Evidence map›Paper›PMID 28963279›Full record

Observational studyBMJ open2017

Urine and serum midkine levels in an Australian chronic kidney disease clinic population: an observational study.

Victoria K Campbell, Chris M Anstey, Ryan P Gately, Drew C Comeau, Carolyn J Clark, Euan P Noble, Kumar Mahadevan, Peter R Hollett, Andrea J Pollock, Sharron T Hall and 3 more

Open access · goldAbstract readMulticenter StudyObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in BMJ open, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Midkine-A novel player in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  6. Review
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

13 authors at 2 institutions in 1 country.

Victoria K CampbellRenal Unit, Nambour General Hospital, Nambour, Australia.
Chris M AnsteySunshine Coast Clinical School, The University of Queensland, Nambour, Australia.
Ryan P GatelyRenal Unit, Nambour General Hospital, Nambour, Australia.
Drew C ComeauRenal Unit, Nambour General Hospital, Nambour, Australia.
Carolyn J ClarkRenal Unit, Nambour General Hospital, Nambour, Australia.
Euan P NobleRenal Unit, Nambour General Hospital, Nambour, Australia.
Kumar MahadevanRenal Unit, Nambour General Hospital, Nambour, Australia.
Peter R HollettRenal Unit, Nambour General Hospital, Nambour, Australia.
Andrea J PollockRenal Unit, Nambour General Hospital, Nambour, Australia.
Sharron T HallCellmid Ltd, Sydney, Australia.
Darren R JonesCellmid Ltd, Sydney, Australia.
Dominic BurgCellmid Ltd, Sydney, Australia.
Nicholas A GrayRenal Unit, Nambour General Hospital, Nambour, Australia.
Nambour General Hospital · AUUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesThe cytokine midkine (MK) is pathologically implicated in progressive chronic kidney disease (CKD) and its systemic consequences and has potential as both a biomarker and therapeutic target. To date, there are no published data on MK levels in patients with different stages of CKD. This study aims to quantify MK levels in patients with CKD and to identify any correlation with CKD stage, cause, progression, comorbid disease or prescribed medication.

methodsIn this observational, single-centre study, demographic data were collected, and serum and urine assayed from 197 patients with CKD and 19 healthy volunteers in an outpatient setting.

resultsThe median serum and urine MK level in volunteers was 754 pg/mL (IQR: 554-1025) and 239 pg/mL (IQR: 154-568), respectively. Compared with serum MK in stage 1 CKD (660 pg/mL, IQR: 417-893), serum MK increased in stage 3 (1878 pg/mL, IQR: 1188-2756; p<0.001), 4 (2768 pg/mL, IQR: 2065-4735; p<0.001) and 5 (4816 pg/mL, IQ: 37477807; p<0.001). Urine MK levels increased from stage 1 CKD (343 pg/mL, IQR: 147-437) to stage 3 (1007 pg/mL, IQR: 465-2766; p=0.07), 4 (2961 pg/mL, IQR: 1368-5686; p=0.005) and 5 (6722 pg/mL, IQR: 3796-10 060; p=0.001). Fractional MK excretion (FeMK) increased from stage 1 CKD (0.159, IQR: 0.145-0.299) to stage 3 (1.024, IQR: 0.451-1.886, p=0.047), 4 (3.39, IQR: 2.10-5.82, p=0.004) and 5 (11.95, IQR: 5.36-24.41, p<0.001). When adjusted for estimated glomerular filtration rate, neither serum nor urine MK correlated with primary CKD diagnosis or CKD progression (small sample). There was a positive correlation between protein:creatinine ratio and FeMK (p=0.003). Angiotensin blockade (adjusted for proteinuria) was associated with lower urine MK (p=0.018) and FeMK (p=0.025).

conclusionMK levels sequentially rise with CKD stage beyond stage 2, and our data support existing animal evidence for an MK/renin angiotensin-system/proteinuria relationship. To what extent this is related to renal clearance versus pathology, or the consequences of chronically elevated MK levels requires further exploration.

Indexed as

Disease ProgressionAdultAgedAged, 80 and overAustraliaBiomarkersCase-Control StudiesComorbidityCreatinineFemaleGlomerular Filtration RateHumansIntercellular Signaling Peptides and ProteinsMaleMiddle AgedMidkineBiomarkersCreatinineIntercellular Signaling Peptides and ProteinsMidkinechronic renal failurecytokineimmunology

Identifiers

PMID28963279
PMCPMC5623449
OpenAlexW2756540376

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.