scholarly journals Nephrotic Syndrome without Hematuria due to Infection-Related Glomerulonephritis Mimicking Minimal-Change Disease in a Child

2016 ◽  
Vol 6 (1) ◽  
pp. 14-20
Author(s):  
Yoichi Iwafuchi ◽  
Tetsuo Morioka ◽  
Takashi Morita ◽  
Kanako Watanabe ◽  
Yuko Oyama ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Mononuclear Cells ◽  
Present Report ◽  
Laboratory Data ◽  
Minimal Change Nephrotic Syndrome ◽  
Minimal Change ◽  
Causative Organism ◽  
History Of ◽  
Leg Edema ◽  
Endocapillary Proliferative Glomerulonephritis

Nephrotic syndrome without hematuria due to infection-related glomerulonephritis is uncommon. The present report describes a case of nephrotic syndrome due to infection-related glomerulonephritis without hematuria and hypertension in an older child. A 14-year-old boy was referred to our hospital because of a 5-day history of fever, nausea, weight gain and recent leg edema without hypertension. Laboratory data showed nephrotic-range proteinuria, hypoalbuminemia, mild hypocomplementemia and acute renal injury without hematuria. Although, due to the clinical presentation, minimal-change nephrotic syndrome was mostly suspected, a renal biopsy showed endocapillary hypercellularity mainly of mononuclear cells with segmental mesangiolytic changes. Fine granular IgG and C3 deposits were noted by an immunofluorescent study; many relatively small electron-dense deposits were observed electron-microscopically. These findings led to the diagnosis of nephrotic syndrome due to infection-related endocapillary proliferative glomerulonephritis, although the causative organism of his nephritis was not detected. He recovered with rest and dietary cure. When we examine an acute nephrotic child, infection-related glomerulonephritis should be considered as the differential diagnosis to avoid unnecessary use of corticosteroids.

Transcriptional and Post-Transcriptional Alterations of I κBα in Active Minimal-Change Nephrotic Syndrome

2001 ◽  
Vol 12 (8) ◽  
pp. 1648-1658 ◽  
Author(s):  
DJILLALI SAHALI ◽  
ANDRÉ PAWLAK ◽  
SABINE LE GOUVELLO ◽  
PHILIPPE LANG ◽  
ASTA VALANCIUTÉ ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Minimal Change Nephrotic Syndrome ◽  
Binding Activity ◽  
Minimal Change ◽  
Peripheral Blood Mononuclear ◽  
Nuclear Extracts ◽  
Blood Mononuclear Cells

Abstract. Minimal-change nephrotic syndrome (MCNS) is a renal disease characterized by heavy glomerular proteinuria and increased production of cytokines by immune cells. Because of the central role of nuclear factor-κB (NF-κB) in the regulation of cytokine expression, its activity during the relapse and remission phases of steroid-sensitive MCNS was analyzed. During relapse, nuclear extracts from peripheral blood mononuclear cells displayed high levels of NF-κB DNA-binding activity, consisting primarily of p50/RelA (p65) complexes. NF-κB p65 and IκBα proteins were barely detected or not detected in cytosolic fractions during relapse, in contrast to remission. The lack of expression of IκBα protein was associated with downregulation of IκBα mRNA and increases in the levels of the mRNA encoding the proteasome α2 subunit proteolytic pathway. In addition, inhibition of proteasome activity induced cytosolic accumulation of phosphorylated IκBα and significant reductions in the NF-κB binding activity in nuclear extracts from peripheral blood mononuclear cells from patients experiencing relapses. These results suggest that alterations in the NF-κB/IκBα regulatory feedback loop may contribute to the immunologic abnormalities that occur in steroidsensitive MCNS.

scholarly journals A Novel Approach to Investigation of the Pathogenesis of Active Minimal-Change Nephrotic Syndrome Using Subtracted cDNA Library Screening

2002 ◽  
Vol 13 (5) ◽  
pp. 1238-1247 ◽  
Author(s):  
Djillali Sahali ◽  
André Pawlak ◽  
Asta Valanciuté ◽  
Philippe Grimbert ◽  
Philippe Lang ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
T Cell ◽  
Cdna Library ◽  
T Cell Receptor ◽  
T Cell Activation ◽  
Mononuclear Cells ◽  
Minimal Change Nephrotic Syndrome ◽  
Cell Receptor ◽  
Minimal Change ◽  
Interleukin 12

ABSTRACT. Clinical and experimental observations suggest that minimal-change nephrotic syndrome (MCNS) results from T cell dysfunction, via unknown mechanisms. For the identification of genes that are potentially involved in MCNS, a subtractive cDNA library was constructed from cDNA from T cell-enriched peripheral blood mononuclear cells obtained from the same patient during relapseversusremission (“relapse minus remission”). This library was screened by differential hybridization with forward (“relapse minus remission”) and reverse (“remission minus relapse”) subtractive cDNAs probes, as well as unsubtracted probes from relapse and remission, and irrelevant nephrotic syndrome (membranous nephropathy). A total of 84 transcripts were isolated, of which 12 matched proteins of unknown function and 30 were unknown clones. Among the 42 known transcripts, at least 18 are closely involved in the T cell receptor-mediated complex signaling cascade, including genes encoding components of the T cell receptor and proteins associated with the cytoskeletal scaffold, as well as transcription factors. In particular, it was demonstrated that the expression levels of Fyb/Slap, L-plastin, and grancalcin were increased during relapse, suggesting that the integration of proximal signaling after T cell engagement involves the preferential recruitment of these cytoskeleton-associated proteins in MCNS. Because very low levels of interleukin-12 receptor β2 mRNA were detected in relapse samples, the interleukin-12 signaling pathway might be defective, suggesting that, in MCNS, T cell activation evolves toward a T helper 2 phenotype. Therefore, the combination of subtractive cloning and differential screening constitutes an efficient approach to the identification of genes that are likely to be involved in the pathophysiologic processes of MCNS.

Sign in / Sign up

Export Citation Format

Share Document