Literature DB >> 20068364

Are sodium transporters in urinary exosomes reliable markers of tubular sodium reabsorption in hypertensive patients?

Cristina Esteva-Font1, Xiaoyan Wang, Elisabet Ars, Elena Guillén-Gómez, Laia Sans, Isabel González Saavedra, Ferran Torres, Roser Torra, Shyama Masilamani, José Aurelio Ballarín, Patricia Fernández-Llama.   

Abstract

BACKGROUND: Altered renal sodium handling has a major pathogenic role in salt-sensitive hypertension. Renal sodium transporters are present in urinary exosomes. We hypothesized that sodium transporters would be excreted into the urine in different amounts in response to sodium intake in salt-sensitive versus salt-resistant patients.
METHODS: Urinary exosomes were isolated by ultracentrifugation, and their content of Na-K-2Cl cotransporter (NKCC2) and Na-Cl cotransporter (NCC) was analyzed by immunoblotting. Animal studies: NKCC2 and NCC excretion was measured in 2 rat models to test whether changes in sodium transporter excretion are indicative of regulated changes in the kidney tissue. Human studies: in hypertensive patients (n = 41), we investigated: (1) a possible correlation between sodium reabsorption and urinary exosomal excretion of sodium transporters, and (2) the profile of sodium transporter excretion related to blood pressure (BP) changes with salt intake. A 24-hour ambulatory BP monitoring and a 24-hour urine collection were performed after 1 week on a low- and 1 week on a high-salt diet.
RESULTS: Animal studies: urinary NKCC2 and NCC excretion rates correlated well with their abundance in the kidney. Human studies: 6 patients (15%) were classified as salt sensitive. The NKCC2 and NCC abundance did not decrease after the high-salt period, when the urinary sodium reabsorption decreased from 99.7 to 99.0%. In addition, the changes in BP with salt intake were not associated with a specific profile of exosomal excretion.
CONCLUSIONS: Our results do not support the idea that excretion levels of NKCC2 and NCC via urinary exosomes are markers of tubular sodium reabsorption in hypertensive patients.
Copyright © 2010 S. Karger AG, Basel.

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Year:  2010        PMID: 20068364      PMCID: PMC2840242          DOI: 10.1159/000274468

Source DB:  PubMed          Journal:  Nephron Physiol        ISSN: 1660-2137


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