Polyuria & Polydipsia Flashcards
What are the 4 steps to urine formation?
- filtration of plasma through glomerulus
- reabsorption
- secretion
- excretion
What is the greatest contributor to the urine concentration gradient?
urea
How does the pituitary gland control water absorption and urine concentration?
- releases ADH in response to an increased plasma osmolarity (sodium, glucose) or low ECF volume
- ADH enhances water permeability, causing it to be passively absorbed along the osmotic gradient
- this results in more concentrated urine
At what USG is urine considered normally concentrated by the renal tubules?
- DOGS = > 1.030
- CATS = > 1.035
(always analyze with Hx of the patient!)
What amount of water intake is necessary for maintenance? What is considered polydipsia?
50-60 mL/kg/day, based on insensible loss caused by breathing or urine excretion
drinking 2x the maintenance —> 100 mL/kg/day
What is the normal amount urine expected to be produced in a day? What is polyuria?
~ 40 mL/kg/day
excessive increase in urination with increased volumes
What is the difference between polyuria and pollakiuria?
POLYURIA - excessive and increased volume
POLLAKIURIA - excessive urination in small amounts (sign of LUT disease)
ASK CLIENTS about size of puddles, frequency, duration, urine stream, or litter box clumps
What are 3 causes of primary polyuria with compensatory polydipsia?
- lack of ADH
- lack of response to ADH
- lack of medullary concentration gradient
What are 3 causes of primary polydipsia with compensatory polyuria?
- physiologic
- behavioral
- pathologic
(psychogenic due to brain tumors or head trauma)
What is central diabetes insipidus?
lack of ADH release due to pituitary disease
What is nephrogenic diabetes insipidus?
lack of response to ADH most commonly caused by substances that interfere with ADH binding to receptors in kidneys
- bacterial endotoxins: E. coli from pyelonephritis, pyometra, or prostatitis
- calcium
- cortisol
What are 3 causes of of loss of medullary concentration gradient?
- hyponatremia, hypokalemia, or decreased BUN, which decreases the osmolality of plasma
- osmotic diuresis - diabetes mellitus or renal glucosuria, where glucose in filtrated urine pulls water
- reduced nephron function - chronic renal failure
What are some disease pathways that lead to primary polyuria?
- central and nephrogenic diabetes insipidus
- endotoxins from pyometra, pyelonephritis, and prostatitis
- hyperadrenocorticism, hypercalcemia: cortisol and calcium block renal receptors for ADH
- DM, renal glucosuria: osmotic
- hypoadrenocorticism: decreased aldosterone causes hyponatremia
- hyperthyroidism: increased renal blood flow
- chronic renal disease: damage to kidneys
- leptospirosis: tubular damage
What are the most common causes of PU/PD in dogs and cats?
DOGS: CKD, hyperadrenocorticism (Cushings), DM
CATS: CKD, hyperthyroidism, DM
How can we ask clients to quantify water intake?
- fill water bowl as normal, measuring total water volume
- refill bowl as needed through the next 24 hours while measuring each refill
- quantify the amonut of water left and subtract it from the total volume
What are the components of the minimum database for diagnosing the cause behind PU/PD?
- UA
- urine culture
- CBC
- chemistry
How is USG helpful for diagnosing the cause of PU/DP?
indicates whether the patient is able to concentrate urine
- hypersthenuria and hyposthenuria = kidneys able to concentrate/dilute urine, unlikely kidney disease
Why is sedimentation on UA helpful for diagnosing the cause of PU/PD?
active sedimentation, like bacteriuria, pyuria, and hematuria, can indicate pyelonephritis
Why is the presence of proteinuria helpful for diagnosing the cause of PU/PD?
indicates renal, tubular, or glomerular disease
Why is the presence of glucosuria helpful for diagnosing the cause of PU/PD?
indicates diabetes mellitus or tubular disease
What are the 3 major values evaluated on normal serum chemistry when trying to diagnose the cause of PU/PD?
- liver enzymes - decreased markers of synthetic function, like glucose, albumin, and BUN —> liver failure causes decreased urea, which also alters medullary concentration
- kidney values - azotemia indicative of kidney disease
- electrolytes - calcium, sodium, potassium
What additional values of serum biochemistry are helpful for diagnosing the cause of PU/PD in cats and dogs?
CATS = total T4 for hyperthyroidism
DOGS = LDDST for hyperadrenocorticism (Cushing’s)
What 3 diagnostics other than routine blood work can be used to diagnose the cause of PU/PD?
- abdominal ultrasounds - observe urinary tract and adrenals (Cushing’s!)
- SDMA - indicates GFR
- desmopressin (DDVAP) trial
How is psychogenic polydipsia diagnosed after ruling out every other option? Why must this be done carefully?
- modified water deprivation test - not given water, still results in concentrated urine
- first morning urine - not given water all night, concentrated urine
How does central and nephrogenic diabetes insipidus compare on the desmopressin (DDAVP) when diagnosing for the cause of PU/PD?
CENTRAL - no ADH produced from pituitary, so oral/conjunctival DDAVP should cause the urine to become concentrated, since the receptors in the kidney still work (+ decrease in water intake)
NEPHROGENIC - ADH not acting on kidney, so even if oral/conjunctival DDAVP is given, the urine will not become concentrated
Why should modified water deprivation tests and desmopressin (DDAVP) trials be done carefully?
withholding water can be dangerous in certain circumstances
rarely, patients with psychogenic polydipsia treated with DDAVP can undergo water toxicity
