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Idiopathic Nephrotic Syndrome In Children: Clinical Aspects

P. Niaudet, O. Boyer
Published 2016 · Medicine

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The most common cause of nephrotic syndrome in children is idiopathic nephrotic syndrome (INS), also called nephrosis [1]. INS is defined by the combination of a nephrotic syndrome (massive proteinuria, hypoalbuminemia, hyperlipidemia, and edema) and nonspecific histological abnormalities of the glomeruli including minimal changes, focal and segmental glomerular sclerosis (FSGS), and diffuse mesangial proliferation. On electron microscopy, glomeruli show an effacement of epithelial cell (podocyte) foot processes and no significant deposits of immunoglobulins or complement by immunofluorescence. In a majority of children, only minimal changes are seen on light microscopy. These children are referred to as having “minimal change disease.” Many authors consider minimal change disease (MCD) and FSGS as separate diseases because of differences in response to corticosteroids and subsequent clinical course. Indeed, these pathologic features carry prognostic significance. Patients with FSGS have more frequently hematuria, are often resistant to corticosteroid treatment, and progress more often to renal failure. Recent data have comforted the belief that MCD and FSGS are different entities. MCD is a functional podocyte disease, whereas FSGS appears to be a structural podocytopathy [2]. The notion of “podocyte dysregulation” [2, 3], the different expression cyclin-dependent kinase inhibitors in MCD and in FSGS, the role of these cell cycle disturbances leading to podocyte proliferation and maturation [4], and the identification of parvovirus B19 in glomeruli of patients with FSGS [5, 6] are in favor of distinct entities. The high circulating levels of the soluble urokinase receptor (suPAR) found in FSGS but not in MCD [7, 8] support the hypothesis that MCD and FSGS as podocytopathies originating from different glomerular permeability factors. In the early stages, FSGS and MCD are indistinguishable [9]. The best illustration of this is the aspect of a transplant biopsy carried out shortly after relapse of proteinuria following transplantation in a patient whose primary renal disease was FSGS. Despite heavy proteinuria, the glomeruli initially show minimal changes. A significant number of patients with FSGS respond to corticosteroids, whereas some steroid-resistant patients have no sclerotic changes on biopsy specimens containing adequate tissue [10]. Therefore, some authors believe that, although histological variants of the INS carry prognostic significance, they cannot at present be considered as separate entities. The term MCD has become synonymous with steroid-responsive nephrotic syndrome although renal biopsy is usually not performed in patients who respond to steroid therapy. Indeed, in many centers, renal biopsy is recommended only for those patients who fail to respond to steroids. Consequently, renal biopsy findings in recent published series are not representative of the true incidence of various histopathological categories seen in INS. It is therefore more appropriate to classify the patients according to their response to steroid therapy. Response to steroid therapy carries a greater prognostic weight than the histological features seen on initial renal biopsy. Thus, two types of INS can be defined: steroid-responsive nephrotic syndrome, in which proteinuria rapidly resolves after starting steroid therapy, and steroid-resistant nephrotic syndrome, in which steroids do not induce remission.
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