ArticleInflammation2011
The effects of inflammation on lipid accumulation in the kidneys of children with primary nephrotic syndrome.
Article in Inflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Systemic inflammation accelerates the development of focal segmental glomerulosclerosis in a mouse model of adriamycin induced nephrosis.Scientific reports · 2025Article
- P2X7R antagonist protects against renal injury in mice with adriamycin nephropathy.Experimental and therapeutic medicine · 2022Article
- The risk factors for children with primary nephrotic syndrome: a systematic review and meta-analysis.Translational pediatrics · 2021Article
- Renal involvement in a patient with the chronic visceral subtype of acid sphingomyelinase deficiency resembles Fabry disease.JIMD reports · 2021Article
- Inflammation Induces Lipid Deposition in Kidneys by Downregulating Renal PCSK9 in Mice with Adriamycin-Induced Nephropathy.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- CD36 Promotes Podocyte Apoptosis by Activating the Pyrin Domain-Containing-3 (NLRP3) Inflammasome in Primary Nephrotic Syndrome.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Calcitriol Prevents Cardiovascular Repercussions in Puromycin Aminonucleoside-Induced Nephrotic Syndrome.BioMed research international · 2018Article
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Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to characterize the relationship between inflammation and lipid accumulation in children with primary nephrotic syndrome (PNS). Local expression of interleukin-1β (IL-1β), transforming growth factor-β1 (TGF-β1), low-density lipoprotein receptor (LDLr), sterol regulatory element binding protein-2 (SREBP-2), SREBP cleavage-activating protein (SCAP), and apolipoprotein B100 (apoB100) was analyzed by immunohistochemistry in kidney tissues obtained from children with PNS. Renal histopathology was evaluated by hematoxylin and eosin and periodic acid-Schiff staining. Serum levels of IL-1β and TGF-β1 were measured by enzyme-linked immunosorbent assays. Expression of IL-1β, TGF-β1, LDLr, SREBP-2, SCAP, and apoB100 was higher in samples from patients with non-minimal change necrotic syndrome (NMCNS) compared to both controls and patients with minimal change necrotic syndrome. Deposition of apoB100 was significantly correlated with expression of IL-1β, TGF-β1, LDLr, SREBP-2, and SCAP and with the glomerulosclerosis index, but not with plasma lipid levels. Expression of IL-1β and TGF-β1 was significantly correlated with expression of LDLr, SREBP-2, and SCAP. These findings suggest that inflammation leads to lipid accumulation in the kidney through disruption of the expression of proteins in the SCAP/SREBP-2/LDLr signaling pathway, which may underlie glomerulosclerosis and tubulointerstitial fibrosis in NMCNS.
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Registered trials
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