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Azotemia

ffelis

Introduction

  • Azotemia is an increased concentration of nonprotein nitrogenous compounds (eg urea and creatinine) in the blood. "Uremia" is the clinical syndrome that occurs as a result of severe azotemia due to abnormal renal function.
  • Causes:
    • Reduced glomerular filtration rate:
      • Reduced renal perfusion (pre-renal azotemia Pre-renal azotemia);
      • Primary renal disease (renal azotemia Uremia);
      • Obstruction to urinary outflow (post-renal azotemia).
    • Uroabdomen leading to reabsorption of urinary nitrogenous compounds (post-renal azotemia).
    • Increased absorption of nonprotein nitrogenous compounds from the gastro-intestinal tract, eg GI bleeding, high protein meal.
    • Increased protein catabolism, eg fever, trauma, burns Burns, hyperthyroidism Hyperthyroidism.
  • A degree of pre-renal azotemia may be super-imposed on pre-existing renal or post-renal azotemia.
    Follow the diagnostic tree for Azotemia Azotemia.

Pathogenesis

Etiology

  • Pre-renal azotemia:
    • Reduced renal perfusion due to low blood volume or low blood pressure (eg dehydration, hypovolemic shock Shock, congestive heart failure Heart: congestive heart failure, cardiac arrhythmias Heart: dysrhythmia, or general anesthesia)   →    reduced glomerular filtration rate, and/or allows passive reabsorption of urea from tubular fluid due to low tubular fluid rates.
  • Renal azotemia:
  • Post-renal azotemia:
    • Obstruction to urinary output, eg due to urethral obstruction Urethra: obstruction.
    • Reabsorption of urine constituents into the circulation following urine leakage into the abdomen, eg due to bladder rupture Bladder: trauma rupture or ureteral rupture Ureter: trauma, usually as a consequence of blunt abdominal trauma.

Predisposing factors

General

Pathophysiology

  • Post-renal azotemia: refer to urethral obstruction Urethra: obstruction and/or uroabdomen.
  • Renal azotemia: refer to acute renal failure Kidney: acute renal failure and chronic renal failure   Kidney: chronic kidney disease.
  • Pre-renal azotemia:
    • Reduced renal perfusion: initially, in the absence of primary renal disease, renal auto-regulatory mechanisms compensate for the tendency to reduce glomerular filtration rate and low vascular volume by increasing sodium and water reabsorption. Urine specific gravity rises to >1.035, if renal function Renal function assessment is adequate.
    • Eventually renal compensatory mechanisms are overwhelmed.  Reduced renal perfusion   →    reduced glomerular filtration rate   →    reduced renal excretory function   →    accumulation of toxic metabolites in the circulation, including nonprotein nitrogenous substances    →    azotemia and eventually uremia Uremia.

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 Edition Eds: Ettinger S J, Feldman E C.  Elsevier Saunders pp 1731-1751.
  • Squires R A (2005) Laboratory evaluation of renal disorders. In: BSAVA Manual of Canine and Feline Clinical Pathology, 2nd Edition.  Eds: Villiers E & Blackwood L. BSAVA Publications, Quedgeley. pp 169-183.
  • Polzon D J (2004) Azotemia and Uremia.  In: The 5-Minute Veterinary Consult, Canine and Feline. Eds: Tilley L P, Smith F W K, Lippincott, Williams and Wilkins. pp 142-143.
  • DiBartola S P (1995) Urinary Emergencies.  In: Handbook of Veterinary Procedures and Emergency Treatment. 6th Edition Eds: Bistner S I and Ford R B. W B Saunders Co, Philadelphia. pp 120-124.

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