ALBUMIN 3.9 - 5.0 LOW
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HYPOALBUMINEMIA, a decreased albumin level less than 3.9 mg/dL. Albumin from week 20 of gestation through adult life is the most abundant protein in human plasma. It represents 55 to 65% of the total protein. Albumin is synthesized in the liver at a rate that is dependent on protein intake and subject to feedback regulation by the plasma level of albumin. Normally, little albumin is filtered through the glomeruli of the kidney and most of that is reabsorbed though the proximal tubule and degraded by lysosomal enzymes into fragments that are returned to the circulation. Hypoalbuminemia results, in most instances, from one or more of the following factors: (1) impaired synthesis; (2) increased catabolism; (3) reduced absorption; (4) protein losses; or (5) altered distribution. The most severe hypoalbuminemia (an albumin level less than 2.5 g/dL) is secondary to protein loss by way of urine or feces. The low oncotic pressure allows water to move out of the blood capillaries into the tissue causing edema or anasarca. Muehrcke's lines (non-palpable, white tranverse lines of the finger nails) are a symptom of severe hypoalbumniemia (less than 2.2 g.dL) and are associated most commonly with cirrhosis, severe malnutrition, or the nephrotic syndrome. Changes in plasma albumin concentrations affect the relative amounts of the bound and free concentrations of the ligands it carries. Because free ligands are those that interact with tissue receptor sites and that can be excreted, plasma levels have important influences on the metabolism of endogenous substances such as calcium, bilirubin, and fatty acids, and on the effects of drugs and hormones. In fact, hypoalbuminemia is a common cause of hypocalcemia. Albumin has a 20-day half-life and thus is not a good indicator of synthetic function when hepatic injury is acute. Rather, albumin is a good indicator of prognosis and severity of liver injury in states of chronic hepatic damage and is a variable in the Child-Pugh classification system for hepatic staging in chronic liver disorders.
Evaluation should begin with determining the source of albumin loss. A urinalysis with heavy proteinuria should be followed by either a 24 hour urine protein level or a random urine sample for protein/creatinine ratio. If the initial testing is indicative of a protein losing nephropathy, then the work-up should proceed as for proteinuria. If the urine studies are not indicative of renal protein losses, then an enteric etiology should be considered (Crohn's disease, lymphangiectasia, or Whipple's disease).