Kidney Week

Abstract: FR-OR47

Salt-Sensitive Blood Pressure Response in CKD Is Not Volume Mediated

Session Information

• Fluid, Electrolyte, and Acid-Base Disorders Research
  November 04, 2022 | Location: W308, Orange County Convention Center‚ West Building
  Abstract Time: 05:24 PM - 05:33 PM

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

• 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical

Authors

• Oppelaar, Jetta J., Amsterdam UMC Locatie AMC, Amsterdam, North Holland, Netherlands

Jetta J. Oppelaar, MD

• van Schijndel, Emma H C, Amsterdam UMC Locatie AMC, Amsterdam, North Holland, Netherlands

Emma H C van Schijndel,

• Van den born, Bert-jan, Amsterdam UMC Locatie AMC, Amsterdam, North Holland, Netherlands

Bert-jan Van den born,

• Olde Engberink, Rik Hg, Amsterdam UMC Locatie AMC, Amsterdam, North Holland, Netherlands

Rik Hg Olde Engberink,

• Vogt, Liffert, Amsterdam UMC Locatie AMC, Amsterdam, North Holland, Netherlands

Liffert Vogt,

Background

Chronic kidney disease (CKD) patients are advised to limit salt intake, because of blood pressure (BP) and albuminuria lowering effects. The salt-sensitive BP response in CKD is classically attributed to the renal incapacity to excrete sodium (Na⁺) resulting in fluid overload. In non-kidney patients BP sensitivity to salt has been shown to be fluid independent and might be linked to vasodysfuction. We aimed to investigate which factor contributes to BP sensitivity to salt in CKD.

Methods

We performed a randomized cross-over study in CKD patients (stage 2a-3, proteinuria >500 mg/d) and healthy controls (HC). All subjects followed both an 8-day low sodium diet (LSD, <50mmol/d) and high sodium diet (HSD, >200mmol/d). After each diet, assessment of the hemodynamic profile included 24-hour BP measurements (Mobil-O-Graph) and cardiac output (using Nexfin^TM), by which SVR was calculated accordingly. Body fluid volume was assessed with multi-frequency body impedance spectroscopy (Fresenius).

Results

We included 13 HC (median age 27 yrs) and 6 CKD patients (median age 49 yrs, proteinuria 1.2 (SD 1.1) grams/day). After HSD, patients with CKD showed a mean daytime systolic BP increase (LSD vs HSD (118.2 (SD 10.6) mmHg vs. 130.8 (SD 7.8) mmHg, p=0.04) while systolic BP in HC did not increase. After HSD, we observed a comparable extracellular fluid (ECV) expansion in CKD and HC subjects (Fig 1A), but no effect on cardiac output (Fig 1B). Delta SVR showed a distinct response in CKD and HC (respectively, 67.6 (SD 313.3) vs -67.5 (SD 106.6) dyn/s/cm^-5, p=0.07). The difference in BP response was not accompanied by differences in urinary Na⁺ excretion after HSD (259 mmol/day vs 247 mmol/day, p=0.73).

Conclusion

Salt sensitivity in CKD is characterized by systolic BP increase. In these patients, this BP increase may not be explained by increased volume expansion due to the renal incapacity to excrete Na⁺. However, in CKD the salt sensitive BP response might coincide with incapacity for vasodilation.