Evidence map›Paper›PMID 39073780›Full record

ArticleEuropean journal of endocrinology2024

Saline suppression testing-induced hypocalcemia and implications for clinical interpretations.

Wasita W Parksook, Jenifer M Brown, Julia Milks, Laura C Tsai, Justin Chan, Anna Moore, Yvonne Niebuhr, Brooke Honzel, Andrew J Newman, Anand Vaidya

Abstract read
In one paragraph

Article in European journal of endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Is It Time to Retire Aldosterone Suppression Testing?American journal of hypertension · 2026
    Review
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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

10 authors.

Wasita W ParksookCenter for Adrenal Disorders, Boston, MA 02115, United States.
Jenifer M BrownCenter for Adrenal Disorders, Boston, MA 02115, United States.
Julia MilksCenter for Adrenal Disorders, Boston, MA 02115, United States.
Laura C TsaiCenter for Adrenal Disorders, Boston, MA 02115, United States.ORCID 0009-0008-5344-2589
Justin ChanCenter for Adrenal Disorders, Boston, MA 02115, United States.
Anna MooreCenter for Adrenal Disorders, Boston, MA 02115, United States.
Yvonne NiebuhrCenter for Adrenal Disorders, Boston, MA 02115, United States.
Brooke HonzelCenter for Adrenal Disorders, Boston, MA 02115, United States.
Andrew J NewmanCenter for Adrenal Disorders, Boston, MA 02115, United States.
Anand VaidyaCenter for Adrenal Disorders, Boston, MA 02115, United States.ORCID 0000-0002-0314-9252

Funding

Unrecognized Primary Aldosteronism as a Pathogenic Mechanism for Chronic Kidney Disease in DiabetesR01DK115392 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Anand Vaidya · 2018 to 2026
$6.0M
Aldosterone, the Mineralocorticoid Receptor, and Cardiovascular Disease in ObesityR01HL153004 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI VAIDYA, ANAND · 2020 to 2024
$4.4M
Primary Aldosteronism Subtypes: Pathophysiology and Steroid SignaturesR01HL155834 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TURCU, ADINA F · 2021 to 2025
$3.5M
Cardiac Perfusion, Structure, and Function across the Primary Aldosteronism SpectrumK23HL159279 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI Jenifer Michelle Brown · 2022 to 2026
$1.0M
American Heart AssociationAmerican Heart Association-American Stroke Association 852429NHLBI NIH HHS K23 HL159279NHLBI NIH HHS K23HL159279NHLBI NIH HHS R01 HL153004NHLBI NIH HHS R01 HL155834NIDDK NIH HHS R01 DK115392NIHNIH HHS R01 DK115392
6 · The paper itself

Abstract

backgroundExtracellular calcium critically regulates physiologic aldosterone production. Moreover, abnormal calcium flux and signaling are involved in the pathogenesis of the majority of primary aldosteronism cases.

methodsWe investigated the influence of the saline suppression test (SST) on calcium homeostasis in prospectively recruited participants (n = 86).

resultsDuring SST, 100% of participants had decreases in serum calcium, with 48% developing frank hypocalcemia. Serum calcium declined from 2.30 ± 0.08 mmol/L to 2.13 ± 0.08 mmol/L (P < .001) with parallel increases in parathyroid hormone from 6.06 ± 2.39 pmol/L to 8.13 ± 2.42 pmol/L (P < .001). In contrast, serum potassium and bicarbonate did not change, whereas eGFR increased and serum glucose decreased (P < .001). Lower body surface area (translating to greater effective circulating volume expansion during SST) was associated with greater reductions in (β = .33, P = .001), and absolutely lower, serum calcium levels (β = .25, P = .001). When evaluating clinically-relevant diagnostic thresholds, participants with post-SST aldosterone levels <138 pmol/L had lower post-SST calcium and 25-hydroxyvitamin D levels (P < .05), and higher post-SST parathyroid hormone levels (P < .05) compared with those with post-SST aldosterone levels >277 pmol/L.

conclusionSST uniformly decreases serum calcium, which is likely to be due to the combination of variable dilution, increased renal clearance, and vitamin D status. These acute reductions in bioavailable calcium are associated with lower post-SST aldosterone. Given the critical role of extracellular calcium in regulating aldosterone production, these findings warrant renewed inquiry into the validity of SST interpretations for excluding primary aldosteronism.

Indexed as

CalciumHyperaldosteronismHypocalcemiaParathyroid HormoneAdultAgedAldosteroneFemaleHumansMaleMiddle AgedProspective StudiesSaline SolutionAldosteroneCalciumParathyroid HormoneSaline Solutionaldosteronecalciumhypocalcemiaparathyroid hormoneprimary aldosteronism

Identifiers

PMID39073780
PMCPMC11322817

What Socratic holds

Textmetadata
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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 Socratic graph.