Clinical Significance of Low-Magnitude Proteinuria in the Cat IVMA CE Self-Study Offering

Within the last decade, proteinuria in cats has been established as a prognostic indicator in chronic kidney disease. Low levels of proteinuria have been shown to be predictive of a poorer prognosis when compared to non-proteinuric cats with a corresponding stage of renal insufficiency. As a result of these findings, there has been increasing attention directed at microalbuminuria. Although multiple tests have been developed for the detection of microalbuminuria in cats, the value of monitoring for microalbuminuria in this species remains unknown. This article reviews the methods of assessment of proteinuria as well as what is currently known about the prognostic and therapeutic significance of low magnitude proteinuria in cats. Proteinuria: pathophysiology and classification Proteinuria is classified by anatomic origin as pre-renal, renal, and post-renal. Pre-renal proteinuria is a result of excessive low molecular weight proteins in the circulation that are filtered by the glomerulus and exceed the reabsorptive capacity of the renal tubule. The classic example of pre-renal proteinuria in the cat is Bence-Jones proteinuria, caused by excess production of immunoglobulin light chains in multiple myeloma. 1 Post-renal proteinuria is the result of inflammation in the lower urinary tract which results in inflammatory proteins being added to the urine after it has been formed in the kidneys. With both pre-renal and post-renal causes, the proteinuria does not result from any abnormality of the kidney itself and these causes must be ruled out when considering the significance of proteinuria. In contrast, renal proteinuria results from some change, either physiologic or pathologic, somewhere in the kidney. In the normal cat, the glomerular filtration barrier keeps the vast majority of plasma proteins in circulation. The proteins are prevented from passing through the barrier because of their large size and negative charge. Small peptides and amino acids do pass through the glomerular filtration barrier and into the filtrate but are either reabsorbed or degraded in the proximal tubule. The resulting effect is that only a minimal amount of protein makes it into the urine of a healthy animal. Renal proteinuria can be either physiologic (functional) or pathologic. Functional renal proteinuria, which can result from strenuous exercise or fever, is typically mild and results in transiently altered renal physiology. 2 This has not been well-studied in animals and is likely of minimal clinical significance in the feline patient. Pathologic proteinuria is the result of either primary or secondary renal dysfunction and is the primary focus of this article. Since both the glomerular filtration barrier keeps proteins out of the filtrate and the renal tubules either absorb or degrade the amino acids and peptides that make it into the filtrate, renal proteinuria can result from glomerular dysfunction, tubular dysfunction, or both. Glomerular proteinuria can result from primary glomerular disease such as amyloidosis or glomerulonephritis, resulting in the classical high-magnitude proteinuria and protein-losing nephropathy but this is uncommon in cats, particularly when compared to dogs, and will not be