ReviewPediatric nephrology (Berlin, Germany)1996
Focal segmental glomerulosclerosis.
Review in Pediatric nephrology (Berlin, Germany), 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed.
- Novel therapy of focal glomerulosclerosis with mycophenolate and angiotensin blockade.Pediatric nephrology (Berlin, Germany) · 2003Trial
- Pulse cyclophosphamide therapy for steroid-resistant focal segmental glomerulosclerosis in children.Annals of Saudi medicineTrial
- Focal Segmental Glomerulosclerosis: Comprehensive Review and Exploration of the Dual Potential of Cyclodextrins in Therapeutic Optimization.International journal of molecular sciences · 2025Review
- To biopsy or not to biopsy a teenager with idiopathic nephrotic syndrome? Biopsy first.Pediatric nephrology (Berlin, Germany) · 2025Article
- The FSGS protein actinin-4 interacts with NKCC2 to regulate thick ascending limb NaCl reabsorption.American journal of physiology. Renal physiology · 2024Article
- Renal tubular gen e biomarkers identification based on immune infiltrates in focal segmental glomerulosclerosis.Renal failure · 2022Article
- Growth hormone induces mitotic catastrophe of glomerular podocytes and contributes to proteinuria.Cell death & disease · 2021Article
- The role of alpha-actinin-4 in human kidney disease.Cell & bioscience · 2015Article
- Article
- Frequency and clinicopathological correlations of histopathological variants of pediatric idiopathic focal segmental glomerulosclerosis.Indian journal of nephrology · 2014Article
- The increasing incidence of initial steroid resistance in childhood nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2012Article
- In vivo, label-free, three-dimensional quantitative imaging of kidney microcirculation using Doppler optical coherence tomography.Laboratory investigation; a journal of technical methods and pathology · 2011Article
- Clinical value of NPHS2 analysis in early- and adult-onset steroid-resistant nephrotic syndrome.Clinical journal of the American Society of Nephrology : CJASN · 2011Article
- A conceptual framework for the molecular pathogenesis of progressive kidney disease.Pediatric nephrology (Berlin, Germany) · 2010Review
- A novel TRPC6 mutation that causes childhood FSGS.PloS one · 2009Article
- Expression of JAKs/STATs pathway molecules in rat model of rapid focal segmental glomerulosclerosis.Pediatric nephrology (Berlin, Germany) · 2009Article
- Complete remission of nephrotic syndrome in an infant with focal segmental glomerulosclerosis: is it renin-angiotensin blockade?Pediatric nephrology (Berlin, Germany) · 2009Article
- Steroid-resistant nephrotic syndrome: the influence of race on cyclophosphamide sensitivity.Pediatric nephrology (Berlin, Germany) · 2006Article
- Predictive factors of chronic kidney disease in primary focal segmental glomerulosclerosis.Pediatric nephrology (Berlin, Germany) · 2006Article
- Paraoxonase 1 192 and 55 polymorphisms in nephrotic children.Pediatric nephrology (Berlin, Germany) · 2006Article
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2 authors.
Funding
Abstract
Over the last 2 decades, we have learnt that focal segmental glomerulosclerosis (FSGS) is a ubiquitous phenomenon underlying the progressive deterioration of many different types of renal diseases in both pediatric and adult populations. FSGS may also be the primary renal lesion, whether in new disease entities such as glycogen storage disease and human immunodeficiency virus infection, or in idiopathic FSGS. Although the mechanism which triggers the development of primary FSGS still remains unknown, laboratory and clinical studies have identified several key pathophysiological events leading to end-stage renal disease. While therapeutic modalities have not changed remarkably, a recent study, although uncontrolled, demonstrated an impressive efficacy of intravenous steroid pulse therapy in inducing remission. Nevertheless, it remains largely unknown whether such a forced remission decreases the overall risk of developing chronic renal failure. Studies have revealed an important pathophysiological role of angiotensin and the therapeutic efficacy of angiotensin converting enzyme inhibitors in progressive loss of renal function in diseases where glomerulosclerosis is secondary; however, it remains to be verified whether these results hold true in primary FSGS. As a result of the improvement in allograft survival rate, the benefit of renal transplant outweighs the risk of recurrence of FSGS, hence transplantation continues to be a vital therapy for FSGS patients who have reached renal failure. Thus, FSGS is not one disease, but rather a range of lesions seen in many settings. The type of lesions and the patient's unique genetic factors contribute to prognosis, and also may dictate choice of optimum therapy.
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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.