Pre-renal azotemia

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.