Renal Sodium Handling and Nighttime Blood Pressure

doi:10.1016/j.semnephrol.2007.07.007

Seminars in Nephrology

Volume 27, Issue 5, September 2007, Pages 565-571

https://doi.org/10.1016/j.semnephrol.2007.07.007 Get rights and content

Summary

Blood pressure follows a circadian rhythm with a physiologic 10% to 20% decrease during the night. There is now increasing evidence that a blunted decrease or an increase in nighttime blood pressure is associated with a greater prevalence of target organ damage and a faster disease progression in patients with chronic kidney diseases. Several factors contribute to the changes in nighttime blood pressure including changes in hormonal profiles such as variations in the activity of the renin-angiotensin and the sympathetic nervous systems. Recently, it was hypothesized that the absence of a blood pressure decrease during the nighttime (nondipping) is in fact a pressure-natriuresis mechanism enabling subjects with an impaired capacity to excrete sodium to remain in sodium balance. In this article, we review the clinical and epidemiologic data that tend to support this hypothesis. Moreover, we show that most, if not all, clinical conditions associated with an impaired dipping profile are diseases associated either with a low glomerular filtration rate and/or an impaired ability to excrete sodium. These observations would suggest that renal function, and most importantly the ability to eliminate sodium during the day, is indeed a key determinant of the circadian rhythm of blood pressure.

Section snippets

The Nighttime Dipping Pattern is Associated With the Development of Cardiovascular Complications

Although the concept still is controversial, evidence has accumulated in recent years suggesting that patients with a blunted overnight decrease in BP are at higher risk to develop target organ damages such as microalbuminuria, chronic renal damage, left ventricular hypertrophy, and cerebrovascular events.6, 9, 10, 11, 12, 13, 14, 15 Thus, in young patients with type 1 diabetes without nephropathy, the absence of nocturnal BP dip is associated with an increased risk of microalbuminuria.¹¹ In a

Nondipping of Nighttime BP: Does the Kidney Play a Role?

As mentioned previously, several neuroendocrine systems and vascular and hematologic factors follow a circadian rhythm that may contribute to the physiologic day-night variations in BP and circadian rhythm of cardiovascular complications. The renal excretion of water, sodium, and other solutes also has been shown to follow a circadian pattern, with higher excretion rates during daytime than during nighttime.¹⁹ Recently, it was hypothesized that the renal capacity to excrete sodium is an

Are There Clinical Data Supporting the Association Between Renal Sodium Excretion and the Decrease in Nighttime BP?

As shown in (Table 1), a nondipping profile of 24-hour BP has been reported in several clinical conditions. These include secondary forms of hypertension such as malignant hypertension,²⁹ primary hyperaldosteronism,30, 31 Cushing’s syndrome,³² or pheochromocytoma.³² A blunted decrease in nighttime BP also has been described in patients with a reduced renal function such as patients with diabetic and nondiabetic nephropathies,24, 33, 34, 35 congestive heart failure,³⁶ organ transplantation,37, 38

Conclusions

BP is known to follow a circadian pattern with a physiologic decrease during the night. To date, little attention has been paid to the nighttime BP for several reasons: the first is that nighttime BP generally is not measured unless a 24-hour recording is performed. Today, with the wider use of ambulatory BP monitoring and the reimbursement of the procedure, physicians are confronted increasingly with the need to provide an interpretation of nighttime BP data. The second difficulty is the

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Cited by (36)

