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Albumin Metabolism in the Nephrotic Syndrome. Implications for Patient Management

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International Yearbook of Nephrology 1991

Part of the book series: International Yearbook of Nephrology 1991 ((IYNE,volume 3))

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Abstract

The urinary loss of as little as 3.5 g of protein a day (1,2), the amount of protein in half a hen’s egg, may cause the entire constellation of the nephrotic syndrome: severe hypoalbuminemia, hyperlipidemia, and edema formation. Although total body albumin stores are quite large, (400 g for a 70 kg person) (3-5) extensive depletion of all albumin pools occurs in the nephrotic syndrome (6-9). The mean value for proteinuria in a number of studies is about 8 g/day (6-9), not all of which is albumin, but viewed in the context of normal protein intake, even this external loss is small in absolute terms. At first glance it would appear to be a fairly simple matter to correct hypoproteinemia by simply replacing the protein lost in the urine with increased dietary protein. Unfortunately, increasing dietary protein intake has no significant beneficial effect in the clinical management of hypoalbuminemia in the nephrotic syndrome (7, 10-12). Increased dietary protein intake fails to increase either serum albumin concentration or body albumin pools in patients with the nephrotic syndrome (7, 11-13), or in animals with experimentally induced renal disease (14). Since the human liver normally synthesizes 12 to 14 grams of albumin a day (15, 16) and can more than double this rate of albumin production (6-9, 16, 17), it is not immediately apparent why hypoalbuminemia results from the urinary loss of this relatively small amount of protein.

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Kaysen, G.A. (1990). Albumin Metabolism in the Nephrotic Syndrome. Implications for Patient Management. In: Andreucci, V.E., Fine, L.G. (eds) International Yearbook of Nephrology 1991. International Yearbook of Nephrology 1991, vol 3. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3946-9_6

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