Evidence map›Paper›PMID 28596971›Full record

ReviewJournal of diabetes research2017

Soluble Urokinase Receptor and the Kidney Response in Diabetes Mellitus.

Ranadheer R Dande, Vasil Peev, Mehmet M Altintas, Jochen Reiser

Open access · goldAbstract readReview
In one paragraph

Review in Journal of diabetes research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  13. Soluble urokinase-type plasminogen activator receptor and incident end-stage renal disease in Chinese patients with chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020
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  19. Increased soluble urokinase plasminogen activator receptor (suPAR) levels in neovascular age-related macular degeneration: a role for inflammation in the pathogenesis of the disease?Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019
    Article
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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

4 authors at 1 institution in 1 country.

Ranadheer R DandeRush University Medical Center, Chicago, IL, USA.
Vasil PeevRush University Medical Center, Chicago, IL, USA.
Mehmet M AltintasRush University Medical Center, Chicago, IL, USA.ORCID 0000-0002-1871-6985
Jochen ReiserRush University Medical Center, Chicago, IL, USA.ORCID 0000-0002-0460-662X
Rush University Medical Center · US

Funding

Role of Circulating suPAR in FSGSR01DK101350 · NIDDK · RUSH UNIVERSITY MEDICAL CENTER · PI REISER, JOCHEN · 2013 to 2017
$2.6M
A Humanized Mouse Model of FSGSR01DK106051 · NIDDK · RUSH UNIVERSITY MEDICAL CENTER · PI REISER, JOCHEN · 2015 to 2017
$628k
NIDDK NIH HHS R01 DK101350NIDDK NIH HHS R01 DK106051
6 · The paper itself

Abstract

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease (ESRD) worldwide. DN typically manifests by glomerular hyperfiltration and microalbuminuria; then, the disease progresses to impaired glomerular filtration rate, which leads to ESRD. Treatment options for DN include the strict control of blood glucose levels and pressure (e.g., intraglomerular hypertension). However, the search for novel therapeutic strategies is ongoing. These include seeking specific molecules that contribute to the development and progression of DN to potentially interfere with these "molecular targets" as well as with the cellular targets within the kidney such as podocytes, which play a major role in the pathogenesis of DN. Recently, podocyte membrane protein urokinase receptor (uPAR) and its circulating form (suPAR) are found to be significantly induced in glomeruli and sera of DN patients, respectively, and elevated suPAR levels predicted diabetic kidney disease years before the occurrence of microalbuminuria. The intent of this review is to summarize the emerging evidence of uPAR and suPAR in the clinical manifestations of DN. The identification of specific pathways that govern DN will help us build a more comprehensive molecular model for the pathogenesis of the disease that can inform new opportunities for treatment.

Indexed as

AlbuminuriaAnimalsDiabetes MellitusDiabetic NephropathiesDisease ProgressionGlomerular Filtration RateHumansHypertensionIntegrinsKidney Failure, ChronicKidney GlomerulusModels, BiologicalPodocytesReceptors, Urokinase Plasminogen ActivatorSignal TransductionIntegrinsReceptors, Urokinase Plasminogen Activator

Identifiers

PMID28596971
PMCPMC5449757
OpenAlexW2616810535

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.