Eating Right for Chronic Kidney Disease Series – Controlling Sodium (Salt) Intake


Sodium, beyond its role in maintaining body fluid balance, is intricately linked to the pathophysiology of chronic kidney disease (CKD). Elevated blood pressure (BP) in CKD patientsis often attributed to sodium sensitivity, leading to sodium and fluid retention and subsequent hypertension. Conversely, studies indicate that salt restriction in non-dialysis CKD patients reduces BP levels and enhances the anti-proteinuric effect of renin–angiotensin–aldosterone (RAAS) system inhibitors. 

Adherence to Low-Salt Diet: Definition and Assessment in CKD Patients

Assessing adherence to low-salt diets poses challenges, with 24-hour urine sample collection considered the gold standard but often impractical. Spot urine samples, estimated using various formulas, provide alternatives, yet their accuracy remains questionable. The Chronic Renal Insufficiency Cohort (CRIC) study reveals that only about 25% of CKD patients achieve sodium intake below 100 mmol/24h. Innovative methods like self-monitoring using urine chloride strips and web-based self-management programs aim to improve adherence, with ongoing trials like SALUTE-CKD shedding light on their efficacy.

Hypertension (Blood Pressure) and Salt in CKD

Hypertension and CKD share a bidirectional relationship, with hypertensive patients having a higher risk of de novo CKD. Salt and water retention play a pivotal role in hypertension development in CKD, contributing to extracellular volume expansion and inappropriate activation of the renin-angiotensin-aldosterone (RAAS) system. CKD patients exhibit increased sodium sensitivity, and experimental studies emphasize the amplified BP response to sodium load in this population.

What’s RAAS ?

The Renin-Angiotensin-Aldosterone System (RAAS) is a complex hormonal cascade that plays a key role in regulating blood pressure, fluid balance, and electrolyte balance within the body. Understanding the intricate workings of the RAAS system is crucial in comprehending its influence on chronic kidney disease (CKD) and blood pressure.

Evolutionary Origins of the RAAS System:

The RAAS system has ancient evolutionary roots, dating back to bony fishes, where its role was primarily focused on adapting to changes in salinity and maintaining electrolyte balance. Over millions of years, this system has evolved to address various challenges posed by shifts in environmental conditions. 
A highly active RAAS offered an evolutionary advantage because salt and volume homeostasis (balance) were
important for survival. Dramatic changes in environment when moving from salt water to fresh water (fish), then to
combined habitat water and land (amphibians) and to land (reptiles, primates), had to be met by an efficient regulatory
system to maintain homeostasis. Such a condition was true until modern humans appeared 150K years ago and beyond. With the invention of salt for conservation in stored food in advanced civilizations and excessive salt content in industrialised nutrition, the RAAS is in constant overdrive, causing salt and volume overload in the body with ensuing hypertension, stroke, CKD & cardiovascular diseases

RAAS System - J Nephropathol. 2014; 3(2): 41–43. Published online 2014 Apr 1. doi: 10.12860/jnp.2014.09 Copyright © 2014 by Journal of Nephropathology

Functioning of the RAAS System:

The RAAS system is activated when there is a decrease in renal blood flow or a drop in blood pressure. This activation leads to the release of renin, an enzyme produced by the kidneys, into the bloodstream. Renin acts on angiotensinogen, a liver-derived protein, converting it into angiotensin I. Further conversion of angiotensin I to angiotensin II occurs through the action of angiotensin-converting enzyme (ACE), primarily in the lungs.
Angiotensin II is a potent vasoconstrictor (a drug, agent, or nerve that causes narrowing of the walls of blood vessels), causing blood vessels to narrow, and stimulates the release of aldosterone from the adrenal cortex. Aldosterone, in turn, promotes sodium and water reabsorption in the kidneys, leading to increased blood volume and, consequently, elevated blood pressure.

Role of RAAS in Chronic Kidney Disease:

  • The RAAS system becomes dysregulated in CKD, contributing to disease progression.
  • Impact on Blood Pressure: The dysregulation of the RAAS system can result in sustained elevation of blood pressure, a common feature of CKD. Increased blood pressure further exacerbates renal damage, creating a vicious cycle.
  • Salt and Volume Overload: Modern dietary habits, including excessive salt intake, contribute to constant overactivation of the RAAS system. This overload of salt and volume in the body is linked to hypertension, stroke, and cardiovascular diseases, all of which are closely intertwined with CKD.

Pharmacological Interventions:

  • ACE Inhibitors (ACEi) and Angiotensin II Receptor Blockers (ARBs): These drugs are commonly prescribed to manage hypertension and mitigate the adverse effects of the RAAS system. ACE inhibitors block the conversion of angiotensin I to angiotensin II, while ARBs prevent angiotensin II from binding to its receptors.
  • Direct Renin Inhibitors (DRIs): A newer class of drugs that directly inhibits renin, the enzyme initiating the RAAS cascade. DRIs offer an alternative approach to controlling the system without interfering downstream like ACE inhibitors and ARBs.
  • Natural RAAS blocker to suppress the renin gene: Vitamin D !!!

Alternative Mechanism of Sodium Toxicity

Recent findings suggest that the skin may act as a reservoir for sodium, operating beyond renal control. High salt intake potentially leads to sodium accumulation in the skin, activating osmoreceptors and influencing local inflammation and vascular proliferation. Sodium stored in the skin, detectable through Na Magnetic Resonance Imaging, is associated with left ventricular mass in CKD patients, highlighting its clinical relevance.

Clinical Effects of Low Salt Diet in Non-Dialysis CKD

A meta-analysis encompassing nine trials demonstrates the significant impact of moderate salt restriction on lowering systolic and diastolic blood pressure in CKD patients. Moreover, this reduction extends to ambulatory blood pressure, emphasizing the efficacy of low-salt diets. Despite the controversies surrounding the long-term effects, these findings underscore the potential benefits of salt restriction in managing hypertension in non-dialysis CKD.

Frequently Asked Questions

Q1: How is adherence to low-salt diets assessed in CKD patients?

Assessment methods include 24-hour urine sample collection, spot urine samples using various formulas, and innovative approaches like self-monitoring with urine chloride strips.

Q2: What role does sodium play in the relationship between hypertension and CKD?

Sodium and water retention contribute to hypertension in CKD, with sodium sensitivity amplified in CKD patients, leading to an inappropriate activation of the renin-angiotensin-aldosterone system.

Q3: What are the alternative mechanisms of sodium toxicity in CKD?

Recent research suggests the skin as a sodium reservoir, influencing local inflammation and vascular proliferation, contributing to increased blood pressure levels in CKD.

Q4: What are the clinical effects of low-salt diets in non-dialysis CKD?

A meta-analysis reveals that moderate salt restriction significantly lowers both systolic and diastolic blood pressure in CKD patients, with similar effects observed in ambulatory blood pressure.


This comprehensive review navigates through the intricate relationship between sodium intake and chronic kidney disease outcomes, providing valuable insights into the management of hypertension in CKD patients through personalized salt restriction strategies.



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