Azotemia

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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 ).
      • Intrinsic 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 , hyperthyroidism.
  • A degree of pre-renal azotemia may be super-imposed on pre-existing renal or post-renal azotemia.

Diagnosis

Clinical signs

  • Signs referable to the underlying cause, and additionally:
    • Evidence of dehydration, nausea, poor coat quality.
    • Uremic breath, weakness.
    • Hypersalivation, uremic stomatitis, ataxia, stupor.

Differential diagnosis

Differentiation of Renal and Pre-renal azotemia:

  • Assess both azotemia and urine specific gravity :
    • Azotemia and urine SG>1.040 indicates pre-renal azotemia with an appropriate renal compensatory response. Treat with intravenous fluids and re-assess the azotemia once the hydration deficit has been corrected.
    • Azotemia and urine SG <1.030 (before administration of any fluid therapy) suggests possible renal dysfunction, with or without a component of pre-renal azotemia.
    • Azotemia and urine SG 1.030-1.040 may be due to a combination of primary renal disease and pre-renal azotemia. Treat with intravenous fluids and re-assess the azotemia once hydration status has been corrected. If azotemia resolves completely renal function is likely to be adequate, although a degree of renal compromise is not ruled out.
    • Azotemia and hyposthenuria SG <1.008 : despite the dilute urine, the azotemia is most likely prerenal and the animal dehydrated. This is a consequence of massive, obligatory polyuria with inadequate compensatory drinking. There is a separate cause for the hyposthenuria (eg liver disease, nephrogenic diabetes insipidus or central diabetes insipidus . Reassess the azotemia after the animal has received asufficient fluid therapy to rehydrate it.

Outcomes

Prognosis

  • Depends on the underlying cause of the azotemia.
  • If pre-renal and post-renal azotemia can be managed effectively a full recovery is possible, but both conditions have the potential to cause permanent renal damage if severe enough, or if left untreated for too long.
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