ArticleClinical proteomics2017
Potential urine proteomics biomarkers for primary nephrotic syndrome.
Article in Clinical proteomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 40 citations in OpenAlex.
- Immune dysregulation in pediatric cancer-associated nephrotic syndrome: current insights.Pediatric nephrology (Berlin, Germany) · 2026Review
- Dental caries prevention as a modifiable precipitating factor of nephrotic syndrome relapse in children: an insight into simple-novel management.International urology and nephrology · 2025Article
- The Spectrum of Minimal Change Disease/Focal Segmental Glomerulosclerosis: From Pathogenesis to Proteomic Biomarker Research.International journal of molecular sciences · 2025Review
- Integrating bioinformatics and metabolomics to identify potential biomarkers of hypertensive nephropathy.Scientific reports · 2025Article
- Urinary Proteomic Shifts over Time and Their Associations with eGFR Decline in Chronic Kidney Disease.Biomolecules · 2025Article
- Hemoglobin-associatedFrontiers in medicine · 2025Article
- Proteomic analysis of laser captured tubular tissues reveals complement activation and mitochondrial dysfunction in autoimmune related kidney diseases.Scientific reports · 2024Article
- Candidate protein biomarkers in chronic kidney disease: a proteomics study.Scientific reports · 2024Article
- Minimal Change Disease: Pathogenetic Insights from Glomerular Proteomics.International journal of molecular sciences · 2024Article
- Urinary proteomics reveals biological processes related to acute kidney injury in Bothrops atrox envenomings.PLoS neglected tropical diseases · 2024Article
- Urinary SPP1 has potential as a non-invasive diagnostic marker for focal segmental glomerulosclerosis.FEBS open bio · 2023Article
- Detection of N‑glycoprotein associated with IgA nephropathy in urine as a potential diagnostic biomarker using glycosylated proteomic analysis.Experimental and therapeutic medicine · 2023Article
- Exploratory Study Analyzing the Urinary Peptidome of T2DM Patients Suggests Changes in ECM but Also Inflammatory and Metabolic Pathways Following GLP-1R Agonist Treatment.International journal of molecular sciences · 2023Article
- Towards the Definition of the Molecular Hallmarks of Idiopathic Membranous Nephropathy in Serum Proteome: A DIA-PASEF Approach.International journal of molecular sciences · 2023Article
- CD44 Expression in Renal Tissue Is Associated with an Increase in Urinary Levels of Complement Components in Chronic Glomerulopathies.International journal of molecular sciences · 2023Article
- Targeted MRM Quantification of Urinary Proteins in Chronic Kidney Disease Caused by Glomerulopathies.Molecules (Basel, Switzerland) · 2023Article
- Advances in proteomic profiling of pediatric kidney diseases.Pediatric nephrology (Berlin, Germany) · 2022Review
- Serum Protein Signatures Using Aptamer-Based Proteomics for Minimal Change Disease and Membranous Nephropathy.Kidney international reports · 2022Article
- Urinary Protein and Peptide Markers in Chronic Kidney Disease.International journal of molecular sciences · 2021Review
- Circulating extracellular vesicles of patients with steroid-sensitive nephrotic syndrome have higher RAC1 and induce recapitulation of nephrotic syndrome phenotype in podocytes.American journal of physiology. Renal physiology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNephrotic syndrome (NS) is a nonspecific kidney disorder, commonly caused by minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), and membranous nephropathy (MN). Here we analyzed urinary protein profiles, aiming to discover disease-specific biomarkers of these three common diseases in NS.
methodsSixteen urine samples were collected from patients with biopsy-proven NS and healthy controls. After removal of high-abundance proteins, the urinary protein profile was analyzed by LC-MS/MS to generate a discovery set. For validation, ELISA was used to analyze the selected proteins in 61 urine samples.
resultsThe discovery set included 228 urine proteins, of which 22 proteins were differently expressed in MCD, MN, and FSGS. Among these, C9, CD14, and SERPINA1 were validated by ELISA. All three proteins were elevated in MCD, MN, and FSGS groups compared with in IgA nephropathy and healthy controls. When a regression model was applied, receiver operating characteristic analysis clearly discriminated MCD from the other causative diseases in NS.
conclusionsWe developed a disease-specific protein panel that discriminated between three main causes of NS. Through this pilot study, we suggest that urine proteomics could be a non-invasive and clinically available tool to discriminate MCD from MN and FSGS.
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.