Higher Nocturnal Blood Pressure and Blunted Nocturnal Dipping Are Associated With Decreased Daytime Urinary Sodium and Potassium Excretion in Patients With CKD
2024, Kidney International Reports
Sodium homeostasis is intimately associated with blood pressure (BP) rhythm, and potassium excretion is closely associated with sodium excretion in the general population. However, the association between circadian sodium and potassium pattern excretion and nocturnal BP in patients with chronic kidney disease (CKD) is not elucidated.
We evaluated the correlation between the day-to-night ratio of urinary sodium and potassium excretion rate, nocturnal blood pressure, and nocturnal BP dipping in a CKD cohort.
A total of 3152 (56.76% males, mean age 47.63 years) individuals with CKD were included in the study. Patients in quartile 1 (with the lowest ratio) exhibited a 12 mmHg or 9 mmHg higher nocturnal systolic blood pressure (SBP) and blunted SBP dipping than those in quartile 4 when urinary sodium or potassium excretion rate was divided into day-to-night ratios (both P < 0.001). In multivariate analyses, lower day-to-night ratio of urinary sodium was independently linked to higher nocturnal SBP and blunted SBP dipping (linear regression coefficient (95% confidence interval [CI]): −6.89 (−9.48 to −4.31), and −3.64 (−5.48 to −1.80), respectively; both P < 0.001). Similarly, compared with the highest quartile of day-to-night ratio of urinary potassium excretion rate, linear regression coefficient (95% CI) for the lowest quartile was −5.60 (−8.13 to −3.07) for nocturnal SBP, and −2.47 (−4.28 to −0.67) for SBP dipping (both P < 0.001). Moreover, urine flow rate and concentrates of sodium or potassium in the urine were positively associated with urinary sodium or potassium excretion during daytime (P < 0.001).
A higher nocturnal BP and a blunted nocturnal BP dipping were both independently linked to a lower excretion of sodium or potassium during the day in patients with CKD. Furthermore, a decreased urine flow rate and a diminished capacity to concentrate sodium or potassium in the urine appear to be the key contributors to a low day-to-night ratio of urinary sodium excretion or potassium rate.
Hypertension in African Americans
2023, Hypertension: A Companion to Braunwald's Heart Disease
Hypertension remains a powerful independent marker of mortality accounting for an estimated 10.8 million deaths globally in 2019. Most of these deaths were from cardiovascular causes. In the United States, age-adjusted death rate for hypertension-related cardiovascular deaths was highest in African Americans and nearly two-fold higher when compared with Whites in 2018. Hypertension incidence and prevalence are significantly higher in African Americans compared with other race-ethnic groups in the United States. In general, African Americans have earlier-onset hypertension, higher average blood pressure (BP) levels, higher average nondipping nocturnal BP, greater 24-hour BP variability on ambulatory monitoring, and a greater prevalence of hypertension-related target organ damage. A definitive pathophysiologic basis for the greater prevalence of hypertension in African Americans remains speculative. Although hypertension treatment has significantly improved, to the point that in the 2011 to 2012 period, hypertension treatment rates were similar among African Americans (76.5%) and Whites (75.8%), control rate in African Americans (49.4%) remains lower than in Whites (54.3%) and also much lower than achievable (>80%) in some integrated health system models. Strategies to improve treatment and control begin with a mutually trusting patient-provider relationship and a commitment to follow through on an action plan informed by evidence-based guidelines. A diligent search is necessary to identify the reasons why BP remains uncontrolled during treatment with maximum or near-maximum doses of drugs from three or more recommended drug classes. Community engagement principles, dissemination and implementation science, and attention to social determinants of health also remain paramount.
Nutritional management of sodium, chloride, and water in kidney disease and kidney failure
2021, Nutritional Management of Renal Disease, Fourth Edition
The regulation of salt and water balance is one the most important and complex physiological processes enabling to maintain homeostasis of the extracellular and intracellular volumes in health as well as in disease conditions. This regulatory process is mediated by multiple factors influencing both the intake of sodium and water and their excretion, essentially by the kidney. In recent years, new mechanisms of regulation of sodium and water balance have been described demonstrating tissue accumulation in the skin and muscles. This has changed substantially the usual concepts of how sodium and water are handled involving not only new storage compartments but also new regulatory pathways such as the immune system and inflammation. There is now evidence that these new mechanisms play also an important role also in patients with chronic kidney disease (CKD) or kidney failure as it will be discussed in this chapter.
In patients with kidney diseases, a reduction in sodium intake and an adequate water intake are always two major components of the nutritional management. Indeed, on a lower sodium diet, blood pressure and proteinuria decrease and there is weak evidence suggesting that renal disease progression may be delayed. Today, most recommendations propose a sodium intake between 2 and 2.3 g Na/day (5–6 g NaCl) in CKD patients. Daily oral fluid intake should be between 1500 and 2000 mL/day in most CKD patients, except those on dialysis who should drink less and those with specific renal diseases such kidney stone diseases and polycystic kidney disease, who need to have a very high urine output.
Hypertension in African Americans
2018, Hypertension: A Companion to Braunwald's Heart Disease
Renal medulla
2016, Nephrologie et Therapeutique
