Evidence map›Paper›PMID 28502983›Full record

ReviewNature reviews. Nephrology2017

Alkaline phosphatase: a novel treatment target for cardiovascular disease in CKD.

Mathias Haarhaus, Vincent Brandenburg, Kamyar Kalantar-Zadeh, Peter Stenvinkel, Per Magnusson

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 1 pooled it
14.3field-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

141 citing papers in PubMed, 1 synthesis or guideline pooled it, 302 citations in OpenAlex.

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81 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

5 authors at 4 institutions in 3 countries.

Mathias HaarhausDivision of Renal Medicine and Baxter Novum, Karolinska Institutet, Karolinska University Hospital, SE-14186 Stockholm, Sweden.
Vincent BrandenburgDepartment of Cardiology and Intensive Care Medicine, RWTH University Hospital Aachen, Pauwelsstraße 30, D-52074 Aachen, Germany.
Kamyar Kalantar-ZadehHarold Simmons Center for Kidney Disease Research and Epidemiology and Division of Nephrology and Hypertension, University of California Irvine, School of Medicine, 101 The City Drive South, City Tower, Suite 400, Mail Code: 4088, Orange, California 92868, USA.
Peter StenvinkelDivision of Renal Medicine and Baxter Novum, Karolinska Institutet, Karolinska University Hospital, SE-14186 Stockholm, Sweden.
Per MagnussonDepartment of Clinical Chemistry and Department of Clinical and Experimental Medicine, Linköping University, SE-58185 Linköping, Sweden.
Karolinska Institutet · SELinköping University · SEUniversitätsklinikum Aachen · DEUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease is the main cause of early death in the settings of chronic kidney disease (CKD), type 2 diabetes mellitus (T2DM), and ageing. Cardiovascular events can be caused by an imbalance between promoters and inhibitors of mineralization, which leads to vascular calcification. This process is akin to skeletal mineralization, which is carefully regulated and in which isozymes of alkaline phosphatase (ALP) have a crucial role. Four genes encode ALP isozymes in humans. Intestinal, placental and germ cell ALPs are tissue-specific, whereas the tissue-nonspecific isozyme of ALP (TNALP) is present in several tissues, including bone, liver and kidney. TNALP has a pivotal role in bone calcification. Experimental overexpression of TNALP in the vasculature is sufficient to induce vascular calcification, cardiac hypertrophy and premature death, mimicking the cardiovascular phenotype often found in CKD and T2DM. Intestinal ALP contributes to the gut mucosal defence and intestinal and liver ALPs might contribute to the acute inflammatory response to endogenous or pathogenic stimuli. Here we review novel mechanisms that link ALP to vascular calcification, inflammation, and endothelial dysfunction in kidney and cardiovascular diseases. We also discuss new drugs that target ALP, which have the potential to improve cardiovascular outcomes without inhibiting skeletal mineralization.

Indexed as

Alkaline PhosphataseCardiovascular DiseasesHumansRenal Insufficiency, ChronicAlkaline Phosphatase

Identifiers

PMID28502983
OpenAlexW2615154579

What Socratic 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 Socratic graph.