Disappearance of Glomerular IgA Deposits in Steroid-Responsive Nephrotic Syndrome
Author(s) -
K. Fukushi,
Hideaki Yamabe,
Kazuhiro Ozawa,
Hiroshi Ohsawa,
Noriyuki Chiba,
Hiroshi Inuma,
Satoshi Seino,
Mariko Miyata,
Kogo Onodera
Publication year - 1989
Publication title -
the nephron journals/nephron journals
Language(s) - English
Resource type - Journals
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000185395
Subject(s) - medicine , nephrotic syndrome , glomerulonephritis , kidney glomerulus , podocyte , nephrology , immunoglobulin a , endocrinology , pathology , immunology , kidney , proteinuria , immunoglobulin g , antibody
Kazuhiko Fukushi, Second Department of Internal Medicine, Hirosaki University, School of Medicine, Hirosaki (Japan) Dear Sir, Nephrotic syndrome or nephrotic range-proteinuria in IgA nephropathy is generally accepted as one of the possible indicators of a poor prognosis [1]. However, several descriptions of steroidresponsive nephrotic syndrome associated with glomerular IgA deposits, with a feature like minimal change nephrosis, have been recently recognized by several investigators [2–12], and several hypotheses for those occasions are realized at present, but the precise pathognomonic cognition is controversial. In our series of steroid-responsive nephrotic syndrome with IgA deposits, we report 2 patients in whom serial renal biopsy revealed the disappearance of glomerular IgA deposits. Case 1. A 30-year-old man developed edema with a prior history of common cold, and was admitted on January 20,1987. Five years earlier, he had been hospitalized for nephrotic syndrome. Shortly after the diagnosis of IgA nephritis (mesangial proliferative glomerulonephritis) was established (fig. 1), he subsequently received corti-costeroid therapy, just when the nephrotic syndrome was remarkable for complete remission. On this admission, urinalysis revealed 7.0 g of daily proteinuria without hematuria. Total protein was 4.7 g/l00 ml and serum creatinine was 0.8 mg/l00 ml. The profiles of immunological and serological parameters were essentially normal. IgA levels were raised to 512 mg/l00 ml, IgG 585 mg/l00 ml, IgM 135 mg/l00 ml. Percutaneous renal rebiopsy included 10 glomeruli on light microscopic examination that showed mild mesangial proliferative glomerulonephritis. On immunofluorescence, not only IgA but other immunoglobulins and complements were negative. Electron microscopic examination was not studied. Corticosteroid therapy completely relieved nephrotic syndrome. Subsequently, elevated serum IgA levels returned to normal values accompanied by remission of nephrotic syndrome.
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