Azotemia

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Uremia-associated vasculitis. [1]

Azotemia is an excess of urea, creatinine, or other nonprotein, nitrogenous substance in blood, plasma, or serum.

Another term, uremia, is a more general term that defines a toxic syndrome as a result of chronic renal disease or other causes of abnormal renal function in animals with azotemia.

Azotemia can be caused by high production of nonprotein nitrogenous substances, low glomerular filtration rate or reabsorption of formed urine into the bloodstream. High production of nonprotein nitrogenous waste substances may be caused by high intake of protein (diet or gastrointestinal bleeding) or accelerated catabolism of endogenous proteins.

Glomerular filtration rate may decline because of reduced renal perfusion (prerenal azotemia), renal insufficiency or failure due to primary renal disease (renal azotemia), or urinary obstruction (postrenal azotemia). Reabsorption of urine may result from leakage of urine from the excretory pathways (also termed postrenal azotemia).

The pathophysiology of uremia is incompletely understood but may be related to 1) metabolic and toxic systemic effects of waste products retained because of renal excretory failure, 2) deranged renal regulation of fluids, electrolytes, and acid-base balance, and 3) impaired renal production of hormones and other substances (eg, erythropoietin and 1,25-dihydroxycholecalciferol).

Azotemia affects most organs of the body, interfering with most cellular processes.

Causes

  • Prerenal Azotemia - reduced renal perfusion due to low blood volume or low blood pressure. Accelerated production of nitrogenous waste products because of enhanced catabolism of tissues in association with infection, fever, trauma, corticosteroid excess, or burns. Increased gastrointestinal digestion and absorption of protein sources (diet or gastrointestinal hemorrhage).
  • Renal Azotemia

Acute or chronic renal failure (ie, primary renal disease affecting glomeruli, renal tubules, renal interstitium, or renal vasculature that impairs renal function by at least 75%)

  • Postrenal Azotemia

Urinary obstruction; rupture of the excretory pathway.

Other causes of azotemia which need to be excluded include:

Dehydration, poor peripheral perfusion, low cardiac output, history of recent fluid loss, high protein diet, or black, tarry stools--rule out prerenal azotemia.

Recent onset of altered urine output (high or low), clinical signs consistent with uremia, exposure to possible nephrotoxicants or ischemic renal injury, or kidney size normal or large--rule out acute renal failure

Progressive weight loss, polyuria, polydipsia, small kidneys, pallor, and signs of uremia that have developed over several weeks to months--rule out chronic renal failure

Abrupt decline in urine output and onset of signs of uremia; occasionally dysuria, stranguria and hematuria; large urinary bladder or fluid-filled abdomen--rule out postrenal azotemia[2].

Urinalysis

A urine specific gravity > 1.035 in cats supports a diagnosis of prerenal azotemia. Administration of fluids or diuretics before urine collection may render low urine specific gravity value uninterpretable. Azotemic cats that have not received fluids and have a urine specific gravity < 1.035 typically have primary renal azotemia. A notable exception to this rule is cats with glomerular disease. Glomerulopathy is sometimes characterized by glomerulotubular imbalance with urine concentrating ability persisting despite sufficient renal glomerular damage to cause primary renal azotemia.

These patients are recognized by moderate to marked proteinuria in the absence of hematuria and pyuria. Urine specific gravity is not of value in differentiating postrenal azotemia from prerenal or primary renal azotemia[3].

Biochemistry

Serial determinations of serum urea nitrogen and creatinine concentrations may be of diagnostic value in differentiating the cause of azotemia. Appropriate treatment to restore renal perfusion typically results in a dramatic reduction in azotemia in patients with prerenal azotemia (typically within 24- to 48 hours). Correcting obstruction to flow or a rent in the excretory pathway typically results in a rapid reduction in the magnitude of azotemia in patients with postrenal azotemia. Concurrent hyperkalemia may be consistent with postrenal azotemia, primary renal azotemia caused by oliguric renal failure, or prerenal azotemia associated with hypoadrenocorticism.

Treatment

Treatment for prerenal azotemia caused by impaired renal perfusion directed at correcting the underlying cause for renal hypoperfusion. The aggressiveness of treatment depends on the severity of the underlying condition and the probability that persistent renal hypoperfusion will lead to primary renal injury or failure. Treatment for primary renal azotemia and associated uremia includes 1) specific measures directed at halting or reversing the primary disease process affecting the kidneys, and 2) symptomatic, supportive, and palliative treatment that a) ameliorates clinical signs of uremia, b) minimizes the clinical impact of fluid, electrolyte, and acid-base imbalances, c) minimizes the effects of inadequate renal biosynthesis of hormones and other substances, and d) maintains adequate nutrition. Treatment for postrenal azotemia directed at eliminating urinary obstruction or correcting leakage from the urinary system. Supplemental fluid administration is often required to prevent dehydration which may develop during the solute diuresis that follows correction of postrenal azotemia.

Fluid therapy is indicated for most azotemic patients. Preferred fluid selections include 0.9% saline and lactated Ringer's solution. The quantity of fluid administered should be estimated on the basis of severity of dehydration or volume depletion. If clinical dehydration is not evident, it may cautiously be assumed that the patient is < 5% dehydrated and a corresponding volume of fluid administered. The bulk of volume replacement should generally be provided over 26 hours, except in patients with overt or suspected cardiac failure. Patients in shock should be treated appropriately[4].

References

  1. Guaguere, E & Prelaud, P (2000) A practical guide to feline dermatology. Merial, France, pp:24.5
  2. DiBartola S (1995) Clinical approach and laboratory evaluation of renal disease. In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine. Philadelphia: WB Saunders, 1995;1706-1719.
  3. Osborne CA & Polzin DJ (1983) Azotemia: a review of what's old and what's new. Part I. Definition of terms and concepts. Compend Cont Ed Pract Vet 5:497-508
  4. Osborne CA & Polzin DJ (1983) Azotemia: a review of what's old and what's new. Part II. Localization. Compend Cont Ed Pract Vet 5:561-5743