Urinary tract Flashcards
What are the criteria for diagnosis of nephrotic syndrome in dogs and cats?
- Hypoalbuminaemia
- Hypercholesterolaemia
- Proteinuria
- Third spacing (ascites, or subcutaneous oedema, or other body cavity effusions)
What is a normal volume of water intake in dogs and cats? What is the cut-off value for definitive polydipsia?
Normal - 80 ml/kg/day in dogs, 50 ml/kg/day for cats
Polydipsia - 100 ml/kg/day
Grey zone - 80 ml - 100 ml /kg/day
Polyuria - > 50 ml/kg/day for both dogs and cats
Describe the pathways of ADH/AVP, including location of production and stimulation of release.
Neural bodies of the magnocellular neurons located within the paraventricular and supra-optical nuclei in the hypothalamus. The axons run through the supra-opticohypophyseal tract and terminate within the posterior pituitary. It is produced within the neural bodies and then bound to neurophysins. Released from the posterior pituitary as a complex, and quickly dissassociates into AVP and neurophysin within the blood.
Stimulated by circumventricular osmoreceptors, as well as change in plasma osmolality of the magnocellular neurons themselves, high pressure baroreceptors within the carotid sinus and aortic arch, as well as low pressure baroreceptors within the pulmonary venous system and atria.
Also stimulated vy angiotensin II.
Describe the effects AVP/ADH has on its target organs
V1
- Located on arterioles and juxtaglomerular cells.
V2
- Located on corticol and medullary collecting ducts, thick ascending loop of Henle, and coagulation system.
V3
- Located in pituitary gland. Stimulates production of ACTH
What are the potential causes central diabetes insipidus?
Central diabetes insipidus
- Caused by inability of magnocellular neurons to produce or secrete AVP
- Can be congenital, although can also be due to trauma, inflammation, structural developmental abnormality, neoplasia, or iatrogenic
What are the causes of primary nephrogenic diabetes insipidus?
Primary nephrogenic diabetes insipidus is inability for the nephrons to respond to AVP
Usually congenital cause.
What are the causes of secondary nephrogenic diabetes insipidus?
Bacterial endotoxaemia e.g. pyelonephritis, pyometra, prostatic abscessation, septicaemia, chronic kidney disease, acute polyuric kidney injury, hypercalcaemia, hypokalaemia, hyperadrenocorticism, hyperaldosteronism, hyperthyroidism, polycythaemia, iatrogenic, leptospirosis
What is the pathophysiology of polyuria secondary to bacterial endotoxaemia?
Bacterial endotoxins, particularly from E. coli competes with the binding site of AVP on the renal tubules, and can cause reversible reduced tubular sensitivity to AVP, interferes with insertion of the aquaporin 2 channels, and reversible renal tubular cell lesions.
What are the pathophysiological mechanisms for polyuria in animals with hyperadrenocorticism?
Excess glucocorticoids act in multiple ways:
- Increase in osmotic setpoint, as well as decreased sensitivity to activate and release of AVP in response to decreased osmolality
- Increased GFR, free water clearance and sodium transport in the proximal tubular epithelium
- Interferes with AVP at the level of the collecting tubules or direct depression of renal tubular permeability to water
- Sometimes pituitary macro-adenoma can cause direct compression on the magnocellular neurons and reduce release of AVP
What is the pathophysiological mechanism for polyuria with hyperaldosterinism?
Unknown mechanism. Proposed it may be due to mineral-corticoid induced resistance to AVP.
What is the pathophysiological mechanism for polyuria and polydipsia in dogs with diabetes mellitus?
Caused by osmotic diuresis. Increased serum glucose levels overwhelms the glucose re-absorption threshold in the kidneys, which results in glucosuria, and subsequent polyuria.
What is the pathophysiological mechansim for polyuria in animals with chronic renal insufficiency?
Accumulated loss of functional nephrons results in increased GFR on individual nephron basis, which results in increased flow through the tubules and reduced absorption of electrolytes and glucose. Resulting osmotic diuresis and polyruia. May also have loss of medullary interstitial concentration gradient, which contributes to osmotic diuresis.
How does hypercalcaemia cause polyuria/ polydipsia?
Increased serum calcium interferes with insertion of aquaporin 2 channels on collecting tubules, inhibits binding of AVP onto receptors, inactivates adenylate cyclase, and decreases transport of sodium and chloride into renal medullary interstitium
According to JVIM 2020 Lourenco et al. study, what are the key findings in regards to treatment of proteinuria in dogs with telmisartan vs. enalapril?
- 80% of dogs treated with telmisartan 1 mg/kg PO SID had > 50% in UPC at 30 days compared to enalapril 0.5 mg/kg PO BID treated dogs (35%).
- Median time to achieve > 50% reduction in UPC was 30 days in telmisartan treated dogs, and 90 days in enalapril treated dogs
- Study not designed for assessment of hypertension management, but there was significantly greater decrease in systolic blood pressure in telmisartan treated dogs compared to enalapril treated dogs (30 days -0.9 enalapril vs. -12.3 telmisartan)
According to ACVIM consensus statement on rational use of gastro-protectants in small animals 2018, what is the consensus for use of PPIs in dogs and cats with chronic renal disease?
In humans with chronic kidney disease, gastrointestinal ulceration is common. Gastroduodenal ulceration is an uncommon finding in dogs and cats with advanced renal disease. Studies on gastrin secretion and gastric pH in cats and dogs with chronic kidney disease had no significant differences. Chronic prolonged use of antacids in humans is associated with increased risk of osteoporosis, PTH and calcium metabolism derangement. Not uncommon for cats to develop renal secondary hyperparathyroidism as well. As such, recommendations is to NOT use PPIs prophylactically in animals with CKD.