Le fait de pouvoir produire une urine hyperosmotique au plasma permet aux mammifères, y compris l’homme, d’excréter dans l’urine des déchets solubles, minéraux et organiques, en minimisant les besoins en eau. La capacité de concentration de l’urine dépend en premier lieu d’une disposition anatomique particulière en « épingle à cheveux » des néphrons et de certains vaisseaux, propre aux mammifères. Elle dépend aussi de l’action de l’hormone antidiurétique qui agit sur la perméabilité à l’eau du canal collecteur, sur toute sa longueur, et sur la perméabilité à l’urée dans sa partie tout à fait terminale, dans la médulla interne. Elle nécessite aussi : (1) un « moteur » produisant un transport actif capable de générer une différence de concentration transépithéliale, créant une augmentation de la concentration de solutés dans l’interstitium environnant ; et (2) l’expression de transporteurs ou de canaux sélectifs localisés de façon très spécifique sur des portions limitées de certains segments du néphron, des canaux collecteurs et des vasa recta artériels, permettant d’accélérer considérablement le transport d’eau ou le passage de certains solutés à travers les membranes cellulaires. Même si certains segments du néphron et du système collecteur sont présents dans le cortex et dans la médulla (notamment le tubule proximal, le segment large ascendant et le canal collecteur), leurs fonctions dans ces différentes zones ne sont pas totalement identiques en raison de leur environnement péritubulaire différent, de la composition du fluide qui les traverse, et de certaines différences de l’épithélium qui les borde. Cet article décrit quelques caractéristiques et fonctions particulières de ces structures dans la médulla rénale, par opposition aux structures correspondantes dans le cortex. Ces fonctions spécifiques des segments de néphron et du canal collecteur dans la médulla ont des conséquences qui peuvent se révéler néfastes dans certaines situations pathologiques.
The ability to produce hyperosmotic urine allows mammals, including humans, to excrete their soluble mineral and organic waste products in the urine with a limited amount of water. The urinary concentrating capacity depends primarily on a special “loop-shaped” architecture of the nephrons and vessels, observed only in mammals. It also depends on the influence of antidiuretic hormone on the permeability to water of the collecting ducts on their entire length, and on the permeability to urea limited to the terminal portion of these ducts in the inner medulla. The ability to concentrate urine also requires (1) an “engine” able to produce an active (energy demanding) transport that generates a transepithelial concentration difference leading to increase the solute concentration in the surrounding interstitium; and (2) the expression of several membrane transporters or channels localized very specifically to limited portions of some nephron segments, collecting ducts and arterial vasa recta. These transporters and channels greatly accelerate the transport of water and some solutes across the cell membranes. Even if some nephron segments and parts of the collecting system are present in both the renal cortex and medulla (namely, the proximal tubule, the thick ascending limb and the collecting duct), their functions in the two renal zones may not be strictly similar, owing to their different peritubular environment, to the composition of the fluid running in their lumen, and to some differences in their epithelium. This paper describes some characteristics and specific functions of these structures in the renal medulla, as opposed to their corresponding structures in the cortex. These specific functions operating in the medulla may lead to various adverse consequences in some pathological situations.
Decreased orthostatic adrenergic reactivity in non-dipping postural tachycardia syndrome
2014, Autonomic Neuroscience: Basic and Clinical
Citation Excerpt :
Finally, although differences in 24-hour natriuresis between groups were not found, we did not explore day-to-night natriuresis ratios. Impaired ability to excrete sodium during the day has been proposed as a major determinant of the circadian rhythm of blood pressure (Burnier et al., 2007). Our results confirm that non-dipping is prevalent in POTS, and suggest that a lower adrenergic reactivity and not peripheral sympathetic denervation or a hyperadrenergic state relates to non-dipping among patients with POTS.
Whether non-dipping – the loss of the physiologic nocturnal drop in blood pressure – among patients with postural tachycardia syndrome (POTS) is secondary to autonomic neuropathy, a hyperadrenergic state, or other factors remains to be determined. In 51 patients with POTS (44 females), we retrospectively analyzed 24-hour ambulatory blood pressure recordings, laboratory indices of autonomic function, orthostatic norepinephrine response, 24-hour natriuresis and peak exercise oxygen consumption. Non-dipping (< 10% day–night drop in systolic blood pressure) was found in 55% (n = 28). Dippers and non-dippers did not differ in: 1) baseline characteristics including demographic and clinical profile, sleep duration, daytime blood pressure, 24-hour natriuresis, and peak exercise oxygen consumption; 2) severity of laboratory autonomic deficits (sudomotor, cardiovagal and adrenergic); 3) frequency of autonomic neuropathy (7/23 vs. 8/28, P = 0.885); 4) supine resting heart rate (75.3 ± 14.0 bpm vs. 74.0 ± 13.8 bpm, P = 0.532); or 5) supine plasma norepinephrine level (250.0 ± 94.9 pg/ml vs. 207.0 ± 86.8 pg/ml, P = 0.08). However, dippers differed significantly from non-dippers in that they had significantly greater orthostatic heart rate increment (43 ± 16 bpm vs. 35 ± 10 bpm, P = 0.007) and significantly greater orthostatic plasma norepinephrine increase (293 ± 136.6 pg/ml vs. 209 ± 91.1 pg/ml, P = 0.028). Our data indicate that in patients with POTS, a non-dipping blood pressure profile is associated with a reduced orthostatic sympathetic reactivity not accounted for by autonomic neuropathy.

