Renal sodium handling and sodium sensitivity

Q: What is the clinical evidence from this study?

Study design: Review. Population: Salt-sensitive hypertension. Intervention: Renal sodium handling and dietary salt/potassium/fructose intake. Primary outcome: Salt sensitivity of blood pressure and hypertension development.

Alissa A. Frame; Richard D. Wainford

doi:10.23876/j.krcp.2017.36.2.117

June 22, 2017Kidney Research and Clinical PracticeOpen Access

Renal sodium handling and sodium sensitivity

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Key result

Impaired renal sodium handling drives salt-sensitive hypertension in ~50% of hypertensive patients.

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Key Points

To synthesize recent scientific discoveries detailing how the kidney regulates sodium excretion and how genetic, inflammatory, neural, and dietary mechanisms contribute to salt-sensitive hypertension.
Narrative review synthesizing findings from clinical genetics, genome-wide association studies (GWAS), and preclinical animal models of hypertension.
Evaluation of integrated regulatory pathways including pressure natriuresis, renal sodium transporters, renal sympathetic nerves, immune cell infiltration, and dietary factors.
Salt sensitivity affects approximately 50% of hypertensive individuals and 25% of normotensive adults, while average global salt intake is approximately 4 g/day, doubling the World Health Organization recommendation of 2 g/day.
Genetic analyses have identified specific loci and variants, including SLC4A5, SH2B3, and NPR1, that directly link renal sodium transport and inflammatory pathways to blood pressure regulation.
Preclinical models demonstrate that renal sympathetic nerve activation and renal immune cell infiltration, such as T-cell accumulation in Dahl salt-sensitive rats, directly impair sodium excretion and elevate blood pressure.

Structured PICO

P

Population

Human populations with normotension or hypertension (where salt sensitivity affects approximately 50% of hypertensive patients and 25% of normotensive adults) and preclinical rodent models (including Dahl salt-sensitive rats, Sprague-Dawley rats, Wistar rats, and knockout mouse models).

O

Outcome

Renal sodium excretion, sodium transporter activity (e.g., NCC, ENaC, NHE3, NKCC2), and blood pressure regulation / salt sensitivity of blood pressuresurrogate

Limitations

Majority of genome-wide association studies are not conducted in identified salt-sensitive versus resistant populations
Role of inflammation in the salt sensitivity of blood pressure in humans has not been investigated
Lack of reproducible role for beta-2 adrenoceptors on sodium chloride cotransporter regulation across studies
Majority of genome-wide association studies (GWAS) are not conducted in identified salt-sensitive versus resistant populations
Ongoing controversy regarding the direct effect of sympathetic outflow and norepinephrine on the regulation, expression, and activity of the sodium chloride cotransporter (NCC)

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Implication

This narrative review synthesizes genetic, inflammatory, dietary, oxidative stress, and sympathetic nervous system mechanisms governing renal sodium handling to identify potential therapeutic targets and inform dietary guidelines for salt-sensitive hypertension.

Abstract

The pathophysiology of hypertension, which affects over 1 billion individuals worldwide, involves the integration of the actions of multiple organ systems, including the kidney. The kidney, which governs sodium excretion via several mechanisms including pressure natriuresis and the actions of renal sodium transporters, is central to long term blood pressure regulation and the salt sensitivity of blood pressure. The impact of renal sodium handling and the salt sensitivity of blood pressure in health and hypertension is a critical public health issue owing to the excess of dietary salt consumed globally and the significant percentage of the global population exhibiting salt sensitivity. This review highlights recent advances that have provided new insight into the renal handling of sodium and the salt sensitivity of blood pressure, with a focus on genetic, inflammatory, dietary, sympathetic nervous system and oxidative stress mechanisms that influence renal sodium excretion. Increased understanding of the multiple integrated mechanisms that regulate the renal handling of sodium and the salt sensitivity of blood pressure has the potential to identify novel therapeutic targets and refine dietary guidelines designed to treat and prevent hypertension.

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Cite This Study

Frame et al. (2017) conducted a review in Salt-sensitive hypertension. Renal sodium handling and dietary salt/potassium/fructose intake was evaluated on Salt sensitivity of blood pressure and hypertension development. Renal sodium handling governed by genetic, inflammatory, dietary, sympathetic nervous system, and oxidative stress mechanisms drives blood pressure salt sensitivity in 50% of hypertensive patients.

synapsesocial.com/papers/6a79aa6364a2339647022393 https://doi.org/10.23876/j.krcp.2017.36.2.117

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Renal sodium handling and sodium sensitivity

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Key Points

Structured PICO

Limitations

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Implication

Abstract

Discussion

Cite This Study

Renal sodium handling and sodium sensitivity

Figures

Key Points

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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