• Azotemia 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 >1.030.
• Treatment: treat underlying cause.
• Prognosis: reversible if treated early; longstanding decreased renal perfusion → renal parenchymal damage.

Presenting signs

• Signs related to the underlying cause of renal hypoperfusion:
  • Lethargy.
  • Vomiting.
  • Prolonged capillary refill time and other signs of poor peripheral perfusion.
  • Increased pulse rate and poor quality pulses.
  • Decreased skin turgor.
  • Dry mucous membranes.
  • Decreased blood pressure.

Special risks

• General anesthesia often causes reduced cardiac output and may induce or exacerbate pre-renal azotemia.
• The use of IV-fluids during anesthesia to maintain effective circulating blood volume and the use of anesthetic drugs with few cardiovascular or renal adverse effects is indicated.
• Non-steroidal anti-inflammatory drugs should be avoided in animals with uncorrected prerenal azotemia.
• Monitoring of blood pressure during general anesthesia is helpful in preventing renal hypoperfusion.