VII.3. Microalbuminuria (MA)

Increased (continuous, at least twofold) protein secretion in the kidney (proteinuria) has been reported to enhance the risk of CVD and death. MA is an independent marker of circulatory diseases and of nephropathies caused by DM.

The primary filtrate is formed physiologically in the glomerulus, which is the initial part of the nephrons in the kidney.  The amount of primary filtrate from the blood is defined by the difference in pressure of the two parts (BP and osmotic pressure). The efflux of a molecule into the filtrate is limited by the size, structure and charge of the molecule, and the structure of the vessel wall (the charge and size of the pores in the endothelial basal membrane). Heparan sulfate molecules present in the vessel walls are negatively charged, and therefore electrostatically repel the negatively charged proteins, and thus inhibit the efflux of proteins into the filtrate. The layer of heparan sulfate is very sensitive and plastic, and it may be changed by different effects such as fever, and then restored. The physiologically filtered small amount of albumin is passed by endocytosis into the kidneys, and hence the urine is physiologically protein-free.

The MA may be increased for hemodynamic reasons (a blood pressure increase) or because of vascular damage (the negative charge of the glomerulus membrane decreased, or the pore size is increased). 

The level of MA increases with age. It is increased by smoking, physical activity and fever. Its range in diabetic patients is 20-200 µg/min or 30-300 mg/day. MA is frequently associated with metabolic diseases (DM, an increased cholesterol level or hyperinsulinemia). It has been suggested that MA is a component of the MetS.