Page 242 - Problem-Based Feline Medicine

234 PART 4 CAT WITH URINARY TRACT SIGNS

– Glomerular disease resulting in leakage of – Renal insensitivity to ADH (nephrogenic dia-
albumin and other poorly absorbable solutes betes insipidus). Renal cells may not respond to
into the renal tubule. adequate concentrations of ADH because of
– Impaired tubular reabsorption of glomerular insufficiency of functioning nephrons, compet-
filtrate solutes such as urea, creatinine, and itive inhibition for ADH receptors, or bacterial
phosphorus as occurs in renal failure and endotoxins. Altered cellular concentrations of
++
+
Fanconi syndrome. Ca , Mg , prostaglandin E, and corticosteroids
– Diuretics which act as a non-absorbable interfere with ADH receptor binding and render
solute, e.g. Mannitol. renal cells unresponsive to ADH (e.g. hyper-
● The medullary osmotic gradient is compromised, adrenocorticism, hypercalcaemia). Endotoxins
which decreases the concentrating ability of the such as E. coli render nephrons insensitive to
kidney, producing urine with a SG of 1.007–1.030. ADH (e.g. in pyometra–endometritis complex).
Causes include:
Polyuria should be differentiated from pollakiuria,
– Interference with the NaCl pump in the loop
which is increased frequency of urination of small
of Henle. This leads to a decrease in reabsorp-
quantities of urine, and is typically associated with
tion of ions, which is followed by a decrease in
bladder disease, especially cystitis. Inappropriate urina-
medullary hyperosmolality. These effects result
tion associated with behavioral disorders should also be
in the reduced movement of water out of the
differentiated from polyuria.
lumen of the distal tubules and collecting ducts
and hence an increased excretion of water and
solutes. Diuretics such as furosemide act via this
WHERE?
mechanism.
– Rapid fluid flow through the tubules or rapid Primary polyuria is most common, and occurs when the
blood flow through the vasa recta washes out ability to concentrate urine is decreased. Polydipsia is
the high concentration of solutes within the compensatory for polyuria.
medulla interstitium, referred to as medullary
Polyuria commonly results from structural and
washout. This impairs the countercurrent sys-
functional renal pathology, such as:
tem, which normally generates a hyperosmotic
● Loss of functioning nephrons.
environment in the renal medulla interstitium to
● Increased solute loading per nephron.
promote the movement of water out of the lumen
● Disruption of the medullary countercurrent system.
of distal tubules and collecting ducts. Medullary
● Decreased renal responsiveness to ADH.
washout can occur secondary to marked
polyuria, for example from diabetes insipidus, or Polyuria may also be influenced by many other organs
following diuretic use. and non-renal etiologies.
– Disruption to urea recycling through the body
Primary polydipsia (psychogenic polydipsia) has not
decreases the urea concentration in the
been reported in the cat.
medullary interstitium and hence decreases
medullary osmolality. Disruption to urea cycling
can be the result of decreased tubular response to WHAT?
antidiuretic hormone (ADH) leading to the
reduced permeability of collection ducts to urea, Renal disease (acute and chronic renal failure), dia-
or from decreased plasma urea concentration betes mellitus, hyperthyroidism and nephrogenic
(cirrhosis, protein depletion). Urine specific diabetes insipidus are the most common causes of
gravity is 1.007–1.030. polyuria and polydipsia.
● Collecting ducts become impermeable to water.
Hyperadrenocorticism, hypoadrenocorticism, acromegaly
This is characterized by urine with a SG
and central diabetes insipidus are uncommon causes.
1.001–1.006, and is due to either:
– Deficiency of ADH (central diabetes insipidus). Psychogenic polydipsia has not been reported.