Felis ISSN 2398-2950

Hyposthenuria

Contributor(s): Jana Gordon, Daniel H Lewis

Introduction

  • Definition: urine Specific Gravity <1.008; Urine Osmolality <300 mOsm/kg.
  • Hyposthenuria implies urine with an osmolality less than that of plasma and indicates decreased reabsorption of water by the kidneys and a normal renal ability to dilute urine.
  • Urine concentration is determined by the action of antidiuretic hormone (ADH) upon the principal cells of the cortical and medullary collecting ducts, and is dependent upon the presence of a hyperosmotic medullary interstitium.

Pathogenesis

Etiology

  • Around 65% of the filtered water is reabsorbed in the proximal convoluted tubule, with a further !0% in the Loop of Henle. The remaining portion of water is reabsorbed under fine control at the level of the collecting duct system.
  • Final urine concentration is determined by the action of anti-diuretic hormone (ADH) upon the principal cells of the collecting ducts. In the presence of hyperosmotic medullary interstitial fluid, ADH permits reabsorption of water along an osmotic gradient. ADH secretion from the posterior pituitary is affected by alterations in both serum osmolality and blood pressure/volume.
  • Diseases or drugs that decrease ADH production, affect ADH receptors, alter renal tubular function or reduce medullary interstitial osmolality (medullary washout) can therefore reduce the ability of the kidneys to reabsorb water.

Predisposing factors

General

  • Any condition causing renal tubular damage, medullary washout or polydipsia.

Specific

  • Central diabetes insipidus (reduced ADH secretion from the pituitary gland).
  • Nephrogenic diabetes insipidus (decreased renal response to ADH).
  • Primary congenital, familial disorder (reported in Huskies).
  • Secondary due to hypercalcemia Hypercalcemia: overview, endotoxemia, hyperadrenocorticism Hyperadrenocorticism (this may also result in decreased ADH secretion), hypokalemia Hypokalemia and hepatic insufficiency.

Pathophysiology

  • Final urine concentration is determined by the action of ADH upon the principal cells of the collecting ducts. ADH activates V2 receptors on the principal cells of the renal collecting ducts, triggering the movement of water channels (Aquaporin 2) to the luminal cell membrane. 
  • The creation of a hyperosmotic medullary interstitial fluid by means of the countercurrent mechanisms of the vasa recta, active reabsorption of sodium and chloride in the Loop of Henle and passive movement of urea out of the medullary collecting ducts. This provides an osmotic gradient favoring the reabsorption of water into the medulla. ADH permits reabsorption along an osmotic gradient by enhancing the permeability of the collecting duct system. diseases or drugs that decrease ADH production, affect ADH receptors, alter renal tubular function or reduce medullary interstitial osmolality (medullary washout) can therefore reduce the ability of the kidneys to reabsorb water.

Diagnosis

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Treatment

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Further Reading

Publications

Refereed papers

Other sources of information

  • DiBartola S (2006) Disorders of Sodium and Water: Hypernatraemia and Hyponatraemia. In: Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice pp 47-79. Ed S. DiBartola, Saunders Elsevier.
  • Archer J (2005) Urine analysis. In: BSAVA Manual of Canine and Feline Clinical Pathology pp 149-168. Eds E.Villiers & L.Blackwood, BSAVA Publications.
  • Eaton D C, Pooler J P (2004) Vanders Renal Physiology. Lange Medical Books/McGraw-Hill.


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