Felis ISSN 2398-2950

Pre-renal azotemia

Synonym(s): Azotaemia

Contributor(s): Philip K Nicholls, Richard Squires, Melissa Wallace

Introduction

  • Azotemia = increased concentration of non-protein nitrogenous waste products, ie urea and creatinine, in the blood.
  • Pre-renal azotemia = azotemia due to inadequate renal perfusion.
  • Pre-renal azotemia may be present concurrently with primary renal and post-renal azotemia.
  • Cause: decreased renal perfusion, may be caused by dehydration, reduced cardiac output, hemorrhagic shock, etc.
  • Signs: dependent on underlying cause but often include vomiting, lethargy, anorexia, diarrhea, etc.
  • Diagnosis: elevated serum BUN and creatinine with urine specific gravity >1.035.
  • Treatment: treat underlying cause.
  • Prognosis: reversible if treated early; longstanding decreased renal perfusion   →   renal parenchymal damage.

Pathogenesis

Etiology

  • Cardiac failure Heart: congestive heart failure  (   →   decreased cardiac output   →    decreased renal perfusion).
  • Dehydration (   →   hypovolemia   →   decreased renal perfusion).
  • Shock Shock (   →   decreased renal perfusion).
  • Severe hemorrhage (   →   hypovolemia   →   decreased renal perfusion).
  • Hypoadrenocorticism Hypoadrenocorticism (   →   hyponatremia   →   hypovolemia   →   decreased renal perfusion).
  • Angiotensin-converting enzyme inhibitors   →    decrease glomerular filtration fraction   →    azotemia.
  • Some other antihypertensives   →    decreased blood pressure   →    decreased renal perfusion.

Pathophysiology

  • Decreased cardiac output or decreased blood volume   →   decreased effective circulating blood volume   →   decreased renal perfusion   →   initially renal autoregulation will preserve glomerular filtration rate and intravascular volume due to increased water reabsorption in the proximal tubules and collecting tubules and increased sodium reabsorption in the distal tubules, but eventually   →   decreased glomerular filtration rate   →   decreased excretory function   →  azotemia  Azotemia.
  • If no renal parenchymal damage in the early stages   →    good urine concentrating ability.
  • Longstanding renal hypoperfusion   →   renal parenchymal damage   →   acute tubular necrosis   →   acute renal failure Kidney: acute renal failure.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

Other sources of information

  • Cowgill L D & Francy T (2005) Acute Uraemia. In: Textbook of Veterinary Internal Medicine. 6th edn. Ettinger S J, Feldman E C (eds). Elsevier, Saunders, pp 1731-1751.
  • Squires R A (2005) Laboratory evaulation of renal disorders. In: BSAVA Manual of Canine and Feline Clinical Pathology. 2nd edn. Villiers E & Blackwood L. BSAVA Publications, Quedgeley, pp 169-183.
  • DiBartola S P (1995) Clinical approach and laboratory evaluation of renal disease. In: Textbook of Veterinary Internal Medicine. Eds: Ettinger S J, Feldman E C. Philadelphia: W B Saunders Co. pp 1706-1719.
  • Graker G F, Lane I F (1995) Acute renal failure. In: Textbook of Veterinary Internal Medicine. Eds: Ettinger S J, Feldman E C. Philadelphia: W B Saunders Co. pp 1720-1733.


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