Idiopathic nephrotic syndrome in adults. Classification based on histologic criteria

J. Churg; M. H. Goldstein; E. Grishman; S. L. Yunis; J. G. Porush

doi:10.1016/0002-8703(66)90226-2

Idiopathic nephrotic syndrome in adults. Classification based on histologic criteria

J. Churg, M. H. Goldstein, E. Grishman, S. L. Yunis, J. G. Porush

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Original language	English
Pages (from-to)	566-568
Number of pages	3
Journal	American Heart Journal
Volume	71
Issue number	4
DOIs	https://doi.org/10.1016/0002-8703(66)90226-2
State	Published - Apr 1966

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10.1016/0002-8703(66)90226-2

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@article{48a8a4daf31c4d029660e45e7ad5785a,

title = "Idiopathic nephrotic syndrome in adults. Classification based on histologic criteria",

author = "J. Churg and Goldstein, {M. H.} and E. Grishman and Yunis, {S. L.} and Porush, {J. G.}",

note = "Funding Information: It is now generally accepted that the manifestations of the nephrotic syndrome result from a primary defect of the renal glomerulus that allows large quantities of protein to pass into the urine. The development of this glomerular lesion may occur during the course of either a primary renal disease or a systemic disease involving the kidney. Prior to the widespread use of the percutaneous renal biopsy, the diagnosis of glomerulonephritis was made almost all adult nephrotic patients with primary renal disease. However, it is well known that many cases of nephrotic syndrome in children lacked the features of classic glomerulonephritis and showed few, if any, glomerular changes.{\textquoteright} Recent experience in this and other laboratories2 has indicated that a significant number of adults with the nephrotic syndrome also do not have the characteristic clinical or pathologic findings of proliferative glomerulonephritis, the form of nephritis which is commonly preceded by streptococcal infection.3 Whether these cases represent a variant of glomerulonephritis or a separate disease entity called lipoid nephrosis, idiopathic nephrosis, or idiopathic uephrotic syndrome (INS) has not been conclusively resolved.4 We believe that the histologic changes noted in these cases are distinctive enough to support the idea that they represent a separate entity. We refer to this group of cases as idiopathic nephrotic syndrome (INS). Confusion has arisen in the literature concerning INS because earlier histologic studies have not allowed a clear separation of this entity from proliferative glomerulonephritis. Be11,5 who was the first to recognize the presence of glomerular changes in INS, introduced the term membranous glomerulonephritis. Although this name has been widely used, it implies a pathogenetic relationship to proliferative glomerulonephritis which has not been proved. Ellis6 designated Type 2 nephritis those cases in which the nephrotic syndrome developed insidiously. Unfortunately, this group includes cases of proliferative glomerulonephritis, INS, and perhaps other diseases associated the nephrotic syndrome. This work was supported by United States Public Healtll Service Research Grant AM-00918 from the National Institute of Arthritis and Metabolic Diseases.",

year = "1966",

month = apr,

doi = "10.1016/0002-8703(66)90226-2",

language = "English",

volume = "71",

pages = "566--568",

journal = "American Heart Journal",

issn = "0002-8703",

publisher = "Elsevier Inc.",

number = "4",

}

TY - JOUR

T1 - Idiopathic nephrotic syndrome in adults. Classification based on histologic criteria

AU - Churg, J.

AU - Goldstein, M. H.

AU - Grishman, E.

AU - Yunis, S. L.

AU - Porush, J. G.

N1 - Funding Information: It is now generally accepted that the manifestations of the nephrotic syndrome result from a primary defect of the renal glomerulus that allows large quantities of protein to pass into the urine. The development of this glomerular lesion may occur during the course of either a primary renal disease or a systemic disease involving the kidney. Prior to the widespread use of the percutaneous renal biopsy, the diagnosis of glomerulonephritis was made almost all adult nephrotic patients with primary renal disease. However, it is well known that many cases of nephrotic syndrome in children lacked the features of classic glomerulonephritis and showed few, if any, glomerular changes.’ Recent experience in this and other laboratories2 has indicated that a significant number of adults with the nephrotic syndrome also do not have the characteristic clinical or pathologic findings of proliferative glomerulonephritis, the form of nephritis which is commonly preceded by streptococcal infection.3 Whether these cases represent a variant of glomerulonephritis or a separate disease entity called lipoid nephrosis, idiopathic nephrosis, or idiopathic uephrotic syndrome (INS) has not been conclusively resolved.4 We believe that the histologic changes noted in these cases are distinctive enough to support the idea that they represent a separate entity. We refer to this group of cases as idiopathic nephrotic syndrome (INS). Confusion has arisen in the literature concerning INS because earlier histologic studies have not allowed a clear separation of this entity from proliferative glomerulonephritis. Be11,5 who was the first to recognize the presence of glomerular changes in INS, introduced the term membranous glomerulonephritis. Although this name has been widely used, it implies a pathogenetic relationship to proliferative glomerulonephritis which has not been proved. Ellis6 designated Type 2 nephritis those cases in which the nephrotic syndrome developed insidiously. Unfortunately, this group includes cases of proliferative glomerulonephritis, INS, and perhaps other diseases associated the nephrotic syndrome. This work was supported by United States Public Healtll Service Research Grant AM-00918 from the National Institute of Arthritis and Metabolic Diseases.

PY - 1966/4

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