Nephron Physiology

Original Paper

Urinary Excretion Rate of Tamm-Horsfall Protein Is Related to Salt Intake in Humans

Torffvit O.a · Melander O.b · Hultén U.L.b

Author affiliations

aDepartment of Medicine, University Hospital of Lund, Lund, bDepartment of Endocrinology, Malmö University Hospital MAS, Malmö, Sweden

Keywords: Tamm-Horsfall proteinSodium excretionTubular functionBlood pressureRenal functionPotassium excretion

Related Articles for ""
Nephron Physiol 2004;97:p31–p36
https://doi.org/10.1159/000077600

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 11, 2003
Accepted: March 08, 2004
Published online: May 24, 2004
Issue release date: May 2004

Number of Print Pages: 1
Number of Figures: 0
Number of Tables: 3


eISSN: 1660-2137 (Online)

For additional information: https://www.karger.com/NEP

Abstract

Background/Aims: Increased salt intake and enhanced salt sensitivity are implicated in the pathogenesis of hypertension. The aim of the present study was to investigate whether the urinary excretion rate of Tamm-Horsfall protein (THP) is dependent on salt intake in healthy, genetically hypertension-prone individuals. Methods: Thirty unrelated subjects (13 men and 17 women, mean age 48.1 ± 6.7 years) with at least one first-degree relative with primary hypertension were studied. After a baseline investigation, the study subjects were put on a low-salt diet (10 mmol of sodium and 70 mmol of potassium per day) for 1 week. During the second week, sodium chloride capsules (230 mmol/day) were added to the diet to achieve a high-salt intake of 240 mmol/day. Urine samples (24-hour and overnight collections) were collected before the baseline investigation and at the end of the high- and low-salt diet weeks. The salt sensitivity was calculated as the difference between the blood pressure during high salt intake and the blood pressure during low salt intake. Results: A low salt intake induced a decrease in the urinary excretion rate of THP during the night (11.7 µg/min) compared with baseline (19.5 µg/min; p < 0.05) and high salt intake (23.1 µg/min; p < 0.01). Furthermore, a greater response in blood pressure to a high salt intake, i.e. high salt sensitivity, was associated with increased excretion of THP in urine during the change to high salt intake (r = 0.38, p < 0.05). Conclusion: We were able to confirm that urinary excretion of THP is dependent on sodium intake. Patients with a high salt sensitivity, i.e. an exaggerated blood pressure response to high salt intake, responded to the high salt intake with an even greater increase in the urinary excretion rate of THP. The mechanism underlying this response is still unknown, but it might indicate that distal nephron function in healthy, genetically hypertension-prone individuals is altered.

© 2004 S. Karger AG, Basel



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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 11, 2003
Accepted: March 08, 2004
Published online: May 24, 2004
Issue release date: May 2004

Number of Print Pages: 1
Number of Figures: 0
Number of Tables: 3


eISSN: 1660-2137 (Online)

For additional information: https://www.karger.com/NEP

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2004, Vol.97, No. 1

May 2004

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