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November 26, 1949


JAMA. 1949;141(13):922-923. doi:10.1001/jama.1949.02910130036011

The genesis of the so-called nephrotic syndrome has not thus far been elucidated. It is convenient from a clinical point of view to regard it as an independent entity. The syndrome is by some believed to be renal in origin, either a disease entity per se or a phase in chronic glomerulonephritis, while others believe it to be of extrarenal origin, caused by some disturbance of the protein metabolism. The syndrome, as pointed out by Bradley and Tyson,1 presents certain uniform and consistent features, such as gross edema, hypoproteinemia, hypercholesteremia, lipidemia and heavy proteinuria in the absence of congestive heart failure.

The plasma protein composition is greatly altered in the nephrotic syndrome. There is a significant reduction in albumin, while the globulin content may rise, especially in amyloidosis, may remain unchanged or may fall. The urinary proteins are probably derived from plasma by a filtration mechanism. The obvious site

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