Chetna M Pathak1, Joachim H Ix2, Cheryl A M Anderson3, Tyler B Woodell4, Gerard Smits5, Martha S Persky5, Geoffrey A Block5, Dena E Rifkin6. 1. School of Medicine, University of California San Diego, San Diego, California. 2. School of Medicine, University of California San Diego, San Diego, California; Division of Nephrology-Hypertension, Department of Medicine, University of California San Diego, San Diego, California; Department of Family Medicine and Public Health, University of California San Diego, San Diego, California; Veterans Affairs San Diego Healthcare System, San Diego, California. 3. School of Medicine, University of California San Diego, San Diego, California; Division of Nephrology-Hypertension, Department of Medicine, University of California San Diego, San Diego, California; Department of Family Medicine and Public Health, University of California San Diego, San Diego, California. 4. Division of Nephrology, Oregon Health Sciences University, Portland, Oregon. 5. Denver Nephrology, Denver, Colorado. 6. School of Medicine, University of California San Diego, San Diego, California; Division of Nephrology-Hypertension, Department of Medicine, University of California San Diego, San Diego, California; Department of Family Medicine and Public Health, University of California San Diego, San Diego, California; Veterans Affairs San Diego Healthcare System, San Diego, California. Electronic address: drifkin@ucsd.edu.
Abstract
OBJECTIVE: In the kidney disease clinic setting, higher-than-usual blood pressure is often ascribed to recent dietary sodium indiscretion. While clinical trials demonstrate a clear relationship between salt intake and blood pressure on the population level, it is uncertain whether real-world variation in sodium intake within individual chronic kidney disease (CKD) patients is associated with fluctuations in blood pressure. METHODS: We analyzed data from the Phosphorus Normalization Trial, in which participants with CKD eating their usual diets completed at least three 24-hour urine collections over 9 months, from which we measured sodium. Blood pressure was measured at the time of 24-hour urine collections. For each individual participant, we assessed the slope of the relationship between sodium intake and mean arterial blood pressure (MAP). RESULTS: Among 119 participants (mean age 67 years and mean estimated glomerular filtration rate 31 mL/minute/1.73 m2), there was substantial variation in sodium intake as measured by 24-hour urine collections (mean intake 3,903 mg/day, standard deviation 1037 mg/day). Individual participants had highly variable associations between their sodium intake and their MAP; 47% (n = 56) had inverse associations between sodium and MAP, whereas the remainder had positive (salt-sensitive) associations. CONCLUSIONS: Among CKD patients, there is substantial variation in sodium intake but no predictable relationship between dietary sodium and blood pressure in individuals. The frequent dismissal of elevated blood pressure readings as related to recent sodium intake in clinic may be a misapplication of large-scale population data to explain individual variability and may contribute to clinical inertia regarding high blood pressure treatment.
RCT Entities:
OBJECTIVE: In the kidney disease clinic setting, higher-than-usual blood pressure is often ascribed to recent dietary sodium indiscretion. While clinical trials demonstrate a clear relationship between salt intake and blood pressure on the population level, it is uncertain whether real-world variation in sodium intake within individual chronic kidney disease (CKD) patients is associated with fluctuations in blood pressure. METHODS: We analyzed data from the Phosphorus Normalization Trial, in which participants with CKD eating their usual diets completed at least three 24-hour urine collections over 9 months, from which we measured sodium. Blood pressure was measured at the time of 24-hour urine collections. For each individual participant, we assessed the slope of the relationship between sodium intake and mean arterial blood pressure (MAP). RESULTS: Among 119 participants (mean age 67 years and mean estimated glomerular filtration rate 31 mL/minute/1.73 m2), there was substantial variation in sodium intake as measured by 24-hour urine collections (mean intake 3,903 mg/day, standard deviation 1037 mg/day). Individual participants had highly variable associations between their sodium intake and their MAP; 47% (n = 56) had inverse associations between sodium and MAP, whereas the remainder had positive (salt-sensitive) associations. CONCLUSIONS: Among CKDpatients, there is substantial variation in sodium intake but no predictable relationship between dietary sodium and blood pressure in individuals. The frequent dismissal of elevated blood pressure readings as related to recent sodium intake in clinic may be a misapplication of large-scale population data to explain individual variability and may contribute to clinical inertia regarding high blood pressure treatment.
Authors: Emma J McMahon; Judith D Bauer; Carmel M Hawley; Nicole M Isbel; Michael Stowasser; David W Johnson; Katrina L Campbell Journal: J Am Soc Nephrol Date: 2013-11-07 Impact factor: 10.121
Authors: Geoffrey A Block; David C Wheeler; Martha S Persky; Bryan Kestenbaum; Markus Ketteler; David M Spiegel; Matthew A Allison; John Asplin; Gerard Smits; Andrew N Hoofnagle; Laura Kooienga; Ravi Thadhani; Michael Mannstadt; Myles Wolf; Glenn M Chertow Journal: J Am Soc Nephrol Date: 2012-07-19 Impact factor: 10.121
Authors: Andrew Smyth; Matthew Griffin; Salim Yusuf; Johannes F E Mann; Donal Reddan; Michelle Canavan; John Newell; Martin O'Donnell Journal: J Ren Nutr Date: 2016-03-12 Impact factor: 3.655