Microalbuminuria is defined as an albumin concentration in urine greater than normal but below the detection limit using a conventional urine dipstick method. In the dog, micro-albuminuria means urine albumin between 1.0 and 30.0 mg/dL.

In two recent studies, the prevalence of microalbuminuria was 30% and 36% in 67 and 159 dogs, respectively, presented to veterinary teaching hospitals for routine health screening, elective procedures, or evaluation of health problems. The prevalence of microalbuminuria was 19% in 86 clinically normal dogs.

In a very large study of 3,041 staff-owned dogs from over 350 veterinary clinics, the overall prevalence of microalbuminuria was 24.7%. The health status of the dogs was not reported. A statistically significant correlation was found between increasing age and microalbuminuria. When grouped by age, microalbuminuria was present in 7.4% of dogs < 3 years old, 8.6% 3-5 years old, 20% 6-8 years old, 36.0% 9-11 years old, and 49.1% 12 years or more years old.

The prevalence of microalbuminuria in cats has not been reported.

Microalbuminuria may be a good indicator of early renal diseases in dogs, particularly those involving the glomerulus. Urine samples from 12 dogs infected with Dirofilaria immitis all showed microalbuminuria that increased in magnitude over time and preceded the development of overt proteinuria in some cases. At the end of the study, 11 dogs had histologic evidence of glomerular disease. In dogs with X-linked hereditary nephropathy, the presence of microalbuminuria was found to be a reliable early marker of developing nephropathy. In Soft-Coated Wheaten Terriers genetically at risk for the development of glomerular disease, the prevalence of microalbuminuria was 76%. The magnitude of microalbuminuria increased over time and 43% of the dogs eventually developed increased urine protein:creatinine ratios.

Other conditions present in dogs with microalbuminuria included: 3 of 3 dogs with cardiovascular disease, 2 of 5 dogs with urogenital disease, 4 of 20 dogs with neoplasia, and 3 of 14 dogs evaluated for other diseases.

Administration of carprofen or amoxicillin/clavulinic acid did not affect the magnitude of microalbuminuria, but use of prednisolone increased the amount of microalbuminuria in 50% of dogs already showing microalbuminuria and in 50% of dogs with normal urine albumin before prednisolone administration.

As a new diagnostic tool for canine renal disease, more information is needed to optimize use of this test in every day practice. What animals should be evaluated and at what age? Those dog breeds predisposed to familial glomerular diseases (e.g., Soft-Coated Wheaten Terriers, Bull Terriers, English Cocker Spaniels) should be routinely screened for microalbuminuria. As hereditary nephritis and proteinuria develop early in life in the latter two of these breeds, the first screening should begin at around 6-8 weeks of age, and continue every 1-2 months of age for the first year of life. By contrast, the familial nephropathy of Soft-Coated Wheaten Terriers occurs later in life, and testing should begin no later than 1 year of age and continue annually throughout life.

For dogs without an identified risk for developing glomerular disease, the logical time to begin routine screening for microalbuminuria is around 6 years old, when concentrations begin to increase with age. If microalbuminuria is detected, the test should be repeated in about 4 weeks. If the microalbuminuria is persistant, the dog may be at risk for development of glomerular disease and should be evaluated for a concurrent infectious, inflammatory or neoplastic disease that may be causing glomerular injury. Urine albumin concentrations should be reevaluated once concurrent diseases are effectively eliminated or managed. May eventually develop overt protein losing nephropathy. Early identification may allow for more appropriate and earlier intervention, and perhaps slow the progression to overt protein-losing nephropathy and renal failure.

References: Pressler et al. J Vet Int Med 15:300, 2001; Jensen et al. J Vet Int Med 15: 300, 2001; Grauer et al. J Vet Int Med 16: 352, 2002; Lees et al. J Vet Int Med 16: 353, 2002. [Material for this topic was contributed by Dr. Shelly L. Vaden, Proc. ACVIM 2003]