PUPD Flashcards
how can you charaterise PUPD?
Polyuria - > 50ml/kg/day of urine
Polydipsia - > 100ml/kg/day intake (dogs) > 50ml/kg/day (Cats)
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.
Therefore we can consider either:
Primary Polydipsia
Primary Polyuria
what are the causes of primary polydipsia?
A difficult thing to prove and often diagnosed as idiopathic.
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.
* Physiological
* Salt toxicity e.g. seawater
* Exercise
* High Environmental temperature
what are the broad causes of primary polyuria?
intrinsic renal problem, or extrinsic effect on the kidneys.
- ADH (Anti-diuretic hormone) increases aquaporin density and increases reabsorption from tubules. ADH, or it’s receptors, are often affected to cause PU.
- Osmotic diuresis – if urine contains solutes above normal values (e.g. glucose in diabetes mellitus) this ‘draws’ water into the tubules increasing output.
- Medullary solute washout – i.e. loss of solutes from the medulla, also leads to a concentration gradient and osmotic water loss.
- Interstitial tonicity reduction – protein restricted diets; reduced concentration gradients across the interstitium.
- Increased GFR – e.g. hypertension will lead to increased filtration in excess of the kidneys resorptive capability.
what are the No ADH production (hypothalamus) or release (pituitary) causes of primary polyuria?
Central Diabetes Insipidus
what are the Reduced ADH sensitivity/response causes of primary polyuria?
- Primary Nephrogenic Diabetes Insipidus (rare)
- Secondary NDI – primarily endocrine/inflammatory but can be other poorly known interactions
- Hyperadrenocorticism (Cushings)
- Hypoadrenocorticism (Addisons)
- Hyperthyroidism
- Hyperaldosteronism (Conns)
- Liver Disease
- Pyelonephritis
- Pyometra
- Hypokalaemia
- Hypercalcaemia (think of all the various causes e.g. hyperPTH, neoplasia)
- Erythrocytosis
- Lepto
- Acromegaly (Excess GH – 25% of Diabetic Mellitus cats!)
- Neoplasia – Leiomyosarcoma, Haemangiosarcoma (unknown mechanism)
- Drugs e.g. steroids
ehat are the osmotic diuresis causes of polyuria?
- Glucose
- **Diabetes Mellitus **
- Primary renal glycosuria
- Fanconi’s syndrome (Basenjis, small breed dogs, secondary to dodgy jerky ingestion!) (Proximal tubular disease and loss of glucose, but amino acids, bicarb, electrolytes, lactate, etc.)
- Sodium
- Post obstructive diuresis (blocked cats – multifactorial, glomerular/renal damage e.g. ADH response is probably also reduced)
- High salt diet
- Addisons
-
Diuretics
- Spironolactone
- Furosemide (loop diuretic – also lose potassium!)
what are the Reduced medullary/interstitial tonicity causes of polyuria?
- Low protein diet
- Medullary washout (e.g. prolonged PUPD, prolonged aggressive fluid therapy)
what are the mixed/unknown causes of primary polyuria?
Chronic Renal Failure
Don’t forget, this could be present from youth in congenital defects e.g. renal dysplasia
Acute Kidney Injury
Phaeochromocytoma (Catecholamine producing tumour of the adrenal gland i.e. adrenaline)
what are the history, signalment nad clinical exam factors that are inportant for differnentiating PUPD?
History and signalment
* Age e.g. congenital in young
* Breed e.g. Fanconi syndrome in small breeds
* Species e.g. HyperT4 and CKD in older cats
* Toxin/drug/medications?
* Vaccination status – Lepto
* Diet!
Clinical Exam
* Body condition – chronic vs acute disease missed by the owners
* Signs of dehydration – primary polyuria
* Neurological disease – central lesion
* Other signs associated with endocrinopathies – e.g. dermatalogical disease (Cushings), or waxing/waning GI disease (addisons)
* Clinical signs of other body systems e.g. jaundice in hepatopathy, increased GI loss in diarrhoea driving thirst, enlarged abdomen and third space loss.
What does it mean if you have these specific gravities in a patient that is PU:
> 1.030 with normal hydration?
1.030 with dehydration?
< 1.030 with normal hydration?
< 1.030 with dehydration?
< 1.006 (Hyposthenuria)?
> 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
> 1.030 with dehydration – check for glucosuria, consistent with diabetes mellitus, Fanconi’s and renal tubular glycosuria.
< 1.030 with normal hydration – Consider primary polydipsia again, but consistently present.
< 1.030 with dehydration – Consider primary polyuria and intrinsic renal disease or extrinsic disease affecting renal function.
< 1.006 (Hyposthenuria) – Diabetes insipidus, primary polydipsia, hypercalcemia, hyperadrenocorticism
How can you rule in Primary polydipsia?
Remember, this is difficult to fully prove sometimes; and you 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 – POCUS!
Endocrine or osmolarity changes – Haem and Biochem (polycythaemia, electrolyte disturbances) and consider HyperT4 in cats and liver disease.
Central disease – Neuro assessment +/- MRI
how do you rule in primary polyuria?
Dependent on the history; rule out major life threatening disease first e.g. pyometra, addisons, acute kidney injury, diabetes mellitus progressing to diabetic ketoacidosis, haemangiosarcoma
Triage - (POCUS, Elecs, BG, UG, U/C/K+)
Intrinsic renal disease
* Further urinalysis including UPCR, urine sediment exam (e.g. casts in tubular disease), culture and sensitivity (e.g. pyelonephritis).
* Biochemistry – Urea, Creatinine, symmetric dimethylarginine (SDMA) (see following slide on azotaemia)
* Further imaging +/- renal biopsy.
Extrinsic disease
* Further urinalysis including urine glucose and culture and sensitivity (ascending infections common in diabetes mellitus, hyperadrenocorticism and hyperthyroidism)
* Haematology and biochemistry (see differentials list)
* Ideally ionised calcium for hypercalcaemia
* Further imaging +/- FNA/Biopsy
* Physiological assessment e.g. inappropriate hypertension in phaeochromocytoma
in a patien with PUPD you can see Azotaemia (elevated urea and creatinine) what is the difference with pre-renal and post-renal azotaemia?
how can you rulel out pre-renal azotaemia?
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 cause, so USG can vary
* Rapidly fluid responsive - this will rule our pre-renal azotaemia
Post-renal – Obstruction or uroabdomen
- PUPD not really a feature – until after removing the obstruction.
- POCUS!
- DANGEROUS Hyperkalaemia can develop rapidly
what is renal azotaemia?
what will the USG be?
Renal – Acute Kidney injury or chronic renal failure (intrinsic disease) (2/3rds renal mass loss)
* USG will be poorly concentrated (functional loss) but NOT dilute (i.e. hyposthenuric) which indicates active dilution from the kidneys (proximal tubules and loop of Henle).
* Cats can develop glomerular disease without issues of concentration and maintain a **normal USG. **
* Phosphorous is likely to be high (GFR dependant)
* In AKI – Phosphorous increase is marked.
* In CKD – Phosphorous increase is more moderate, and consistent with the creatinine elevation
* DANGEROUS Hyperkalaemia can develop in AKI (oliguria or anuria)
* Albumin and UPCR – Protein losing nephropathy
* Non-regen anaemia – CKD (reduced EPO production from the kidney)
