerular disease without issues of concentration and maintain a normal UG.
  • Phosphorous is likely to be high (GFR dependant).
  • Low albumin and UPCR - protein losing nephropathy
  • Non-regenerative anaemia - seen in later stages of CKD
• Why do a water deprivation test?

  Differentiates between primary polydipsia, central diabetes insipidus and nephrogenic diabetes insipidus.
• Problems with the water deprivation test?

  Before doing have to make sure that the kidneys are functioning. If an animal with renal disease is deprived of water it will die.
• Interpreting the water deprivation test

  Primary polydipsia - SG improves with just water deprivation, as they should concentrate their urine. If they continue to not concentrate then is primary polyuria.

  CDI - SG improves with vasopressin

  NDI - SG never improves

  Fatal amounts if fluid loss in the PU patient is possible so test requires close monitoring via hospitalisation.