Using urine specific gravity values to localize azotemia in veterinary care
In previous issues of dvm360 (see the http://dvm360.com/osborne "The whole story"), we discussed various aspects of urine specific gravity values and their implications on patient health. Here, we discuss urine specific values and localization of azotemia.
Keep in mind that some azotemic cats with primary renal failure retain comparably greater urine concentrating capacity than dogs do. In dogs with progressive disease resulting in primary renal failure, azotemia usually follows loss of the ability to concentrate urine to a specific gravity of at least 1.030. In some cats with primary renal failure, azotemia may precede loss of the ability to concentrate urine to values of 1.040 to 1.045.
Prerenal azotemiaCauses and pathogenesis. Extraurinary diseases may cause varying degrees of alteration in glomerular filtration because of reduced renal blood flow. Inadequate perfusion of normal glomeruli with blood, regardless of cause, may cause prerenal azotemia.
Prerenal azotemia is initially associated with structurally normal kidneys that are capable of quantitatively normal renal function, provided compromised renal perfusion is corrected before the onset of ischemic nephron damage. Progression of prerenal azotemia to intrarenal (primary) renal failure due to persistent ischemia prolongs and reduces the likelihood of complete recovery.
Consider prerenal azotemia if abnormal elevations in blood urea nitrogen (BUN) and creatinine concentrations are associated with adequately concentrated urine (1.035 in dogs; 1.040 in cats) in patients with no specific evidence of generalized glomerular disease. Adequately concentrated urine in association with azotemia indicates that enough functional nephrons are present to prevent primary renal azotemia. Significantly elevated BUN or creatinine concentrations due to primary renal failure cannot be detected in dogs until about 70 to 75 percent of the nephron population is nonfunctional. Elevated urine specific gravity associated with prerenal azotemia probably reflects a compensatory response by the body to combat low perfusion pressure and blood volume by secreting antidiuretic hormone (and possibly other substances) to conserve water filtered through glomeruli. Appropriate volume replacement therapy to restore renal perfusion is typically followed by a dramatic drop in urea and creatinine concentrations to normal in about one to three days.
Another form of potentially reversible prerenal azotemia associated with primary renal disease may develop in patients with glomerulonephropathy and severe hypoalbuminemia. At the level of the glomerulus, hypoalbuminemia enhances the glomerular filtration rate because of reduced colloidal osmotic pressure. However, decreased renal blood flow and glomerular filtration that occur in association with a marked reduction in vascular volume secondary to a reduction in colloidal osmotic pressure result in a proportionate degree of retention of substances normally cleared by the kidneys (e.g., creatinine, urea). These two mechanisms have opposite effects on glomerular filtration. So carefully interpret an abnormal increase in BUN or creatinine concentration (or a reduction in creatinine clearance) in hypoproteinemic nephrotic patients. Azotemia is not indisputable evidence of severe primary glomerular lesions since a component of the azotemia may be associated with a potentially reversible decrease in renal perfusion caused by hypoalbuminemia.
Diagnosis. Diagnosis of prerenal azotemia is based on the following:
> Elevated serum BUN or creatinine concentrations
> High urine specific gravity (1.035 in dogs; 1.040 in cats) or osmolality
> Detection of underlying cause
> Rapid correction of azotemia after administration of appropriate therapy to restore renal perfusion.
Prognosis. The prognosis of prerenal azotemia depends on reversibility of the primary cause. The prognosis is favorable for renal function if perfusion is rapidly restored. However, complete loss of renal perfusion in excess of two to four hours may result in generalized ischemic renal disease. With the exception of shock, this degree of reduced renal perfusion is uncommon. Thus, the onset of generalized renal disease would be expected to require a longer period of altered renal perfusion.