Polyuria and Polydipsia

How common is primary nephrogenic diabetes insipidus?

(Not having receptors able to respond to ADH) Has never been properly diagnosed in vet med

Osmotic solute in the urine

Creates primary polyuria. The kindney maintains concentration ability but solvents keep water from being reabsorbed. Ex diabetes mellitus and primary glucosuria

If urine is not concentrated at the end of the water deprivation test what is the diagnosis?

DI, either central or nephrogenic

Pollakiuria

Frequent small amounts of urine

Theory as to why pyometra causes PU/PD

Bacteria in pyometra is usually E.coli which can produce a toxin which prevents the kidney from concentrating urine. This theory has not been proven.

Primary polyuria due to reduced or absent ADH production and release

Central diabetes insipidus-something wrong in the pituitary gland, making it unable to make ADH

Secondary nephrogenic diabetes insipidus

Conditions which interfere with the kidneys ability to concentrate urine 1. hypercalcemia 2. Hyperadrenocorticism 3. Liver failure 4. Pyelonephritis 5. Pyometra

What do you need to form concentrated urine?

1. ADH production and release 2. Renal tubules responding to ADH (functional receptors etc) 3. Osmotic gradient (renal tubules and medullary interstitium) Loss of any of these will result in polyuria

When not to do a water deprivation test

1. Azotemia (either dehydrated or kidney disease) 2. Dehydration-don't have a starting point for the test 3. Already concentrated (SG >1.030 in dogs and 1.040 in cats)

A water deprivation test is used to differentiate what?

1. Central diabetes insipidus 2. Nephrogenic DI 3. Psychogenic polydipsia

Potential complications with water deprivation test

1. Dehydration 2. AKF (if early renal disease) 3. Urosepsis (if pyelonephritis) 4. Acute water overload and cerebral edema from unlimited water access after restriction

Most common cause of PU/PD in an old cat

1. Diabetes mellitus 2. Chronic kidney disease 3. Hyperthyroidism

Top differentials for PU/PD

1. Diabetes mellitus 2. Diabetes insipidus (central and nephrogenic) 3. Hyperthyroidism 4. Hyperadrenocorticism 5. Hypercalcemia 6. Kidney disease 7. Liver disease 8. Psychogenic polydipsea 9. Hypokalemia 10. Primary glucosuria 11. Acromegaly 12. Pyometra 13. Drugs-ex corticosteroids

Causes of primary polydipsia without polyuria

1. Dry food 2. Fever 3. Elevated ambient temperature Tends to be transient

Thirst is inhibited by what?

1. ECF expansion 2. Hi BP 3. Drinking 4. Fullness 5. Increased Na+ (???)

What to start with to rule out causes of PU/PD?

1. History 2. Physical exam 3. Minimum data base (at least CBC, chem and UA)

Which ddx for PU/PD can be ruled out with chemistry

1. Hypercalcemia (Need to measure ionized) 2. Hypokalemia 3. Creatinine-kidney disease 4. Tests for liver function (BUN, Cholesterol, albumin, glucose)

Things that stimulate ADH release

1. Hyperosmolarity 2. Low BP 3. Fever 4. Pain 5. Nausea 6. Low glucose 7. Stress 8. Exercise 9. Drugs

How to diagnose causes of PU/PD not diagnosed with history, chem, CBC and UA?

1. Hyperthyroidism-T4 2. Liver disease-Bile acids 3. Acromegaly-insulin like growth factor 1 4. Pyometra (ultrasound) 5. Hyperadrenocorticism-low dose dex suppression 6. Psychogenic polydipsia and diabetes insipidus (central and nephrogenic)-rule out everything else, then do a water deprivation test to differentiate between these.

Problems with water deprivation test

1. May be difficult to interpret 2. Misdiagnosis if other diseases not ruled out first. 3. May not differentiate partial DI from psychogenic

Primary polyuria due to failure of renal tubule response to ADH

1. Primary nephrogenic diabetes insipidus 2. Secondary nephrogenic diabetes insipidus .

Causes for reduction in the osmotic gradient

1. Reduced Na -Renal failure (most common) -Hypoadrenocorticism -Renal medullary washout 2. Reduced BUN -liver failure

Primary polyuria

1. Reduced or absent ADH produced and released 2. Failure of the renal tubules respond to ADH 3. Reduction of the osmotic gradient (renal tubules or medullary interstitium)

Specific gravity in most PU/PD cases is what?

<1.025

Primary glucosuria

A renal tubular defect making tubules unable to reabsorb glucose, resulting in primary polyuria.

