Combinations of azotemia
Pathogenesis. Severely diseased kidneys have impaired ability to compensate for stresses imposed by disease states, dietary indiscretion
and changes in environment. In patients with previously compensated primary renal disease, uremic crises are commonly precipitated
or complicated by a variety of concomitant extrarenal factors.
Extrarenal mechanisms that may be associated with uremic crises include the following:
> Factors that accelerate endogenous protein catabolism increase the quantity of metabolic by-products in the body since the
kidneys are incapable of excreting them. Protein by-products contribute significantly to the production of uremic signs in
patients with renal failure.
> Stress states (fever, infection, change of environment) are associated with glucocorticoid release from the adrenal glands.
> Glucocorticoids stimulate conversion of proteins to carbohydrates (gluconeogenesis) and, thus, increase the quantity of protein
waste products in the body.
> Abnormalities that decrease renal perfusion (i.e., decreased water consumption, vomiting, diarrhea) cause prerenal uremia.
> Nephrotoxic drugs in a patient with chronic renal failure may precipitate an acute uremic crisis by damaging nephrons.
Diagnosis. Combinations of causes of azotemia should be considered based on:
> A previous history of compensated primary renal failure
> Detection of primary extrarenal disease processes as well as generalized renal disease
> Detection of clinical dehydration—dehydration associated with azotemia and impaired urine concentration is reliable evidence
that a portion of the azotemia is prerenal in origin.
> How the patient responds to therapy—uremic crises precipitated by reversible extrarenal disorders may rapidly respond to
supportive and symptomatic therapy (rapid and significant reduction in the magnitude of azotemia). Uremic crises caused by
progressive irreversible destruction of nephrons usually respond slower (a marginal reduction in the magnitude of azotemia).
Prognosis. Withhold formulating a prognosis until the magnitude of azotemia is reassessed after correcting the prerenal or postrenal
components of azotemia.
Dr. Carl A. Osborne is the director of the Minnesota Urolith Center and a professor at the College of Veterinary Medicine
at the University of Minnesota. Dr. Eugene Nwaokorie is pursuing a PhD at the University of Minnesota.