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proteinuria(prot?en-ur'e-a, pro?ten?) [ protein + -uria]
Normally, the glomerular membrane allows only low molecular weight proteins to enter the filtrate, and then most of this protein is reabsorbed via the renal tubules. Loss of protein in the urine is a common finding in diseases that damage the glomeruli and/or tubules of the kidneys. Common illnesses that contribute to urinary protein loss include diabetes mellitus, hypertension, kidney stones, multiple myeloma, polycystic kidney disease, and renal artery stenosis. All of these illnesses may result in progressive kidney failure. The degree of proteinuria can be measured with timed collections of all the urine a person produces (such as 24-hr collection with first specimen discarded and final specimen retained in a day) or by spot urine collections, i.e., by collecting a single specimen and estimating daily protein losses. The urine must not be contaminated with toilet tissue or feces. Controlling high blood pressure and hyperglycemia, taking ACE inhibitors or angiotensin receptor blockers, and limiting dietary protein intake can all have a beneficial effect on patients with urinary protein losses. Minimal proteinuria is more commonly associated with renal diseases that have less glomerular involvement, e.g., pyelonephritis. Moderate proteinuria occurs in various renal diseases or in diseases in which renal failure is a late complication (diabetes mellitus, heart failure). Heavy proteinuria is usually associated with nephritic syndrome. Many therapeutic agents (such as amphotericin B, aminoglucosides, gold preparations, polymixins) cause renal damage, resulting in proteinuria. Benign proteinuria can result from changes in body positioning. Functional proteinuria can be associated with physical exercise as well as emotional or physiologic stress and is usually transient. Proteinuria is associated with progressive kidney failure, the eventual need for dialysis, and an increased risk of death from cardiovascular diseases.