Evidence map›Paper›PMID 30567514›Full record

Observational studyBMC nephrology2018

Association of plasma somatostatin with disease severity and progression in patients with autosomal dominant polycystic kidney disease.

A Lianne Messchendorp, Edwin M Spithoven, Niek F Casteleijn, Wendy A Dam, Jacob van den Born, Wouter F Tonnis, Carlo A J M Gaillard, Esther Meijer, DIPAK Consortium

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in BMC nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 23% 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, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  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

9 authors at 3 institutions in 1 country.

A Lianne MesschendorpDepartment of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. a.l.messchendorp@umcg.nl.
Edwin M SpithovenDepartment of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Niek F CasteleijnDepartment of Urology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Wendy A DamDepartment of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Jacob van den BornDepartment of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Wouter F TonnisDepartment of Pharmaceutical Technology and Biopharmacy, University of Groningen, Groningen, The Netherlands.
Carlo A J M GaillardDivision of Internal Medicine and Dermatology, University Medical Center Utrecht, University of Utrecht, Utrecht, The Netherlands.
Esther MeijerDepartment of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
DIPAK Consortium
University of Groningen · NLUniversity Medical Center Groningen · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSomatostatin (SST) inhibits intracellular cyclic adenosine monophosphate (cAMP) production and thus may modify cyst formation in autosomal dominant polycystic kidney disease (ADPKD). We investigated whether endogenous plasma SST concentration is associated with disease severity and progression in patients with ADPKD, and whether plasma SST concentrations change during treatment with a vasopressin V2 receptor antagonist or SST analogue.

methodsIn this observational study, fasting concentrations of SST were measured in 127 ADPKD patients (diagnosed upon the revised Ravine criteria) by ELISA. cAMP was measured in 24 h urine by Radio Immuno Assay. Kidney function was measured (mGFR) as

resultsIn 127 ADPKD patients, 41 ± 11 years, 44% female, eGFR 73 ± 32 ml/min/1.73m

conclusionsFasting plasma SST concentration is not associated with disease severity or progression in patients with ADPKD. Treatment with lanreotide caused a decrease in SST concentration. These data suggest that plasma SST cannot be used as a biomarker to assess prognosis in ADPKD, but leave the possibility open that change in SST concentration during lanreotide treatment may reflect therapy efficacy.

Indexed as

AdultAntidiuretic Hormone Receptor AntagonistsAntineoplastic AgentsCyclic AMPDisease ProgressionFastingFemaleGlomerular Filtration RateHumansKidneyMagnetic Resonance ImagingMaleMiddle AgedOrgan SizePeptides, CyclicPolycystic Kidney, Autosomal DominantAntidiuretic Hormone Receptor AntagonistsAntineoplastic AgentsCyclic AMPlanreotidePeptides, CyclicSomatostatinTolvaptanADPKDBiomarkercAMPDisease progressionSomatostatin

Identifiers

PMID30567514
PMCPMC6299932
OpenAlexW2905402457

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.