ReviewJournal of clinical medicine2022
Biomarkers in Primary Focal Segmental Glomerulosclerosis in Optimal Diagnostic-Therapeutic Strategy.
Review in Journal of clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Multi-Modal, Machine Learning-Driven Framework Integrating Multi-Omics for Personalized Chronic Kidney Disease Management.Journal of clinical medicine · 2026Review
- Living Donor Kidney Transplantation in High-Recurrence Kidney Diseases: Precision Risk Stratification and Management.Kidney international reports · 2026Review
- Trehalose alleviates nephropathy in focal segmental glomerulosclerosis via the upregulation of the WT-1/EZH2 pathway.Frontiers in pharmacology · 2025Article
- Post-transplant glomerular diseases: update on pathophysiology, risk factors and management strategies.Clinical kidney journal · 2024Review
- Identification of Genes Associated with Familial Focal Segmental Glomerulosclerosis Through Transcriptomics and In Silico Analysis, IncludingInternational journal of molecular sciences · 2024Article
- Potential biomarkers of recurrent FSGS: a review.BMC nephrology · 2024Review
- Urinary biomarkers associated with podocyte injury in lupus nephritis.Frontiers in pharmacology · 2024Review
- Evaluation of glomerular sirtuin-1 and claudin-1 in the pathophysiology of nondiabetic focal segmental glomerulosclerosis.Scientific reports · 2023Article
- Therapeutic Potential Targeting Podocyte Mitochondrial Dysfunction in Focal Segmental Glomerulosclerosis.Kidney diseases (Basel, Switzerland) · 2023Review
- The most common founder pathogenic variant c.868G > A (p.Val290Met) in theFrontiers in medicine · 2023Article
- A randomized controlled trial of preemptive rituximab to prevent recurrent focal segmental glomerulosclerosis post-kidney transplant (PRI-VENT FSGS): protocol and study design.Frontiers in nephrology · 2023Article
- The Potential Applications of Raman Spectroscopy in Kidney Diseases.Journal of personalized medicine · 2022Review
- Recurrence of focal segmental glomerulosclerosis: An updated review of pathophysiology, biomarkers, and therapeutic strategies.Cell transplantationReview
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Focal segmental glomerulosclerosis (FSGS) involves podocyte injury. In patients with nephrotic syndrome, progression to end-stage renal disease often occurs over the course of 5 to 10 years. The diagnosis is based on a renal biopsy. It is presumed that primary FSGS is caused by an unknown plasma factor that might be responsible for the recurrence of FSGS after kidney transplantation. The nature of circulating permeability factors is not explained and particular biological molecules responsible for inducing FSGS are still unknown. Several substances have been proposed as potential circulating factors such as soluble urokinase-type plasminogen activator receptor (suPAR) and cardiolipin-like-cytokine 1 (CLC-1). Many studies have also attempted to establish which molecules are related to podocyte injury in the pathogenesis of FSGS such as plasminogen activator inhibitor type-1 (PAI-1), angiotensin II type 1 receptors (AT1R), dystroglycan(DG), microRNAs, metalloproteinases (MMPs), forkheadbox P3 (FOXP3), and poly-ADP-ribose polymerase-1 (PARP1). Some biomarkers have also been studied in the context of kidney tissue damage progression: transforming growth factor-beta (TGF-β), human neutrophil gelatinase-associated lipocalin (NGAL), malondialdehyde (MDA), and others. This paper describes molecules that could potentially be considered as circulating factors causing primary FSGS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.