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Control of water balance and investigation of polyuria and polydipsia
/content/chapter/10.22233/9781910443866.chap9
Control of water balance and investigation of polyuria and polydipsia
- Author: Robert E. Shiel
- From: BSAVA Manual of Canine and Feline Endocrinology
- Item: Chapter 9, pp 62 - 70
- DOI: 10.22233/9781910443866.9
- Copyright: © 2023 British Small Animal Veterinary Association
- Publication Date: August 2023
Abstract
This chapter discusses the challenges in identifying and quantifying polyuria and polydipsia, and explores the various causes and underlying pathophysiology. The chapter provides an overview of the diagnostic investigation of these conditions, including the use of routine clinicopathological tests, urine culture, tests of endocrine and organ function, and diagnostic imaging. It also discusses the differentials for polyuria and polydipsia based on signalment, history, and physical examination. The chapter concludes with a brief reference to additional tests that may be conducted to differentiate between central diabetes insipidus and primary polyuria.
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/content/chapter/10.22233/9781910443866.chap9
Figures
/content/figure/10.22233/9781910443866.chap9.fig9_2
9.2
Relationships between plasma osmolality (POsm), plasma arginine vasopressin (PAVP) concentration, urine osmolality (UOsm) and urine volume (U Volume). (a) Small changes in plasma osmolality are associated with relatively large increases in PAVP concentration. (b) Urine osmolality is increased proportional to the PAVP concentration, until maximal urine-concentrating ability is reached (plateau). The height of this plateau is dependent upon the renal medullary concentration gradient. (c) Urine volume rapidly decreases in response to increases in PAVP concentration. The shaded areas represent the reference interval for PAVP in healthy dogs.
(Reproduced from
Robinson and Verbalis (2008)
with permission from the publisher. © Elsevier) © 2023 British Small Animal Veterinary Association
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10.22233/9781910443866/fig9_2.png
9.2
Relationships between plasma osmolality (POsm), plasma arginine vasopressin (PAVP) concentration, urine osmolality (UOsm) and urine volume (U Volume). (a) Small changes in plasma osmolality are associated with relatively large increases in PAVP concentration. (b) Urine osmolality is increased proportional to the PAVP concentration, until maximal urine-concentrating ability is reached (plateau). The height of this plateau is dependent upon the renal medullary concentration gradient. (c) Urine volume rapidly decreases in response to increases in PAVP concentration. The shaded areas represent the reference interval for PAVP in healthy dogs.
(Reproduced from
Robinson and Verbalis (2008)
with permission from the publisher. © Elsevier)
/content/figure/10.22233/9781910443866.chap9.fig9_3
9.3
Relationship between plasma arginine vasopressin (PAVP) and blood volume (VOL) or plasma osmolality (OSM) in rats. Plasma hypertonicity serves as the primary stimulus for AVP release; very small changes are associated with significant linear increases in AVP secretion. A greater degree of volume depletion is required to promote AVP release, which is exponential, and the magnitude of release may exceed that due to osmolality changes.
(Reproduced from
Dunn et al. (1973)
with permission from the publisher) © 2023 British Small Animal Veterinary Association
10.22233/9781910443866/fig9_3_thumb.gif
10.22233/9781910443866/fig9_3.png
9.3
Relationship between plasma arginine vasopressin (PAVP) and blood volume (VOL) or plasma osmolality (OSM) in rats. Plasma hypertonicity serves as the primary stimulus for AVP release; very small changes are associated with significant linear increases in AVP secretion. A greater degree of volume depletion is required to promote AVP release, which is exponential, and the magnitude of release may exceed that due to osmolality changes.
(Reproduced from
Dunn et al. (1973)
with permission from the publisher)
/content/figure/10.22233/9781910443866.chap9.fig9_4
9.4
Arginine vasopressin (AVP) production and action in the kidney. 1 = AVP is synthesized in the hypothalamus as a preprohormone and stored in vesicles within the posterior pituitary. Secretion of AVP from the posterior pituitary is stimulated by increasing plasma osmolality sensed by the osmoreceptors in the hypothalamus or by decreased total circulating plasma volume sensed as a change in pressure within the atria, veins and the carotid sinus. 2 = Circulating AVP acts primarily in the distal tubule and the collecting ducts of the kidney. Arginine vasopressin interacts with its receptor (V2) and, via a cascade of events, facilitates the transient insertion of water channels (aquaporin-2), which increases the permeability of these epithelial cells to water. By an independent pathway, AVP also regulates urea transport within the inner medullary collecting duct. AVP causes an increase in transepithelial transport of urea, which is important for maintenance of the urea gradient. 3 = The fluid in the distal tubule is dilute, allowing passive movement of water from the tubule to the hypertonic medullary interstitium along an osmotic gradient. 4 = Maintenance of the osmotic gradient is dependent on the counter-current multiplier system between the loop of Henle and the vasa recta blood supply, which concentrates solutes (urea and sodium) within the medullary interstitium. cAMP = cyclic adenosine monophosphate. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
(Reproduced from the BSAVA Manual of Canine and Feline Nephrology and Urology) © 2023 British Small Animal Veterinary Association
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9.4
Arginine vasopressin (AVP) production and action in the kidney. 1 = AVP is synthesized in the hypothalamus as a preprohormone and stored in vesicles within the posterior pituitary. Secretion of AVP from the posterior pituitary is stimulated by increasing plasma osmolality sensed by the osmoreceptors in the hypothalamus or by decreased total circulating plasma volume sensed as a change in pressure within the atria, veins and the carotid sinus. 2 = Circulating AVP acts primarily in the distal tubule and the collecting ducts of the kidney. Arginine vasopressin interacts with its receptor (V2) and, via a cascade of events, facilitates the transient insertion of water channels (aquaporin-2), which increases the permeability of these epithelial cells to water. By an independent pathway, AVP also regulates urea transport within the inner medullary collecting duct. AVP causes an increase in transepithelial transport of urea, which is important for maintenance of the urea gradient. 3 = The fluid in the distal tubule is dilute, allowing passive movement of water from the tubule to the hypertonic medullary interstitium along an osmotic gradient. 4 = Maintenance of the osmotic gradient is dependent on the counter-current multiplier system between the loop of Henle and the vasa recta blood supply, which concentrates solutes (urea and sodium) within the medullary interstitium. cAMP = cyclic adenosine monophosphate. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
(Reproduced from the BSAVA Manual of Canine and Feline Nephrology and Urology)