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Renal Sodium Handling and Nighttime Blood Pressure

Summary

Section snippets

The Nighttime Dipping Pattern is Associated With the Development of Cardiovascular Complications

Nondipping of Nighttime BP: Does the Kidney Play a Role?

Are There Clinical Data Supporting the Association Between Renal Sodium Excretion and the Decrease in Nighttime BP?

Conclusions

Am J Hypertens

Kidney Int

Med Hypotheses

Am J Hypertens

Circadians rhythms and clinical medicine with applications to hypertension

Am J Hypertens

Diurnal rhythms and other sources of blood pressure variability in normal and hypertensive subjects

Time-dependent structure and control of arterial blood pressure

Ann NY Acad Sci

Circadian rhythm of blood pressure: internal and external time triggers

Chronobiol Int

Altered circadian rhythm of blood pressure in shift worker

J Hum Hypertens

Stroke prognosis and abnormal nocturnal blood pressure falls in older hypertensives

Hypertension

Reproducibility and clinical value of nocturnal hypotension: prospective evidence from the SAMPLE study

J Hypertens

Impact of nocturnal fall in blood pressure on early cardiovascular changes in essential hypertension

J Hypertens

Disturbed circadian rhythm of urinary albumin excretion in non-dipper type of essential hypertension

Am J Nephrol

Increase in nocturnal blood pressure and progression to microalbuminuria in type 1 diabetes

N Engl J Med

Prediction of stroke by ambulatory blood pressure monitoring versus screening blood pressure measurements in a general population: the Ohasama study

J Hypertens

Circadian blood pressure variation related to morbidity and mortality from cerebrovascular and cardiovascular diseases

Ann N Y Acad Sci

The majority of nondipping men do not have increased cardiovascular risk—a population based study

J Hypertens

Prediction of mortality by ambulatory blood pressure monitoring versus screening blood pressure measurements: a pilot study in Ohasama

J Hypertens

Association of impaired diurnal blood pressure variation with a subsequent decline in glomerular filtration rate

Arch Intern Med

Predicting cardiovascular risk using conventional vs ambulatory blood pressure in older patients with systolic hypertensionSystolic Hypertension in Europe Trial Investigators

JAMA

Prognostic value of ambulatory blood pressure recordings in patients with treated hypertension

N Engl J Med

The relationship between blood pressure and sodium and potassium excretion during the day and at night

J Hypertens