ReviewSeminars in immunopathology2007
Minimal change nephropathy and focal segmental glomerulosclerosis.
Review in Seminars in immunopathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 62 citations in OpenAlex.
- Article
- Scaffold protein SH3BP2 signalosome is pivotal for immune activation in nephrotic syndrome.JCI insight · 2024Article
- New Insights into the Treatment of Glomerular Diseases: When Mechanisms Become Vivid.International journal of molecular sciences · 2022Review
- An elderly-onset neuroblastoma concomitant with minimal change nephrotic syndrome: the first autopsy case report.CEN case reports · 2021Article
- Interleukin-18 binding protein attenuates renal injury of adriamycin-induced mouse nephropathy.International journal of clinical and experimental pathology · 2019Article
- Article
- The level of urinary semaphorin3A is associated with disease activity in patients with minimal change nephrotic syndrome.International journal of nephrology and renovascular disease · 2017Article
- Cell biology and genetics of minimal change disease.F1000Research · 2016Review
- IQGAP1 regulates actin cytoskeleton organization in podocytes through interaction with nephrin.Cellular signalling · 2015Article
- Rapid progression to end-stage renal disease in a child with a sporadic ACTN4 mutation.Clinical nephrology. Case studies · 2015Article
- Minimal change nephrotic syndrome associated with non-Hodgkin lymphoid disorders: a retrospective study of 18 cases.Medicine · 2014Article
- Immunopathogenesis of idiopathic nephrotic syndrome with relapse.Seminars in immunopathology · 2014Review
- Actin-associated Proteins in the Pathogenesis of Podocyte Injury.Current genomics · 2013Article
- Our experience with rituximab therapy for adult-onset primary glomerulonephritis and review of literature.International urology and nephrology · 2013Review
- LPS and PAN-induced podocyte injury in an in vitro model of minimal change disease: changes in TLR profile.Journal of cell communication and signaling · 2013Article
- Upregulation of nuclear factor-related kappa B suggests a disorder of transcriptional regulation in minimal change nephrotic syndrome.PloS one · 2012Article
- Mycophenolate mofetil (MMF) treatment efficacy in children with primary and secondary glomerulonephritis.Archives of medical science : AMS · 2011Article
- Induction of podocyte-derived VEGF ameliorates podocyte injury and subsequent abnormal glomerular development caused by puromycin aminonucleoside.Pediatric research · 2011Article
- Minimal change disease as a modifiable podocyte paracrine disorder.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2011Review
- Safe administration of celecoxib to a patient with repeated episodes of nephrotic syndrome induced by NSAIDs.Clinical drug investigation · 2011Article
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
The terms minimal change nephropathy and focal segmental glomerulosclerosis describe histopathological entities diagnosed by renal biopsy, typically in patients presenting with heavy proteinuria and its consequences including nephrotic syndrome. Numerous alterations in the immune response have been reported, but there is uncertainty about whether these play a causal role. In both conditions, there is evidence of injury to glomerular epithelial cells (podocytes), a cell type with limited potential for repair or replacement. The mechanisms of injury are poorly understood but may include immunologically mediated processes such as the effects of soluble mediators produced by lymphocytes. Empirical immunosuppressive therapy with corticosteroids, alkylating agents, and/or calcineurin antagonists is often effective, but the potential for toxicity of these drugs is enormous, and more specific forms of treatment are needed. The focus in recent years has been on the podocyte, and in particular the potential importance of mutations/polymorphisms in podocyte-specific genes as predisposing factors, mechanisms of podocyte injury including study of the role of podocytes as active participants in disease pathogenesis, indices of podocyte injury as markers of disease activity or possible diagnostic tools, and strategies for podocyte repair including the recognition that existing therapies may have effects (beneficial or adverse) on podocytes. Future improvements in the understanding of these diseases and in our ability to successfully treat them can be confidently expected as a result of rapid advances in the study of podocyte biology in health and disease.
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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.