PU/PD- Pathophysiology and Diagnostic Approach. Polyuria/Polydipsia PU/PD. Michael Geist, DVM, DACVIM VCA- Animal Specialty Group San Diego, Ca

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1 PU/PD- Pathophysiology and Diagnostic Approach Michael Geist, DVM, DACVIM VCA- Animal Specialty Group San Diego, Ca Polyuria/Polydipsia Drinking too much? >100ml/kg/day Water intake is variable Have owners quantify at home Urinating too much? >50ml/kg/d Difficult to measure in pets outside hospital May be present without meeting definition in conjunction with low USG PU/PD Determine morning Urine Specific Gravity (USG) If USG is high, PU/PD is not present If USG is consistently low investigate

2 USG No such thing as normal or abnormal Use terms appropriate and inappropriate Eg. Drinking large volume of H20 hyposthenuria is appropriate Consider species: Cat vs. Dog Cat: dry food- >1.040 wet- >1.030 Dog: range Surrogate for osmolality Osmolality the concentration of a solution in terms of osmoles of solutes per kilogram of solvent (2 x Na) + (BUN / 2.8) + (Glucose / 18) Effective osmole= ability to cause fluid shifts/draw H20 Na, glucose Ineffective osmole= diffuses across membranes into compartments urea USG and Osmolality Term Expected Range of USG Hyposthenuria <1.008 <300 Range of Osmolality (mosm/kg) Isosthenuria (dog) (cats) Minimally concentrated urine Hypersthenuria (dogs) (cats) >1.035 (dogs) >1.045 (cats) >310 (dogs) >330 (cats) >1,500

3 Determinant of Osmolality ADH- anti-diuretic hormone/ Arginine Vasopressin Produced in neurohypophysis/posterior pituitary Regulates body s retention of H20 Increases blood pressure (vasoconstriction) Stimulant for increase: Increased plasma osmolality/decreased plasma volume Kidney- Acts on distal convoluted tubule and collecting ducts AVPR2 receptor insertion of Aquaporin2 water channels H20 resorption down osmotic gradient ADH Action Causes of PU/PD -Primary Polyuria vs Primary Polydipsia Diabetes Mellitus Hyperthyroidism Kidney Failure (A or C) Hyperadrenocorticism Hypoadrenocorticism Pyelonephritis Hypokalemia Hypercalcemia Liver Failure Portosystemic Shunt Acromegaly Pyometra Leiomyosarcoma Pheochromocytoma Drugs Post-obstructive diuresis Iatrogenic Renal glucosuria/fanconi s Polycythemia

4 PU/PD Mechanisms Primary Polyuria Osmotic Diuresis Impaired tubule response to ADH/block ADH receptor ADH deficiency/lack of ADH release from neurohypophysis Loss of renal medullary hypertonicity Damaged counter-current mechanism Primary Polydipsia Psychogenic Osmotic Diuresis Osmotic Diuresis Diabetes Mellitus Fanconi Syndrome and other tubulopathies Polyuric Acute Renal Failure Acromegaly (2 to DM) Post-obstructive diuresis

5 Impaired Tubule Response to ADH/Nephrogenic Diabetes Insipidus Impaired Tubule Response to ADH/ Secondary Nephrogenic DI Hyperadrenocorticism Hypercalcemia Bacterial Endotoxin (pyelonephritis, pyometra, etc) Hypokalemia Primary nephrogenic diabetes insipidus Leiomyosarcoma Hyperaldosteronism +/- Acromegaly Lack of ADH release

6 ADH deficiency Central Diabetes Insipidus +/- Acromegaly- partial? Decreased Renal Medullary Hypertonicity Decreased Renal Medullary Hypertonicity Hypoadrenocorticism Hyponatremia Renal medullary solute washout Can be secondary to anything that causes PU/PD Liver failure/pss Diuretics Fluid Therapy Damaged counter-current mechanism Renal failure

7 Psychogenic Polydipsia Primary Psychogenic Liver failure PSS Hyperthyroidism? Recap of Causes of PU/PD Primary Polyuria Diabetes Mellitus Hyperthyroidism Kidney Failure (A or C) Hyperadrenocorticism Hypoadrenocorticism Pyelonephritis Hypokalemia Hypercalcemia Liver Failure Portosystemic Shunt Post-obstructive diuresis Acromegaly Pyometra Leiomyosarcoma Pheochromocytoma Drugs Iatrogenic Renal glucosuria/fanconi s Polycythemia Primary Polydipsia psychogenic Diagnostic approach to PU/PD History Physical Exam Minimum Database U/A (morning urine sample is ideal for USG) Hyposthenuria, isosthenuria, minimally concentrated Urine Culture CBC Serum Biochemistry T4 These tests can rule-out most causes!

8 Additional Testing Abdominal Ultrasound Kidney structure and architecture Stones/mineralization Adrenal size/mass Liver structure/architecture Other masses/lymph nodes Bile Acids- pre and post-prandial Leptosporosis serology MRI GFR testing Iohexol clearance test easy to perform Rule-out Cushing s (HAC) Urine Cortisol:Creatitine (UCCR) highly sensitive, non specific Reserve for cases where you have a low index of suspicion for HAC Get morning samples from two or three different days Low Dose Dexamethasone Suppression Test )LDDST more sensitive ACTH Stimulation Test Pituitary dependent: Sn=60% Sp= 85-90% Functional adrenal tumor: Sn= 85% Sp= 85-90% U Tennessee Adrenal Panel (extended steroid panel) AUS Endogenous ACTH What are we left with? Primary Central Diabetes Insipidus Psychogenic Polydipsia Primary Nephrogenic Diabetes Insipidus What is an appropriate work-up???

9 Water Deprivation Test DO NOT DO A WATER DEPRIVATION TEST!!! Purpose: whether an animal can produce concentrated urine in the face of water deprivation Very dangerous life-threatening dehydration Time consuming Cost The benefits of results do not outweigh the risks under any circumstances DDAVP Trial Primary Nephrogenic DI is exceedingly rare and there is no specific treatment Therefore we are likely dealing with: CDI vs Psychogenic A response to DDAVP should give you a diagnosis of CDI (trauma, neoplasia, congenital, idiopathic) Cushing s patients can respond to DDAVP Empirical dose: 20kg dog: 0.1mg PO q8 40kg dog: 0.2mg PO q8 Or can use nasal solution as eye drops can be wasteful and cumbersome Recheck USG and measure water intake over next 3-7 days Should see a response within a few days then taper dose as needed Questions? Thank You