Evidence map›Paper›PMID 28289910›Full record

ArticleClinical and experimental nephrology2017

Acid-base disturbances in nephrotic syndrome: analysis using the CO

Tomomichi Kasagi, Hirokazu Imai, Naoto Miura, Keisuke Suzuki, Masabumi Yoshino, Hironobu Nobata, Takuhito Nagai, Shogo Banno

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Clinical and experimental nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 98% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Different effect of aldosterone on corrected HCOHypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
  2. Revisiting Stewart's Approach toward Assessment of Unidentified or Complex Acid-Base Disorders.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2022
    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

8 authors at 1 institution in 1 country.

Tomomichi KasagiDivision of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan. kasagi.tomomichi.284@mail.aichi-med-u.ac.jp.ORCID http://orcid.org/0000-0002-9150-1446
Hirokazu ImaiDivision of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Naoto MiuraDivision of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Keisuke SuzukiDivision of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Masabumi YoshinoDivision of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Hironobu NobataDivision of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Takuhito NagaiDivision of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Shogo BannoDivision of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Japan.
Aichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Stewart model for analyzing acid-base disturbances emphasizes serum albumin levels, which are ignored in the traditional Boston model. We compared data derived using the Stewart model to those using the Boston model in patients with nephrotic syndrome.

methodsTwenty-nine patients with nephrotic syndrome and six patients without urinary protein or acid-base disturbances provided blood and urine samples for analysis that included routine biochemical and arterial blood gas tests, plasma renin activity, and aldosterone. The total concentration of non-volatile weak acids (A

resultsAccording to the Boston model, 25 of 29 patients (90%) had alkalemia. Eighteen patients had respiratory alkalosis, 11 had metabolic alkalosis, and 4 had both conditions. Only three patients had hyperreninemic hyperaldosteronism. The Stewart model demonstrated respiratory alkalosis based on decreased PaCO

conclusionsPatients with nephrotic syndrome had primary respiratory alkalosis, decreased A

Indexed as

Acid-Base EquilibriumModels, BiologicalAcid-Base ImbalanceAdultAgedAged, 80 and overBicarbonatesBiomarkersCarbon DioxideCase-Control StudiesFemaleGlomerular Filtration RateHumansHypoalbuminemiaKidneyMaleALB protein, humanBicarbonatesBiomarkersCarbon DioxideSerum Albumin, HumanAcid–base disturbanceMetabolic acidosisNephrotic syndromeRenin–angiotensin–aldosterone systemRespiratory alkalosis

Identifiers

PMID28289910
PMCPMC5648741
OpenAlexW2595023552

What OpenQuestion holds

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LicenceCC BY
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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.