High salt intake promotes a decline in renal function in hypertensive patients: a 10-year observational study

Abstract

We investigated the influence of long-term salt load on renal function in hypertensive patients. The subjects were 133 hypertensive patients (80 women and 53 men, mean age 60±9 years) who underwent at least five successful 24 h home urine collections during the 10-year observation period. Blood pressure (BP) and 24-h urinary salt and creatinine excretion levels were measured. BP decreased from 143±12/85±8 to 129±14/68±11 mm Hg during the 10.5-year observation period, and this decrease was associated with patients taking an increased number of antihypertensive drugs (1.3±1.0 to 2.2±1.1). The estimated glomerular filtration rate (eGFR) also significantly decreased from 71.7±14.6 to 64.7±16.5 ml min(-1) (P<0.01), and the change in eGFR was -0.68 ml min(-1) per year on average. The average salt excretion was 8.6±2.2 g per day and showed a significant negative correlation with the change in eGFR (r=-0.21, P=0.02). Subjects with an average salt excretion<8 g per day showed a significantly slower decline in renal function than those with an average salt excretion 8 g per day (the change in eGFR: -0.41±1.10 vs. -0.83±1.19 ml min(-1) per year, P<0.05). In the multivariate analysis, the average salt excretion (partial r=-0.19, P=0.03) and baseline eGFR (partial r=-0.23, P=0.01) were significantly associated with the change in eGFR. This association was independent of BP change or an increased number of antihypertensive drugs. The results suggest that long-term salt load promotes a decline in renal function in hypertensive patients; thus, salt restriction is encouraged, to prevent renal damage.

High-salt diet inhibits tumour growth in mice via regulating myeloid-derived suppressor cell differentiation

“…Two-tailed Student's t test; each dot represents one mouse; *p < 0.05, **p < 0.01 and ***p < 0.001 vs. the NSD group. People in many countries currently consume a diet high in salt, sugar, fat and cholesterol, which has widespread implications in renal, cardiovascular and endocrine homoeostasis, as well as cancer 59,60 . Although some previous studies have shown that salt or salted food is involved in an increased risk of gastric cancer 61 , others have suggested little or only weak correlations 60,62 .…”

High Salt Diet Affects the Reproductive Health in Animals: An Overview

“…Furthermore, surface water in saline regions comprises up to 0.9-1.7% salt, which leads to an exacerbation of the enhanced salt consumption [4]. Several types of animal disorders have been observed such as lipid accumulation, kidney damage, hypertension, and failure in renal function as a result of an excess intake of salt [5]. Moreover, nowadays, there is an increasing proof to examine the relation between high salt consumption and many disorders that include obesity, water retention, osteoporosis, cancer, obesity, vascular dementia, and diabetes [6][7][8].…”

Factors associated with a vicious cycle involving a low nephron number, hypertension and chronic kidney disease

“…Whereas studies agree that the average number of nephrons is approximately one million per kidney, larger studies have shown a maximal 13-fold variation in the normal human nephron number. 6,7 In addition, a few recent autopsy studies have indicated that the nephron number is lower in the kidneys of patients with hypertension than in the kidneys of normotensive age-matched controls. 8,9 Furthermore, the findings of a low nephron number in Australian aborigines, who exhibit an extremely high rate of renal failure, are consistent with the link between a low nephron number and CKD.…”

“…A reduction in the nephron number results in a reduced sodium excretory capacity, enhanced susceptibility to HTN and diminished renal functional reserve, thereby limiting the extent of compensation for renal injury and progressive renal insufficiency. [4][5][6] It has long been accepted that the human kidney contains, on average, one million nephrons. However, numerous studies conducted in the past 20 years have demonstrated that there is much greater variability in the total nephron number in normal human kidneys than previously suspected.…”