Microalbuminuria and progressive renal disease

Microalbuminuria is a predictor of excess cardiovascular morbidity and mortality in both hypertensive and diabetic subjects. The reasons for this are multifactorial and relate to metabolic and haemodynamic problems seen in this population. In diabetic patients, microalbuminuria correlates more with glycosylated haemoglobin than with the duration of diabetes. The pathogensis of microalbuminuria includes alterations in glomerular shunting of albumin, increased intraglomerular pressure and increased amounts of certain growth factors that alter cell permeability. The urine Micral test is an easy way to screen for the presence of microalbuminuria. The increase in microalbuminuria over time can be documented by annual quantitation using a radioimmunoassay technology. Aggressive control of BP is vitally important in order to preserve renal function. Antihypertensive agents that lower both intraglomerular pressure and volume are preferable, since they consistently attenuate both the increase in microalbuminuria and structural changes within the glomerulus. In addition to BP control, other measures known to reduce the rise in microalbuminuria include a reduced dietary protein intake and good long-term blood glucose control. Unfortunately, there is no definitive study, in humans, that conclusively demonstrates a preservation of renal function directly relates to an attenuated rise in microalbuminuria. Thus, while microalbuminuria is clearly a risk factor for development of diabetic nephropathy and an indicator of hypertensive renal disease, its reduction has not demonstrated functional or structural benefit in humans. This is in large part due to the inpracticality of such a trial because of the duration needed to see an effect. Interestingly, a beneficial effect on renal survival has been shown with albuminuria reduction independent of BP reduction.