Pre-renal azotemia

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

Diagnosis

Clinical signs

  • Dry mucous membranes.
  • Increased capillary refill time.
  • Poor quality peripheral pulses..
  • Increase in pulse rate.
  • Decreased skin turgor.
  • Evidence of underlying cause of renal hypoperfusion.
  • Bradycardia (hypoadrenocorticism).

Differential diagnosis

  • Renal azotemia.
  • Post-renal azotemia.

Outcomes

Prognosis

  • Good: if underlying cause can be treated and renal perfusion restored to normal.
  • Guarded: if kidney has been underperfused for a long time, renal damage may have occurred.

Expected response to treatment

  • Resolution of azotemia.

Reasons for treatment failure

  • If concurrent renal azotemia and pre-renal azotemia, the azotemia will not fully resolve on restoration of renal perfusion.
  • If underlying cause cannot be treated effectively.
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