Urine output relies a lot on what hormone?

ADH

Stage 2 of water deprivation test

Abrupt water deprivation 1. Requires close monitoring 2. Goal is to achieve maximal ADH secretion and concentration of urine at loss of 3-5% body weight 3. If urine concentrates->psychogenic polydipsia 4. Baseline (PE, BUN, creatinine, TP and electrolytes, empty bladder completely and check SG. Obtain exact body weight and restrict all food and water) 5. Monitor patient ever 1-2 hrs (PE, Weigh, completely empty bladder and check SG, BUN) 6. Check creatining, PCV, TP, electrolytes every 4-6 hrs

Psychogenic polydipsia

Animals compulsively drink water but are otherwise normal. 1. Primary 2. Liver failure-one of the earliest signs of hepatic encephalopathy is PD 3. Hyperthyroidism-in cats

Na relationship with ADH

As Na goes up, ADH is released to retain water.

Definition of polydipsia (numerical)

Dogs >100 ml/kg/day Normal water consumption is larger in dogs <4 kg 1 kg dog ->132 ml/kg/day is normal Cats >45 ml/kg/day

Stage 3 of water deprivation test

Done if urine is not concentrated ADH response test 1. Give DDAVP then check SG after 2 hrs 2. If concentrates->central DI 3. If does not concentrate->primary nephrogenic DI

DDAVP trial

Give supplemental DDAVP for 5-7 days. If decreased water intake->central DI If minimal change->psychogenic polydipsia or primary nephrogenic Cushing's disease may have minimum or moderate response to DDAVP

Stage 1 of water deprivation test

Gradual restriction of water over 3 days (ideally at home) Day 1: 120-150 ml/kg water divided into -8 portions Day 2: 80-100 ml/kg water Day 3: 60-80 ml/kg water Minimize medullary washout

ADH release

Hypothalamus->posterior pituitary->kidney reabsorption of H20->decreased urine output

Definition of polyuria (numerical)

In dogs >50 ml/kg/day In cats >40 ml/kg/day

What differentials for PU/PD might be detected with a urinalysis?

Increased glucose-diabetes mellitus and primary glucosuria May show inflammation as well, culture typically not done

Cycle of ADH release

Increased plasma osmolality->increased ADH release->increased water reabsorption->decreased plasma osmolality->decreased ADH release If you are very volume depleted you may have ADH release independent of osmolality

Incontinence

Lack of voluntary control. Enuresis

Polyuria

Large amounts of urine

Thirst is stimulated by what?

Low BP, fever, pain, drugs

Main action of ADH

Make collecting ducts more permeable to water which is driven out due to the concentration gradient.

How is medullary hypertonicity maintained?

Na is primarily reabsorbed in the proximal tubule. In the thick ascending loop Na is reabsorbed without water and recirculated into the descending loop. This creates a lot of Na in renal interstitium.

PU/PD with SG <1.007

Not a problem with the kidney. Could be psychogenic polydipsea (liver failure may cause this) or diabetes insipidus.

PU/PD with a specific gravity of 1.035

Patient may have glucosuria, may be able to concentrate urine and may occur with psycogenic polydipsea (at hospital don't drink a lot of water)

If urine is concentrated at the end of the water deprivation test what is the diagnosis?

Psychogenic PD

Most common cause of PU/PD in an intact female dog

Pyometra

Stage 4 of water deprivation test

Reintroduce gradually over 6 hrs to avoid acute water overload and cerebral edema. Patient needs to be rehydrated, but needs to be done gradually.

How to treat psychogenic polydipsia

Restrict water after trying prozac

Risks associated with water deprivation test

Risk of life threatening dehydration and decompensation.

What is the most common cause of polyuria?

Secondary nephrogenic diabetes insipidus

Renal medullary washout

Situation in which there is chronic polyuria making renal tubular flow very fast and unable to absorb much Na from tubules. Tends to be in combination of several diseases.

What happens following water loss

Water loss->hyperosmolarity ->thirst and increased water intake->water balance->urine output. Some water is metabolized and some evaporated.

When do we stop the water deprivation test?

When patient... 1. Has lost 5% body weight 2. Is clinically dehydrated, vomiting, lethargic, abnormal mentation 3. Is azotemic 4. When urine SG > 1.030 5. At this point should have enough stimulus for ADH secretion, if not concentrating, not psychogenic

How does renal failure result in reduced osmotic gradient?

Without working nephrons, the kidney is unable to maintain hyperosmolarity