Recurrence of Idiopathic Nephrotic Syndrome After Renal Transplantation

Hoyer, John R.; Raij, Leopoldo; Vernier, Robert L.; Simmons, Richard L.; Najarían, John S.; Michael, Alfred F.

doi:10.1016/s0140-6736(72)91734-5

Cited by 279 publications

(112 citation statements)

References 19 publications

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“…Proteinuria recurs after initial renal transplantation in approximately 30% of patients whose underlying diagnosis is FSGS (2,21). Recurrence may exceed 85% in patients with a history of allograft loss because of recurrence.…”

Section: Posttransplant Recurrence Of Ns/fsgsmentioning

confidence: 99%

Circulating Permeability Factors in Idiopathic Nephrotic Syndrome and Focal Segmental Glomerulosclerosis

McCarthy

Sharma

Savin

2010

Clinical Journal of the American Society of Nephrology

280

247

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Section: Posttransplant Recurrence Of Ns/fsgsmentioning

confidence: 99%

Circulating Permeability Factors in Idiopathic Nephrotic Syndrome and Focal Segmental Glomerulosclerosis

McCarthy

Sharma

Savin

2010

Clinical Journal of the American Society of Nephrology

280

247

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“…1,5 The most likely pathologic process is that T cells promote the production of a circulating factor that alters the glomerular permeability of the renal filtration barrier. 5,6 This concept came from the observation that proteinuria recurred in the very first samples of urine from patients who received a transplant 7 and was supported by studies demonstrating increased protein excretion in rats after the injection of serum from patients who relapsed after transplantation for FSGS. 8 Nevertheless, both the nature of pathogenic circulating factor and the mechanisms by which the immune system is involved in the pathologic process of FSGS and MCNS remain unknown.…”

mentioning

confidence: 99%

A Humanized Mouse Model of Idiopathic Nephrotic Syndrome Suggests a Pathogenic Role for Immature Cells

Sellier‐Leclerc

Duval²,

Riveron

et al. 2007

Journal of the American Society of Nephrology

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Idiopathic nephrotic syndrome is characterized by glomerular proteinuria in the absence of infiltrating cells or immunoglobulin deposits. Although it is suspected that T cells secrete a circulating factor that leads to proteinuria by altering the permeability of the glomerular filtration barrier, the precise etiology of this syndrome is unknown. Because an animal model that mimics human idiopathic nephrotic syndrome does not exist, we developed a humanized mouse model of the disease by injecting CD34 ϩ stem cells or CD34 Ϫ peripheral blood mononuclear cells from afflicted patients into immunocompromised mice. Even though both CD34 ϩ and CD34 Ϫ cells induced the engraftment of human CD45 ϩ leukocytes in mice, only the injection of CD34 ϩ stem cells induced albuminuria. Ultrastructural analysis of glomeruli from the resulting proteinuric mice revealed effacement of podocyte foot processes, similar to the pathology observed in the human disease. Therefore, our data suggest that the cells responsible for the pathogenesis of idiopathic nephrotic syndrome are more likely to be immature differentiating cells rather than mature peripheral T cells.

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“…In non genetic forms, the primary disorder seems to involve the immune system. To date, little is known about immune mechanisms which ultimately lead to the disorganisation of the glomerular filtration barrier and since the first report of INS recurrence following renal transplantation, the pathophysiology of this disease has become a challenge for nephrologists 18 . It has been postulated for a long time that INS results from a T cell dysfunction, leading to the release of a circulating factor responsible for glomerular damages 19 .…”

Section: Discussionmentioning

confidence: 99%

Potential Role of Soluble ST2 Protein in Idiopathic Nephrotic Syndrome Recurrence Following Kidney Transplantation

Bruneau

Berre

Hervé

et al. 2009

American Journal of Kidney Diseases

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France.DS and JD contributed equally to this work. No differences were detected in these sera before transplantation. Moreover, recurrent patients displayed the same sST2 isoform as the two control groups. In vitro, a mouse podocyte cell line was profoundly altered by incubation with sera of recurrent patients. However, purified sST2 from these patients was not able to reproduce these damages. In addition, induction of high sST2 levels in rats did not trigger proteinuria. Collectively, these data suggest that sST2 is a marker of INS recurrence that could be of interest for its diagnosis in ambiguous clinical situations. Nonetheless, sST2 does not seem to be directly implicated in INS development. This work was supported in part by

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Recurrence of Idiopathic Nephrotic Syndrome After Renal Transplantation

Cited by 279 publications

References 19 publications

Circulating Permeability Factors in Idiopathic Nephrotic Syndrome and Focal Segmental Glomerulosclerosis

Circulating Permeability Factors in Idiopathic Nephrotic Syndrome and Focal Segmental Glomerulosclerosis

A Humanized Mouse Model of Idiopathic Nephrotic Syndrome Suggests a Pathogenic Role for Immature Cells

Potential Role of Soluble ST2 Protein in Idiopathic Nephrotic Syndrome Recurrence Following Kidney Transplantation

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