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Polyuria Polydipsia

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Slide 1 :

Polyuria-Polydipsia Rhonda L. Schulman, DVM, DACVIM University of Illinois

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Water Metabolism Body water is tightly regulated Volume & Osmolality monitored

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Osmolality Refers to the # of particles in solution Maintained within very narrow ranges Sodium is the principal determinant 2(Na + K) + glucose + BUN 18 2.8

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Water conservation ? Volume Renin secretion ? Angiotensin formation Angiotensin is a dipsinogen Angiotensin promotes AVP release ? Osmolality AVP is released AVP leads to less urine produced (without AVP, will have a water diuresis)

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Vasopressin = Antidiuretic hormone (ADH) = AVP = Arginine vasopressin In pigs, it is lysine vasopressin Synthesized & secreted by the neurohypophysis Includes nuclei in the hypothalamus which terminate in the pituitary

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Water Metabolism

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Solute Diuresis = osmotic diuresis large amounts of a poorly reabsorbed solute such as glucose, mannitol, or urea

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Water diuresis Seen in the absence of AVP Limited reabsorption of solute-free water Large urine volumes with low osmolality

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Polyuria-Polydipsia (PU/PD) Water intake > 100 ml/kg/day Urine output > 50 ml/kg/day

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Polyuria-Polydipsia (PU/PD) Primary Polydipsia Primary Central Diabetes Insipidus (CDI) Nephrogenic Diabetes Insipidus (NDI) Renal insufficiency Pyelonephritis Post-obstructive diuresis Hyperadrenocorticism Hypoadrenocorticism Hyperthyroidism

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Nephrogenic Diabetes Insipidus (NDI) Hepatic insufficiency Pyometra Hypercalcemia Hypokalemia Glucosuria Renal medullary solute washout Primary NDI

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Primary polydipsia Excessive intake of water Often seen in puppies May result from the dog “playing with the water” Polyuria compensates for the overhydration

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Central Diabetes Insipidus (CDI) Lack of AVP production &/or secretion May be partial or complete Any disturbance/injury of the hypothalamus &/or pituitary is a potential cause Idiopathic Trauma Neoplasia Cysts Inflammation

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Nephrogenic Diabetes Insipidus (NDI) Many diseases interfere with: the interaction of AVP and the kidneys or the kidneys ability to respond to AVP or the renal medullary concentration gradient

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Nephrogenic DI Renal insufficiency ? # of functioning nephrons ? ?GFR per individual nephron ? solute reabsorption ? solute diuresis Decreased concentration gradient

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Nephrogenic DI Pyelonephritis The infection and inflammation disrupt the medullary concentration gradient. E. Coli interferes w/ the kidneys’ ability to respond to AVP

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Nephrogenic DI Post-obstructive diuresis Azotemia = ? BUN ? osmotic diuresis

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Nephrogenic DI Hyperadrenocorticism The mechanism is unknown ? interference w/ the action of AVP on the kidneys ? ? GFR ? diuresis ? Direct depression of kidneys’ ability to reabsorb ? ? AVP release

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Nephrogenic DI Hypoadrenocorticism Mineralocorticoid deficiency ? ? Na ? medullary solute washout

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Nephrogenic DI Hyperthyroidism Mechanism is unknown ? ?GFR?diuresis ? Psychogenic PD

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Nephrogenic DI Hepatic insufficiency ? BUN may impair concentration gradient Hepatic encephalopathy may cause 1° polydipsia

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Nephrogenic DI Pyometra E. Coli endotoxins interfere with the kidneys’ ability to respond to AVP

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Nephrogenic DI Hypercalcemia Calcium interferes with the kidneys’ ability to respond to AVP. Calcium may also disrupt the medullary concentration gradient

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Nephrogenic DI Hypokalemia ?? K makes the kidney less responsive to AVP ?? K interferes with the concentration gradient ?? K may interfere with release of AVP from the pituitary (CDI)

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Nephrogenic DI Glucosuria The excessive glucose in the urine causes an osmotic diuresis

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Nephrogenic DI Renal medullary solute washout ?Na and urea ? ? hypertonicity Impaired concentration ability This typically results from another condition.

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Concentration Gradient

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Nephrogenic DI Primary NDI A congenital defect in which the kidneys are unable to respond to AVP

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Iatrogenic causes of PU/PD Drugs glucocorticoids diuretics anticonvulsants thyroid hormone supplements amphotericin B methoxyfluorane Excessive salt

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Work-up for PU/PD

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Work-up for PU/PD

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Work-up for PU/PD

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Work-up for PU/PD Culture the urine US &/or X-ray the abdomen ACTH stimulation test Hyperadrenocorticism Hypoadrenocorticism Bile Acids for liver dz

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Water Deprivation Test Only after ruling out other causes!!!

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Water Deprivation Test-Part 1 Monitor water intake for a few days 3 days prior, Restrict water to 120-150 ml/kg/day 2 days prior, Restrict water to 100-120 ml/kg/day 1 day prior, Restrict the water to 60-80 ml/kg/day

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Water Deprivation Test-Part 1 This should help re-establish the medullary concentration gradient. Depending on how much the patient has been drinking, you may want to do this even more slowly.

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Water Deprivation Test-Part 2 In-hospital portion of the test Take away all food and water Empty the bladder & measure the urine s.g. Weigh the patient Measure PCV/TS, Creat, BUN Check patient’s overall well-being and CNS function

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Water Deprivation Test-Part 2 Hourly checks of: Body weight Urine specific gravity Overall well-being Bloodwork should be checked every few hours

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Water Deprivation Test-Part 2 The test is finished when: The urine concentrates to ? 1.030 The patient loses 3-5% of body weight The patient becomes dehydrated, azotemic or ill 5% weight loss should maximally stimulate ADH release

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Water Deprivation Test If the patient loses 5% of its weight but doesn’t concentrate its urine, give exogenous ADH Every 30 minutes for 2 hours, then check: urine s.g. patient’s overall well-being and CNS function BUN

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Water Deprivation Test Central DI patients should be able to concentrate urine within 2 hours of being given AVP Following the test, allow limited access to water for the next 2 hours

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Water Deprivation Test

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Alternative Water Dep Test Administer 1-2 drops of DDAVP into the conjunctival sac 1-2x/day Patients with central DI will improve within 5-7 days

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Treatment-CDI DDAVP: 1-4 drops sid-bid Chlorpropamide may enhance the renal response to ADH only useful in more mild/partial cases takes 1 week to be effective may cause hypoglycemia.

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Treatment-CDI Thiazide diuretics inhibit Na reabsorption leads to a decreased urine volume Useful in mild cases Use with a low sodium diet Low sodium diet No treatment is required

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Treatment-NDI Thiazide diuretics Low sodium diet No treatment

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Treatment-Psychogenic Mild water restriction Behavioral modification Enrich the patient’s environment

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	SlidesOnline 1 Years ago. Category: other

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523 Views, 0 favourite
Renal insufficiency; Pyelonephritis; Post-obstructive diuresis; Hyperadrenocorticism; Hypoadrenocor more Renal insufficiency; Pyelonephritis; Post-obstructive diuresis; Hyperadrenocorticism; Hypoadrenocorticism; Hyperthyroidism. Nephrogenic Diabetes Insipidus ... less

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