Evidence map›Paper›PMID 29703839›Full record

ReviewJournal of the American Society of Nephrology : JASN2018

The Complexity and Heterogeneity of Monoclonal Immunoglobulin-Associated Renal Diseases.

Sanjeev Sethi, S Vincent Rajkumar, Vivette D D'Agati

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
12.5field-weighted citation impact, top 1% of its field
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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

  1. Pooled it
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  18. Atypical Anti-Glomerular Basement Membrane Disease.Kidney international reports · 2023
    Review
  19. Article
  20. Article

13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Sanjeev SethiDepartment of Laboratory Medicine and Pathology and sethi.sanjeev@mayo.edu.
S Vincent RajkumarDivision of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota; and.
Vivette D D'AgatiDepartment of Pathology, College of Physicians and Surgeons, Columbia University, New York, New York.
Columbia University · USMayo Clinic · US

Funding

Project 4: Targeting Resistance to T-Cell Directed Therapy in Multiple MyelomaP50CA186781 · NCI · MAYO CLINIC ARIZONA · PI Rafael Fonseca · 2015 to 2026
$25.5M
NCI NIH HHS P50 CA186781
6 · The paper itself

Abstract

Monoclonal gammopathies are characterized by the overproduction of monoclonal Ig (MIg) detectable in the serum or urine resulting from a clonal proliferation of plasma cells or B lymphocytes. The underlying hematologic conditions range from malignant neoplasms of plasma cells or B lymphocytes, including multiple myeloma and B-cell lymphoproliferative disorders, to nonmalignant small clonal proliferations. The term MGUS implies presence of an MIg in the setting of a "benign" hematologic condition without renal or other end organ damage. The term MGRS was recently introduced to indicate monoclonal gammopathy with MIg-associated renal disease in the absence of hematologic malignancy. Most MIg-associated renal diseases result from the direct deposition of nephrotoxic MIg or its light- or heavy-chain fragments in various renal tissue compartments. Immunofluorescence microscopy is essential to identify the offending MIg and define its tissue distribution. Mass spectrometry is helpful in difficult cases. Conditions caused by direct tissue deposition of MIg include common disorders, such as cast nephropathy, amyloidosis, and MIg deposition diseases, as well as uncommon disorders, such as immunotactoid glomerulopathy, proliferative GN with MIg deposits, light-chain proximal tubulopathy, and the rare entities of crystal-storing histiocytosis and crystalglobulinemia. Indirect mechanisms of MIg-induced renal disease can cause C3 glomerulopathy or thrombotic microangiopathy without tissue MIg deposits. Treatment of MIg-associated renal disease is aimed at eliminating the clonal plasma cell or B-cell population as appropriate. Both the renal and the underlying hematologic disorders influence the management and prognosis of MIg-associated renal diseases.

Indexed as

AmyloidosisHumansImmunoglobulin Heavy ChainsImmunoglobulin Light ChainsKidney DiseasesKidney GlomerulusKidney TubulesLaser Capture MicrodissectionMass SpectrometryParaproteinemiasTerminology as TopicImmunoglobulin Heavy ChainsImmunoglobulin Light Chainskidney diseasemultiple myelomaRenal pathology

Identifiers

PMID29703839
PMCPMC6050917
OpenAlexW2802006033

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.