These laboratory data are most consistent with prerenal azotemia with an elevated BUN , TP, PCV combined with a concentrated urine specific gravity. Post renal azotemia is also a possibility, but in most circumstances post renal azotemia is accompanied by anuria and the serum potassium would be increased.

Increased BUN with isosthenuric urine suggests intrinsic renal disease. The elevated potassium is most compatible with oliguric acute renal failure. Chronic renal failure is more often associated with polyuria and normal to low serum potassium. Although urine sodium is substantially influenced by dietary sodium and CRF patients can have increased urinary sodium, usually CRF patients do not "waste" (excrete) large amounts of sodium. Urine sodium loss is a more consistent feature of ARF due to acute disruption of tubular function without time for adaptive (compensatory) mechanisms to "kick in." The increased TP and PCV support hemoconcentration often observed in patients with ARF due to gastrointestinal losses and reduced intake.

These laboratory data are most consistent with hypoadrenocorticism (Addison's disease) characterized by a low serum sodium in conjunction with a high urine sodium and a high serum potassium. The high sodium in the urine is inducing diuresis - resulting in the marginal ability to concentrate urine. Patients with Addison's disease classically have gastrointestinal losses of fluid due to vomiting and diarrhea and most likely the azotemia is prerenal due to fluid losses. The patient cannot concentrate its urine because of the natriuretic effect due to low aldosterone. We cannot exclude the possibility that the BUN increase is due to intrinsic renal disease on the basis of this single set of lab data. These parameters should be re-evaluated after the patient's Addison's disease is stabilized with mineralocorticoid. Hypoadrenocorticism is an example of a disease in which a patient can have prerenal azotemia yet have an impaired ability to concentrate their urine. This is an exception to the rule that combinations of azotemia and isosthenuria are due to intrinsic renal disease. In the case of Addison's disease, the azotemia is usually prerenal. A mild increase in serum calcium is sometimes observed in patients with Addison's disease.