Lipid nephrosis

Primary glomerular disease membranous glomerulonephritis, lipid nephrosis... 

Marsh, J. B., and D. L. Drabkin Experimental reconstruction of metabolic pattern of lipid nephrosis key role of hepatic protein synthesis in hyperhpemia. Metabolism 9,9466 (1960). 

PEM is frequently associated with changes in serum markers such as protein, lipid, and nitrogen (Hendrickse, 1991). Decreased serum albumin levels have been used as a standard PEM indicator. Since albumin has a long half-life of 18 days in the plasma and a large pool size that decreases in various illnesses (such as hepatic insufficiency and nephrosis), it is not a specific marker for recent nutritional inadequacies. Prealbumin (or transthyretin), by virtue of its higher catabolic rate (half-life = 1.9 days) and small pool size, is a very sensitive and fairly specific indicator of acute malnutrition and shortterm responses to nutritional replacements in patients of all ages (Bernstein and Ingenbleek, 2002). 

In accordance with our interpretation of the term lipidoses as hereditary disorders of lipid metabolism, a review of secondary hyperlipidemias has not been attempted here. Since they are considered as associated phenomena of disorders such as diabetic ketoacidosis, nephrosis or pancreatitis, their exclusion seems to be justifiable. 

Endogenous hyperlipemia occurs in uncontrolled diabetes and, at times, in starvation, pregnancy, lactation, severe anemia, nephrosis, and after hemorrhage. The lipid changes appear to be associated with a decrease in plasma protein concentration or in oxygen-carrying capacity of blood (Chapter 7). 

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