- 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 >1.035.
- Treatment : treat underlying cause.
- Prognosis : reversible if treated early; longstanding decreased renal perfusion → renal parenchymal damage.
- 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).
- Renal azotemia.
- Post-renal azotemia.
- 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.