Azotaemia

Introduction

Azotaemia refers to biochemical evidence of increase in the blood concentrations of urea and creatinine. Azotaemia occurs almost exclusively with renal dysfunction, resulting in accumulation of these two, but not the only, waste products of protein metabolism. Urea and Creatinine vary in the extent of the increase induced by renal pathologies (creatinine can show substantial increases from baseline, whereas smaller increases in urea are significant as levels generally increase by a much smaller factor) and also the time taken for the increase. The severity of the increase in the urea concentration is considered to be proportional to the severity of the clinical syndrome, as urea (60D) is known to have distribution equal to the total body water, unlike that of creatinine. The severity in the increased concentration of creatinine, however, may not necessarily represent a severe damage to the kidneys. It is recommended that creatinine clearance and not the mere concentration of creatinine should be used as an indicator to judge the severity of illness.

Clinical Significance

Azotaemia may cause the clinical syndrome of uraemia, affecting multiple organ systems, and may involve retention of an array of different toxins in the body, which a healthy kidney would have excreted in the urine.

The causes of azotaemia can broadly be classified into pre-renal, renal and post-renal, however clinical differentiation is always challenging, as the manifestation is almost always, overlapping.

Pre-renal azotaemia

This occurs when the kidney receives insufficient oxygen via blood flow to maintain its normal metabolic processes. Conditions that can cause this include:

• Dehydration/hypovolaemia, which reduces renal blood flow.
• Heart failure which results in a reduced cardiac output, thereby reducing renal blood flow.
• Anaemia reduces the amount of oxygen delivered to the kidneys.
• Portal hypertension may result in splanchnic pooling of blood and reduced renal blood flow.

Renal azotaemia

This occurs following a direct insult to the kidney from several possible causes including:

• Exogenous toxins including heavy metals, aminoglycosides, tetracyclines, polymixin B, cisplatin, antifreeze (ethylene glycol), NSAIDs, lilies in cats and grapes in dogs.
• Endogenous toxins including haemoglobin, myoglobin and calcium.
• Infections such as pyelonephritis, interstitial nephritis (as caused by Leptospira spp. or granulomatous nephritis (as caused by the dry form of Feline Infectious Peritonitis).
• Glomerulonephritis and amyloidosis.
• Neoplasia, notably adenocarcinoma in dogs and lymphoma in cats.

Post-renal azotaemia

This occurs following obstructions within the urinary tract:

• Urolithiasis
• Rupture of the urinary tract, often due to trauma and causing uroabdomen.
• Neoplasia, including transitional cell carcinoma of the bladder and prostatic neoplasia.