Approach to PUPD Flashcards
Polyuria definition
- > 50ml/kg/day of urine
Polydispsia definition
- > 100ml/kg/day intake (dogs)
- > 50ml/kg/day intake (cats)
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
Broad causes of primary polyuria
- intrinsic renal problem
- or extrinsic effect on the kidneys
Causes of primary polyuria
- Problems with ADH or its receptors (e.g. no ADH production/release, or reduced ADH sensitivity/response)
- Osmotic diuresis
- Medullary solute washout
- Interstitial tonicity reduction
- Increased GFR
What is ADH and what does it do?
= Anti-diuretic hormone
- increases aquaporin density and increases reabsorption from tubules
How does central diabetes insipidus affect ADH?
- no ADH production (hypothalamus) or release (pituitary)
Causes of reduced ADH sensitivity/response
- 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 (various causes e.g. hyperPTH, neoplasia)**
– Erythrocytosis
– Lepto
– Acromegaly (Excess GH – 25% of DM cats)
– Neoplasia – Leiomyosarcoma, Haemangiosarcoma (unknown mechanism)
– Drugs e.g. steroids**
How does osmotic diuresis cause polyuria?
- if urine contains solutes above normal values (e.g. glucose in diabetes mellitus) this ‘draws’ water into the tubules increasing output
Causes of osmotic diuresis
Glucose
- Diabetes Mellitus**
- Primary renal glycosuria
- Fanconi’s syndrome
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)
Fanconi’s syndrome
- Basenjis, small breed dogs
- secondary to dodgy jerky ingestion
- Proximal tubular disease -> reduced resorption of solutes -> loss of glucose, amino acids, bicarb, electrolytes, lactate, etc.
Causes of reduced medullary/interstitial tonicity causing primary polyuria
- Low protein diet
- Medullary washout (e.g. prolonged PUPD, prolonged aggressive fluid therapy)
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)
Diagnostic approach - 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
Diagnostic approach - 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.
USG - key question to ask yourself when interpreting results
- is it appropriate to the patients hydration status?
Interpretation of USG >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
Interpretation of USG >1.030 with dehydration
- check for glucosuria, consistent with diabetes mellitus, Fanconi’s and renal tubular glycosuria.
Interpretation of USG <1.030 with normal hydration
- Consider primary polydipsia again, but consistently present
Interpretation of USG <1.030 with dehydration
- Consider primary polyuria and intrinsic renal disease or extrinsic disease
affecting renal function
Interpretation of USG <1.006 (Hyposthenuria)
- Diabetes insipidus, primary polydipsia, hypercalcemia, hyperadrenocorticism
What to do when you suspect primary polydipsia
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
What serum osmolality supports primary polydipsia?
- low serum osmolality
What to do when you suspect primary polyuria?
Dependent on the history; rule out major life threatening disease first e.g.
- pyometra
- addisons
- AKI
- DM progressing to diabetic ketoacidosis
- haemangiosarcoma
Triage
- POCUS, Elecs, BG, UG, U/C/K+
What to do if you suspect 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
What to do if you suspect extrinsic disease
- Further urinalysis including urine glucose and C&ST (ascending infections common in diabetes mellitus, HAC and hyperthyroidism)
- Haematology and biochemistry
- Ideally ionised calcium for hypercalcaemia
- Further imaging +/- FNA/Biopsy
- Physiological assessment e.g. inappropriate hypertension in phaeochromocytoma
What is azotaemia?
- elevated urea and creatinine
3 causes of azotaemia
- Pre-renal - fluid loss i.e. haemoconcentration and reduced renal blood flow
- Renal - AKI or CRF (intrinsic dz) (2/3rd renal mass lost)
- Post-renal – Obstruction or uroabdomen
Why does pre-renal azotaemia become renal also?
- reduced renal blood flow -> renal hypoxia
Pre-renal azotaemia:
- potential cause?
- what element is likely to be high?
- USG?
- fluid responsive?
➢ 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
Post-renal azotaemia:
- PUPD?
- care re what?
- investigation?
➢ PUPD not really a feature –until after removing the obstruction.
➢ POCUS
➢ DANGEROUS - Hyperkalaemia can develop rapidly
Renal azotaemia
- USG
- what element is likely to be high?
- care re what?
- other notes
➢ 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-regenerative anaemia–CKD (reduced EPO production)
Use of water deprivation test
- Differentiates between primary polydipsia, central diabetes insipidus and nephrogenic diabetes insipidus.
Water deprivation test - how to
- 3-5 days of gradual water restriction, then complete removal of water until 5% dehydration achieved
– Vasopressin (DDAVP – ADH analogue) is then administered.
Water deprivation test - primary polydipsia result (specific gravity)
- SG improves with just water deprivation
Water deprivation test - CDI result (specific gravity)
- SG improves with vasopressin
Water deprivation test - NDI result (specific gravity)
- SG never improves
Why do you need to be careful with the water deprivation test?
- Fatal amounts of fluid loss in the PU patient is possible
- close monitoring
- realistically hospital only
Water deprivation test alternative
- trial Vasopressin therapy
- a response is consistent with CDI
- can be done in first opinion but vasopressin is expensive
