Evidence map›Paper›PMID 32792490›Full record

ReviewNature reviews. Disease primers2020

Podocytopathies.

Jeffrey B Kopp, Hans-Joachim Anders, Katalin Susztak, Manuel A Podestà, Giuseppe Remuzzi, Friedhelm Hildebrandt, Paola Romagnani

Open access · bronzeAbstract readReview
In one paragraph

Review in Nature reviews. Disease primers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 340 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
340citing papers in PubMed, 5 pooled it
33.6field-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

340 citing papers in PubMed, 5 syntheses or guidelines pooled it, 522 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Article
  7. Article
  8. Review
  9. New therapeutic hope for rare podocytopathies.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Proteinuria in adolescence.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  19. Review
  20. Article

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

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

7 authors at 7 institutions in 3 countries.

Jeffrey B KoppKidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH, Bethesda, MD, USA.
Hans-Joachim AndersDivision of Nephrology, Department of Medicine IV, University Hospital, LMU Munich, Munich, Germany.
Katalin SusztakDepartment of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Manuel A PodestàDepartment of Health Sciences, Università degli Studi di Milano, Milan, Italy.
Giuseppe RemuzziIstituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.
Friedhelm HildebrandtDivision of Pediatric Nephrology, Boston Children's Hospital, Boston, MA, USA.
Paola RomagnaniDepartment of Clinical and Experimental Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy. paola.romagnani@unifi.it.
Boston Children's Hospital · USLMU Klinikum · DEMario Negri Institute for Pharmacological Research · ITNational Institute of Diabetes and Digestive and Kidney Diseases · USUniversity of Florence · ITUniversity of Milan · ITUniversity of Pennsylvania · US

Funding

Focal Segmental Glomerulosclerosis: Genetics & MechanismsZIADK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$15.7M
Role of the Notch Pathway in Kidney InjuryR01DK076077 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2007 to 2026
$8.0M
Focal segmental glomerulosclerosis: TreatmentZIADK043412 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$7.4M
Focal segmental glomerulosclerosis: HIV-associated nephropathyZIADK043411 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HEYMANN, JURGEN · 2009 to 2024
$7.3M
Epigenetics of Chronic Kidney DiseaseR01DK087635 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2009 to 2026
$7.0M
Identification and function of new genes causing childhood nephrotic syndromeR01DK076683 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HILDEBRANDT, FRIEDHELM · 2007 to 2021
$5.3M
APOL1 associated kidney diseaseR01DK105821 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SUSZTAK, KATALIN · 2016 to 2024
$4.6M
Epigenetic drivers and biomarkers of diabetic kidney diseaseDP3DK108220 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SUSZTAK, KATALIN · 2015 to 2015
$2.4M
FOCAL SEGMENTAL GLOMERULOSCLEROSIS--PATHOGENESIS AND TREATMENTZ01DK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 1997 to 2008
$1.0M
Intramural NIH HHS Z01 DK043308NIDDK NIH HHS DP3 DK108220NIDDK NIH HHS R01 DK076077NIDDK NIH HHS R01 DK076683NIDDK NIH HHS R01 DK087635NIDDK NIH HHS R01 DK105821
6 · The paper itself

Abstract

Podocytopathies are kidney diseases in which direct or indirect podocyte injury drives proteinuria or nephrotic syndrome. In children and young adults, genetic variants in >50 podocyte-expressed genes, syndromal non-podocyte-specific genes and phenocopies with other underlying genetic abnormalities cause podocytopathies associated with steroid-resistant nephrotic syndrome or severe proteinuria. A variety of genetic variants likely contribute to disease development. Among genes with non-Mendelian inheritance, variants in APOL1 have the largest effect size. In addition to genetic variants, environmental triggers such as immune-related, infection-related, toxic and haemodynamic factors and obesity are also important causes of podocyte injury and frequently combine to cause various degrees of proteinuria in children and adults. Typical manifestations on kidney biopsy are minimal change lesions and focal segmental glomerulosclerosis lesions. Standard treatment for primary podocytopathies manifesting with focal segmental glomerulosclerosis lesions includes glucocorticoids and other immunosuppressive drugs; individuals not responding with a resolution of proteinuria have a poor renal prognosis. Renin-angiotensin system antagonists help to control proteinuria and slow the progression of fibrosis. Symptomatic management may include the use of diuretics, statins, infection prophylaxis and anticoagulation. This Primer discusses a shift in paradigm from patient stratification based on kidney biopsy findings towards personalized management based on clinical, morphological and genetic data as well as pathophysiological understanding.

Indexed as

HumansKidneyNephrotic SyndromePodocytesPrevalenceProteinuria

Identifiers

PMID32792490
PMCPMC8162925
OpenAlexW4211122976

What OpenQuestion holds

Textmetadata
LicenceTDM
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.