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Major Concepts Defined

Definitions

Azotemia is an increase in nitrogen containing waste products such as urea and creatinine in the blood.

Uremia is a syndrome characterized by a constellation of clinical signs caused by the retention of wastes normally excreted by the kidneys.

An azotemic patient is not always uremic but a uremic patient is always azotemic.

Renal disease implies a pathologic or functional lesion of any size, distribution, cause or degree of functional impairment in one or both kidneys. Renal disease may be subclinical due to the large renal reserve.

Renal failure is present when kidney function deteriorates to a point at which the integrity of the internal environment of the animal can no longer be maintained. So like the association between azotemia and uremia, animals with renal failure have concomitant renal disease but the opposite is not true. The abnormalities associated with renal failure include fluid, electrolyte and acid base imbalances, excretory deficits and decreased renal hormone production. Because the kidney has so many functions the clinical signs of failure are diverse and polysystemic.

Azotemia can be caused by prerenal, postrenal and intrinsic renal causes. Therefore the presence of azotemia does not always indicate the presence of kidney disease. Pre renal and post renal disorders can both lead to intrinsic renal disease if the situations are not corrected.

In order for the kidneys to eliminate wastes such as creatinine from circulation the following conditions must be met: (failure to meet any of this conditions can result in waste retention)

  • the heart must generate sufficient cardiac output to provide the kidneys with adequate renal blood flow
  • there must be sufficient blood volume and blood pressure to generate at least a mean blood pressure of 70 mmHg in order to maintain adequate renal blood flow
  • there must be sufficient numbers of functional nephrons to filter wastes (normal GFR)
  • urine must be able to be eliminated from the bladder (no obstruction to urine outflow)

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Prerenal azotemia is due to a decrease in renal blood flow which leads to a reduction in glomerular filtration rate (GFR). As GFR decreases, there is a smaller amount of waste products presented to the to the kidneys for elimination, resulting in elevation of waste products in the blood. Pre renal factors which can lead to decreased renal blood flow and GFR include:
  • decreased cardiac output (CO) due to primary cardiac disease
  • anything which decreases circulating blood volume

    dehydration caused by vomiting and diarrhea
    blood loss
    shock leading to redistribution or pooling of blood

Laboratory abnormalities in patients with pre renal azotemia usually include:

  • increased BUN and creatinine
  • increased PCV and albumin reflecting dehydration
  • blood sodium may be increased or normal depending upon the type of dehydration which exists (e.g. isotonic, hypotonic, hypertonic)
  • urine specific gravity is high (usually well in excess of 1.035) consistent with the elimination of a small volume of urine which is the appropriate kidney response to dehydration (to conserve water)
  • urine creatinine concentration is high, consistent with the kidneys excreting as much creatinine as possible in a smaller volume of water
  • urine sodium concentration is low (<10mEq/l). In order for the kidneys to conserve water they must also conserve sodium.

Treatment of pre renal azotemia includes fluid therapy and correction of the underlying cause. Prognosis is good if the underlying cause is treatable If the prerenal insult persists the patient may develop intrinsic renal disease.

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 Postrenal azotemia results from an obstruction of the urinary outflow tract or discontinuity of the outflow tract with extravasation of urine into body compartments. Obstruction can be by calculi, neoplasms, blood clots or foreign bodies, strictures, herniation of bladder into a perineal hernia, neurologic abnormalities, or feline urologic syndrome (FUS) in cats. Prostatic hypertrophy usually does not cause obstruction in the dog. Prostatic abscess or tumor can cause obstruction.

Signs may include anuria (no urine) if the obstruction is total or oliguria (small volume) if partial. If urine can be obtained, the laboratory findings are the same as those of prerenal azotemia.

Diagnostic tests should include a physical exam, radiographs (survey and contrast), and urethral catheterization. Potassium is commonly elevated as potassium is a small molecule and is reabsorbed from the urine back into blood.

Treatment is to treat the underlying cause. The prognosis is good if the underlying cause can be treated

Postrenal azotemic states can progress to intrinsic renal disease due to increased pressure in the renal tubules or due to hypotension and prerenal influences caused by dehydration.

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Intrinsic renal disease or failure can be divided into Acute renal failure (ARF) and Chronic renal failure (CRF).

It is important to differentiate acute from chronic renal failure to determine prognosis. ARF has a poor short term prognosis but good long prognosis. CRF has a good short term prognosis but poor long term prognosis. Some differentiating features include:

 

Acute renal failure Chronic renal failure
History
recent drug administration, toxin exposure,
surgery/hypovolemia
polyuria, polydipsia
Urine output oliguria polyuria
Kidney size normal to large small
Anemia absent present
Metabolic bone disease absent present
Urine specific gravity 1.007-1.017 (isosthenuric) 1.007-1.017 (isosthenuric)

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Summary- Classification of azotemia

Prerenal Postrenal Renal
Urine specific gravity >1.025 dog

>1.030 cat

>1.025 dog
>1.030 cat
1.007-1.017
Urine sodium <20 mEq/L <20 mEq/L >40 mEq/L (variable)

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