ReviewPediatric nephrology (Berlin, Germany)2017
Mechanical challenges to the glomerular filtration barrier: adaptations and pathway to sclerosis.
Review in Pediatric nephrology (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 83 citations in OpenAlex.
- Mechanisms of Podocyte Injury in Kidney Allografts.Kidney360 · 2026Review
- Elevated Piezo levels cause structural and functional alterations inLife science alliance · 2026Article
- Article
- Clinicopathological and prognostic study of idiopathic membranous nephropathy with tip or non-tip variant focal segmental glomerulosclerosis: a single-center cohort study.Renal failure · 2025Article
- TRPC6 effects on albumin permeation, nephrin shedding, and apoptosis in podocytes: Role of calcineurin and metalloproteases.Physiological reports · 2025Article
- Mechanical Stress and Protective Mechanisms in Podocytes: Insights into Hypertensive Nephropathy.International journal of molecular sciences · 2025Review
- Engineered 3D Kidney Glomerular Microtissues to Model Podocyte-Centric Diseases for the Validation of New Drug Targets.Advanced healthcare materials · 2025Article
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- Piezo1, F-Actin Remodeling, and Podocyte Survival and Regeneration.Journal of the American Society of Nephrology : JASN · 2025Article
- Purinergic Receptor Activation Protects Glomerular Microvasculature from Increased Mechanical Stress in Angiotensin II-Induced Hypertension: A Modeling Study.International journal of molecular sciences · 2025Article
- Application of SGLT-2 inhibitors in non-diabetic CKD: mechanisms, efficacy, and safety.Frontiers in medicine · 2025Review
- Pathogenesis of Focal Segmental Glomerulosclerosis and Related Disorders.Annual review of pathology · 2025Review
- Case Report: Atypical anti-GBM nephritis coexisting with Henoch-Schönlein purpura nephritis: exploring the pathogenic nexus.Frontiers in immunology · 2025Article
- Epigenetics of Hypertensive Nephropathy.Biomedicines · 2024Review
- Piezo activity levels need to be tightly regulated to maintain normal morphology and function in pericardial nephrocytes.Scientific reports · 2024Article
- Pharmacological Blockade of the Adenosine ACells · 2024Article
- Modeling the interaction between tubuloglomerular feedback and myogenic mechanisms in the control of glomerular mechanics.Frontiers in physiology · 2024Article
- Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- A Patient with Acute Kidney Injury Associated with Massive Proteinuria and Acute Hyperuricemia after Epileptic Seizures.Internal medicine (Tokyo, Japan) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocytes are lost as viable cells by detachment from the glomerular basement membrane (GBM), possibly due to factors such as pressure and filtrate flow. Distension of glomerular capillaries in response to increased pressure is limited by the elastic resistance of the GBM. The endothelium and podocytes adapt to changes in GBM area. The slit diaphragm (SD) seems to adjust by shuttling SD components between the SD and the adjacent foot processes (FPs), resulting in changes in SD area that parallel those in perfusion pressure.Filtrate flow tends to drag podocytes towards the urinary orifice by shear forces, which are highest within the filtration slits. The SD represents an atypical adherens junction, mechanically interconnecting the cytoskeleton of opposing FPs and tending to balance the shear forces.If under pathological conditions, increased filtrate flows locally overtax the attachment of FPs, the SDs are replaced by occluding junctions that seal the slits and the attachment of podocytes to the GBM is reinforced by FP effacement. Failure of these temporary adaptive mechanisms results in a steady process of podocyte detachment due to uncontrolled filtrate flows through bare areas of the GBM and, subsequently, the labyrinthine subpodocyte spaces, presenting as pseudocysts. In our view, shear stress due to filtrate flow-not capillary hydrostatic pressure-is the major challenge to the attachment of podocytes to the GBM.
Indexed as
Identifiers
What OpenQuestion holds
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.