ReviewFrontiers in pediatrics2016
Pathology of Podocytopathies Causing Nephrotic Syndrome in Children.
Review in Frontiers in pediatrics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- IgM nephropathy is a controversial entity: a distinct nephropathy or part of the podocytopathy spectrum? A systematic review of the literature.BMC nephrology · 2026Pooled it
- Anti-ANGPTL3 antibody and IL-22 fusion protein mitigate nephrotic syndrome via mitochondrial protection, anti-apoptosis, and autophagy suppression.Antibody therapeutics · 2026Article
- Nephrotic syndrome in children: A review.Medicine · 2026Review
- Perinatal Stroke and Cerebral Sinovenous Thrombosis Caused by Congenital Nephrotic Syndrome NPSH1 (Finnish Type): A Case Report.Neuropediatrics · 2025Article
- Immune Checkpoint Signatures in Minimal Change Disease and Membranous Nephropathy: Divergent Pathways of a Shared Imbalance.International journal of molecular sciences · 2025Article
- Review
- A Case Report of Giant Congenital Melanocytic Nevus Complicated by Minimal Change Disease, With Genetic Analysis.Clinical case reports · 2025Article
- Clinical Characteristics and Renal Outcomes in Patients with IgM Nephropathy: A Retrospective Single-Center Study.International journal of general medicine · 2025Article
- Differentiating primary and secondary FSGS using non-invasive urine biomarkers.Clinical kidney journal · 2024Article
- Urinary matrix metalloproteinase-7 is a sensitive biomarker to evaluate renal tubular injury in patients with minimal change disease and focal segmental glomerulosclerosis.Clinical kidney journal · 2024Article
- Primary Focal Segmental Glomerulosclerosis Plasmas Increase Lipid Droplet Formation and Perilipin-2 Expression in Human Podocytes.International journal of molecular sciences · 2022Article
- Anti-ANGPTL3-FLD monoclonal antibody treatment ameliorates podocyte lesions through attenuating mitochondrial damage.Cell death & disease · 2022Article
- MELAS syndrome with rare manifestations misdiagnosed as vasculitis in the absence of lactic acidosis: A case report.Annals of medicine and surgery (2012) · 2022Article
- CXCL16/ERK1/2 pathway regulates human podocytes growth, migration, apoptosis and epithelial mesenchymal transition.Molecular medicine reports · 2022Article
- Review
- Role of Arachidonic Acid and Its Metabolites in the Biological and Clinical Manifestations of Idiopathic Nephrotic Syndrome.International journal of molecular sciences · 2021Review
- oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.Molecular medicine reports · 2020Article
- CG/CA genotypes represent novel markers in theJournal of genetics · 2020Article
- Mitochondrial biogenesis induced by the β2-adrenergic receptor agonist formoterol accelerates podocyte recovery from glomerular injury.Kidney international · 2019Article
- Podocin and uPAR are good biomarkers in cases of Focal and segmental glomerulosclerosis in pediatric renal biopsies.PloS one · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nephrotic syndrome (NS) in children includes a diverse group of diseases that range from genetic diseases without any immunological defects to causes that are primarily due to immunological effects. Recent advances in molecular and genomic studies have resulted in a plethora of genetic defects that have been localized to the podocyte, the basic structure that is instrumental in normal filtration process. Although the disease can manifest from birth and into adulthood, the primary focus of this review would be to describe the novel genes and pathology of primary podocyte defects that cause NS in children. This review will restrict itself to the pathology of congenital NS, minimal change disease (MCD), and its variants and focal segmental glomerulosclerosis (FSGS). The two major types of congenital NS are Finnish type characterized by dilated sausage shaped tubules morphologically and diffuse mesangial sclerosis characterized by glomerulosclerosis. MCD has usually normal appearing biopsy features on light microscopy and needs electron microscopy for diagnosis, whereas FSGS in contrast has classic segmental sclerosing lesions identified in different portions of the glomeruli and tubular atrophy. This review summarizes the pathological characteristics of these conditions and also delves into the various genetic defects that have been described as the cause of these primary podocytopathies. Other secondary causes of NS in children, such as membranoproliferative and membranous glomerulonephritis, will not be covered in this review.
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