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Urinalysis: The forgotten fellow (Proceedings)

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Apr 01, 2008

Day in and day out, clinical pathology is used to make diagnoses, assess response to treatment and to screen healthy animals for occult disease. What many call a "baseline database" includes a serum chemistry profile of some type, a complete blood count with blood smear evaluation and a complete urinalysis (dipstick and sediment examination). All too often, a urinalysis is not performed. Potential reasons include difficulty in obtaining samples, uncertainty in examining samples in house, sample handling issues during delay before processing and perceived lack of value. There are many reasons why a urinalysis should be performed as part of an initial work up on ALL cases, with serial examinations performed as needed.

The first, and arguably most important reason to perform a urinalysis CONCURRENTLY with a serum chemistry profile and complete blood count is in the evaluation of azotemia. Upon initial evaluation of a patient, it is absolutely imperative that a urinalysis be performed. Many commonly employed therapies will iatrogenically alter the kidney's ability to concentrate urine. Diet, glucocorticoids and diuretics are examples of things that can drastically alter the kidney's ability to concentrate urine; therefore, a urinalysis must be done prior to the initiation of therapy. Although of importance, the dipstick and sediment examination are not as crucial. To this end, even if only a few drops can be obtained using ultrasound guidance or catheterization, it is certainly to your advantage to obtain a urine specific gravity (USG). Your problem list and clinical decisions as to additional diagnostics, treatment, prognosis, etc. can be greatly affected. Likewise, if a case is ultimately referred, the receiving clinician will better be able to pick up the data and continue forward with USG information in hand.

Azotemia is defined as the excess of urea and other non-protein nitrogenous wastes in the blood. Although technically "serum" urea nitrogen, most people refer to it as "blood" urea nitrogen. That being said, urea is such a small molecule (60 Da), that it readily diffuses throughout the body, including into erythrocytes. Azotemia is generally sub-divided into three main categories: pre-renal, renal and post-renal. The bottom line is the magnitude of increase in BUN or creatinine cannot be used alone to subcategorize.

There are several causes of pre-renal azotemia. One cause is a decreased renal perfusion due to hypovolemia. Examples of this include: dehydration, shock and cardiac disease. Decreased flow rate allows greater resorption of BUN. Creatinine should also be similarly elevated. USG is generally elevated secondary to ADH secretion. A noted exception is hypoadrenocorticism. Another cause can be due to increased protein catabolism, such as with necrosis, starvation, prolonged exercise, infection, fever or corticosteroids. This hypercatabolic state leads to an increased generation of ammonia, which leads to an increase in production of urea. This leads to only a mild increase in BUN due to large renal reserve capacity. Creatinine should not be increased. High protein diets can also cause a pre-renal azotemia. An example of this mechanism is upper gastrointestinal bleeding and home-made diets. Creatinine should not be increased in these cases. Creatinine can be slightly elevated secondary to marked rhabdomyolysis; however, the elevation is mild. The BUN:Creatinine ratio may suggest certain etiologies (e.g. upper gastrointestinal bleeding); however, this index is insensitive and is fraught with overlap. With pre-renal azotemia, the fractional excretion of sodium (FE Na) should be very low. Pre-renal azotemia can, and often is, seen in combination with the other types of azotemia.

Renal azotemia implies that >75% of renal functioning mass is non-functional. GFR is significantly decreased; therefore, BUN / Creat are a poor indicator of renal disease, as they will not increase until a significant amount of disease is present. Once azotemia is present, BUN doubles each time the remaining functional mass decreases by half. At this stage of the disease, modest increases in BUN are highly significant. At this stage of disease, the kidney's ability to concentrate urine is usually compromised; however, cats occasionally are azotemic, yet retain some concentrating ability. In the face of physiologic states where water should be conserved, the USG for a dog should be greater than 1.030 and 1.035 for a cat. Primary glomerular disorders may develop azotemia without compromise of concentrating ability. Always be wary of non-renal diseases masquerading as CRF, such as hypoadrenocortisism.