Evidence map›Paper›PMID 36751492›Full record

ReviewGlomerular diseases2021

Hereditary Nephritis and Thin Glomerular Basement Membrane Lesion.

Mark A Lusco, Agnes B Fogo

Open access · goldAbstract readReview
In one paragraph

Review in Glomerular diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Genetic kidney disease in adults-the pathologists' perspective.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Pathological diagnosis of Alport syndrome.Kidney research and clinical practice · 2025
    Article
  6. Article
  7. 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

2 authors at 1 institution in 1 country.

Mark A LuscoDepartment of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Agnes B FogoDepartment of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Vanderbilt University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hereditary nephritis (HN) and thin glomerular basement membrane (GBM) lesion share a common clinical presentation of persistent hematuria, thin GBM by kidney biopsy electron microscopic examination, and a mutation in type IV collagen. However, the clinical course and treatment for these entities are different with varying patterns of heredity. Ultrastructural examination of a renal biopsy specimen is essential for the morphologic diagnosis of HN and thin GBM lesion, whereas light microscopy may only give limited diagnostic clues. Additional workup including immunostaining for subtypes of type IV collagen may provide further information on underlying genetic mutations. The diagnosis of HN may lead to treatment with renin-angiotensin system blockade in patients at risk of early-onset renal failure to delay progression to end-stage renal disease. Additionally, patients with isolated microscopic hematuria and thin GBM lesion are at increased risk for chronic kidney disease when associated with other comorbidities; those patients should receive regular clinical assessment to prevent renal function decline.

Indexed as

Alport syndromeHereditary nephritisThin glomerular basement membraneType IV collagen

Identifiers

PMID36751492
PMCPMC9677744
OpenAlexW3169901111

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.