Evidence map›Paper›PMID 28194476›Full record

ReviewDer Internist2017

[Diagnosis and treatment of chronic kidney disease].

M Girndt

Abstract readReview
PubMed Publisher
In one paragraph

Review in Der Internist, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Urinary exosomes as promising biomarkers for early kidney disease detection.American journal of clinical and experimental urology · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. The role of N6-methyladenosine (mFrontiers in medicine · 2023
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. 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

1 author at 1 institution in 1 country.

M GirndtKlinik für Innere Medizin II, Martin-Luther-Universität Halle-Wittenberg, Ernst-Grube-Str. 40, 06120, Halle (Saale), Deutschland. matthias.girndt@medizin.uni-halle.de.
Martin Luther University Halle-Wittenberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease is defined by decreased glomerular filtration rate or proteinuria. Diabetic nephropathy and hypertensive renal damage are responsible for the majority of cases. The initiation of therapy has to consider if causal treatment of the underlying disease is possible and indicated. In all patients, even if specific treatment is not possible, therapy should aim at reducing progression of kidney failure. Chronic kidney diseases tend to intrinsic deterioration that persists after cessation of the causative damaging pathomechanism. Progression of disease can be delayed; the most important measures include strict blood pressure control, reduction of proteinuria, and avoidance of further renal harm. Kidney disease induces typical sequelae such as left ventricular hypertrophy, vascular calcification, anemia, and renal osteodystrophy. While these are well understood nowadays therapeutic options are limited. The uremic syndrome is to be avoided by renal replacement therapy.

Indexed as

Disease ProgressionHumansHypertension, RenalKidney Failure, ChronicProteinuriaRenal Insufficiency, ChronicDiabetic nephropathyHyperphosphatemiaHypertensionHypertrophy, left ventricularRenal replacement therapy

Identifiers

PMID28194476
OpenAlexW2588757352

What OpenQuestion holds

Textmetadata
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.