Evidence map›Paper›PMID 21183621›Full record

ArticleMolecular & cellular proteomics : MCP2011

Protein microarrays discover angiotensinogen and PRKRIP1 as novel targets for autoantibodies in chronic renal disease.

Atul J Butte, Tara K Sigdel, Persis P Wadia, David B Miklos, Minnie M Sarwal

Abstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Review
  2. Review
  3. Developments and Applications of Functional Protein Microarrays.Molecular & cellular proteomics : MCP · 2020
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Applications of translational bioinformatics in transplantation.Clinical pharmacology and therapeutics · 2011
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Atul J ButteDepartment of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA. abutte@stanford.edu
Tara K Sigdel
Persis P Wadia
David B Miklos
Minnie M Sarwal

Funding

TUMOR SPECIFIC CYTOTOXIC T-LYMPHOCYTES IN BONE MARROW TRANSPLANTATIONP01CA049605 · NCI · STANFORD UNIVERSITY · PI David B. Miklos · 1989 to 2026
$73.3M
MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Repositioning drugs for the treatment of small cell lung cancerR01GM079719 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BUTTE, ATUL J · 2006 to 2015
$4.4M
Defining Biomarkers in Pediatric Renal TransplantationR01AI061739 · NIAID · STANFORD UNIVERSITY · PI SARWAL, MINNIE M · 2004 to 2007
$1.6M
NCI NIH HHS P01 CA049605NIAID NIH HHS R01 AI061739NIAID NIH HHS T32 AI007290NIGMS NIH HHS R01 GM079719
6 · The paper itself

Abstract

Biomarkers for early detection of chronic kidney disease are needed, as millions of patients suffer from chronic diseases predisposing them to kidney failure. Protein microarrays may also hold utility in the discovery of auto-antibodies in other conditions not commonly considered auto-immune diseases. We hypothesized that proteins are released as a consequence of damage at a cellular level during end-organ damage from renal injury, not otherwise recognized as self-antigens, and an adaptive humoral immune response to these proteins might be detected in the blood, as a noninvasive tracker of this injury. The resultant antibodies (Ab) detected in the blood would serve as effective biomarkers for occult renal injury, enabling earlier clinical detection of chronic kidney disease than currently possible, because of the redundancy of the serum creatinine as a biomarker for early kidney injury. To screen for novel autoantibodies in chronic kidney disease, 24 protein microarrays were used to compare serum Ab from patients with chronic kidney disease against matched controls. From a panel of 38 antigens with increased Ab binding, four were validated in 71 individuals, with (n=50) and without (n=21) renal insufficiency. Significant elevations in the titer of novel auto-Ab were noted against angiotensinogen and PRKRIP1 in renal insufficiency. Current validation is underway to evaluate if these auto-Ab can provide means to follow the evolution of chronic kidney disease in patients with early stages of renal insufficiency, and if these rising titers of these auto-Ab correlate with the rate of progression of chronic kidney disease.

Indexed as

Amino Acid MotifsAmino Acid SequenceAngiotensinogenAnimalsAutoantibodiesCell DifferentiationEmbryonic Stem CellsHumansKidney Failure, ChronicMiceMolecular Sequence DataPhosphopeptidesPhosphoproteinsPhosphorylationProtein Array AnalysisProteomeAngiotensinogenAutoantibodiesPhosphopeptidesPhosphoproteinsPrkrip1 protein, mouseProteomeRNA-Binding Proteins

Identifiers

PMID21183621
PMCPMC3047141

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Registered trials

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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.