Evidence map›Paper›PMID 7819016›Full record

ReviewPediatric nephrology (Berlin, Germany)1994

Development biology of the renal kallikrein-kinin system.

S S el-Dahr

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

0 citing papers in PubMed, 14 citations in OpenAlex.

No citing paper in PubMed yet.

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.

S S el-DahrDepartment of Pediatrics, Tulane University School of Medicine, New Orleans, Louisiana 70112.
Tulane University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kinins are endothelium-dependent vasodilators and natriuretic paracrine peptides that participate in the regulation of blood pressure, renal hemodynamics and sodium excretion. Several lines of evidence suggest an important role for intrarenal kinins and their receptors in kidney growth and development. (1) The developing rat kidney expresses all the components of the tissue kallikrein-kinin system: tissue kallikrein, low molecular weight (LMW) kininogen, kininase II and kinin receptors. Also, the developing liver expresses high molecular weight and LMW kininogens. Thus, a complete kinin-generating system exists in the developing kidney. (2) Gene transcription, mRNA and protein abundance, and enzymatic activity of renal kallikrein are all markedly up-regulated during postnatal kidney growth, and a positive correlation exists between renal kallikrein synthesis and the maturational rise in renal blood flow. (3) Rat glomerular mesangial cells in culture express the kinin receptors and proliferate in response to bradykinin, suggesting that endogenous kinins and their receptors modulate glomerular growth. (4) The newborn period is characterized by an activation of kinin receptor gene expression, and chronic pharmacological blockade of kinin receptors suppresses DNA synthesis in the developing but not adult kidney. Collectively, these data provide the basis for the hypothesis that endogenous kinins and the kinin receptors play an important role in the developmental biology of the metanephric kidney.

Indexed as

AnimalsDevelopmental BiologyGene ExpressionHumansKallikrein-Kinin SystemKidneyReceptors, BradykininReceptors, Bradykinin

Identifiers

PMID7819016
OpenAlexW2084541172

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.