Proteinuria refers to abnormal urinary excretion of protein. Detection of proteinuria is important. It is associated with renal and cardiovascular disease; it identifies diabetic patients at risk of nephropathy and other micro vascular complications; and it predicts end organ damage in hypertensive patients. Although proteinuria may arise through various mechanisms, it is most often an indication of abnormal glomerular function.
The glomerular basement membrane through which blood is filtered does not usually allow passage of albumin and large proteins, and proteinuria is most often due to abnormally ‘leaky’ glomeruli. The extent of this ‘leakiness’ varies enormously. When patients become hypoproteinaemic and hypoalbuminaemic due to excessive proteinuria, the normal balance of osmotic and hydrostatic forces at capillary level is disturbed, leading to loss of fluid into the interstitial space (edema).
Some proteins are so small that, unlike albumin and other larger proteins; they pass through the glomerulus freely. The best-known examples are beta-2-microglobulin and alpha-1- microglobulin. Others include retinol-binding protein and N-acetylglucosaminidase. If these proteins are detected in excess in the urine, this reflects tubular rather than glomerular dysfunction, i.e. an inability of the renal tubules to reabsorb them.
RISK FACTORS: Additional proteinuria risk factors include; Diabetes, Obesity, Advanced age (over 65), Family history of kidney disease, Preeclampsia (high blood pressure and proteinuria in pregnancy), Race and ethnicity etc.
PRECAUTIONS AND TREATMENT:
The primary treatment for proteinuria will be to control both blood pressure and blood glucose levels, which may be achieved through lifestyle changes and could include taking additional medication and low protein diet on regular basis.