Circadian Blood Pressure Rhythm Is Disturbed by Nephrectomy

Goto, Norihiko; Uchida, Kazuharu; Morozumi, Kunio; Ueki, Tsuneo; Matsuoka, Susumu; Katayama, Akio; Haba, T; Tominaga, Yoshihiro; Fukuda, Michio; Nakao, Akimasa; Kimura, Genjiro

doi:10.1291/hypres.28.301

Cited by 43 publications

(24 citation statements)

References 51 publications

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“…30,[32][33][34]37 RENAL DYSFUNCTION AND NON-DIPPER CIRCADIAN RHYTHMS Because glomerular filtration capability is one of the major factors determining salt sensitivity, 7,24,28,36 the nocturnal dip in BP may be less pronounced as a function of GFR loss. We recently showed this quantitative relationship in CKD 38,39 and healthy donors after nephrectomy, 40 in both of whom there was an inverse relationship between GFR and the night/day ratio of BP. These findings are compatible with high salt sensitivity of BP in glomerulopathy, even when GFR is maintained at a relatively normal level, 41,42 ultimately becoming much higher as renal function deteriorates.…”

Section: Salt Sensitivity and Circadian Rhythm Of Blood Pressurementioning

confidence: 85%

“…[47][48][49][50][51][52] Because the degree of non-dipping was closely correlated with the degree of renal function loss, as discussed above, 38,40 however, non-dipping might be consequently correlated with the progression of nephropathy. Our clear results especially obtained after kidney donation 40 that instead it might be a phenotype of renal functional loss, together with well known facts that in patients with renal dysfunction the nocturnal BP dip is lost and circadian rhythms manifest as those of non-dippers, 38,40,47,50,53,54 suggest that the circadian rhythm of BP is determined mostly by the kidneys. The importance of kidneys in the genesis of circadian BP rhythm is consistent with reports that the circadian rhythm of BP is normalized from non-dipper to dipper after kidney transplantation, 55 and also by salt intake restriction and diuretics.…”

Section: Salt Sensitivity and Circadian Rhythm Of Blood Pressurementioning

confidence: 99%

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Salt sensitivity and circadian rhythm of blood pressure: the keys to connect CKD with cardiovasucular events

2010

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In healthy subjects, blood pressure (BP) drops by 10-20% during the night. Conversely, in patients with the salt-sensitive type of hypertension or chronic kidney disease, nighttime BP does not fall, resulting in an atypical pattern of circadian BP rhythm that does not dip. This pattern is referred to as the 'non-dipper' pattern. Loss of renal functional reserve, due to either reduced ultrafiltration capacity or enhanced tubular sodium reabsorption, induces the salt-sensitive type of hypertension. When salt intake is excessive in patients with salt-sensitive hypertension, the defect in sodium excretory capability becomes evident, resulting in elevated BP during the night. This nocturnal hypertension compensates for diminished natriuresis during the daytime and enhances pressure natriuresis during the night. Nocturnal hypertension and the non-dipper pattern of circadian BP rhythm cause cardiovascular events. When excess salt intake is loaded in patients who are in a salt-sensitive state, glomerular capillary pressure is also elevated, resulting in glomerular sclerosis and eventual renal failure. In this way, salt sensitivity and excess salt intake contribute to both cardiovascular and renal damage at the same time. We propose that salt sensitivity of BP and excess salt intake have important roles in the genesis of the cardiorenal connection. Salt sensitivity and circadian rhythm of BP are the keys to understanding the connections between cardiovascular and renal complications.

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Section: Salt Sensitivity and Circadian Rhythm Of Blood Pressurementioning

confidence: 85%

Section: Salt Sensitivity and Circadian Rhythm Of Blood Pressurementioning

confidence: 99%

Salt sensitivity and circadian rhythm of blood pressure: the keys to connect CKD with cardiovasucular events

2010

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“…[1][2][3] Because glomerular filtration capability is one of the major factors determining sodium sensitivity, 4,5 as a function of loss of glomerular filtration rate, the nocturnal dip in BP may be less pronounced. We recently illustrated this quantitative relationship in CKD 6 and healthy donors after unilateral nephrectomy, 7 where in fact there was an inverse relationship between glomerular filtration rate and the night: day ratio of BP. Therefore, we have postulated that reduced renal capacity to excrete sodium into urine causes nocturnal elevation of BP, ie, nondippers, to compensate for diminished daytime natriuresis by enhancing pressure natriuresis during sleep.…”

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confidence: 91%

Patients With Renal Dysfunction Require a Longer Duration Until Blood Pressure Dips During the Night

et al. 2008

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Abstract-We have postulated that the diminished renal capacity to excrete sodium causes nocturnal blood pressure (BP) elevation, which enhances pressure natriuresis in compensation for impaired daytime natriuresis. If such a mechanism holds, high BP during sleep at night may continue until excess sodium is sufficiently excreted into urine. This study examined whether the duration, defined as "dipping time," until nocturnal mean arterial pressure began to fall to Ͻ90% of daytime average became longer as renal function deteriorated. Ambulatory BP measurements and urinary sodium excretion rates were evaluated for daytime and nighttime to estimate their circadian rhythms in 65 subjects with chronic kidney disease. Key Words: chronic kidney disease Ⅲ natriuresis Ⅲ blood pressure Ⅲ circadian rhythm Ⅲ nondipper Ⅲ cardiovascular events I n healthy subjects, blood pressure (BP) normally dips during the night by 10% to 20% from daytime. In some patients with hypertension or chronic kidney disease (CKD), however, BP fails to dip during the night, and these patients have been called "nondippers," whereas those with a normal nocturnal BP dip are called "dippers." We reported previously in patients with essential hypertension that, as BP became sodium sensitive, nocturnal dip in BP was diminished. 1-3 Because glomerular filtration capability is one of the major factors determining sodium sensitivity, 4,5 as a function of loss of glomerular filtration rate, the nocturnal dip in BP may be less pronounced. We recently illustrated this quantitative relationship in CKD 6 and healthy donors after unilateral nephrectomy, 7 where in fact there was an inverse relationship between glomerular filtration rate and the night: day ratio of BP. Therefore, we have postulated that reduced renal capacity to excrete sodium into urine causes nocturnal elevation of BP, ie, nondippers, to compensate for diminished daytime natriuresis by enhancing pressure natriuresis during sleep. 1,3,6,8,9 If pressure natriuresis during sleep compensates for reduced daytime renal sodium excretion, high BP during sleep at night may continue until excess sodium is sufficiently excreted into urine. In this study, to ascertain the renal mechanisms of nondippers, we examined whether a longer duration is in fact required until a nocturnal BP begins to fall as renal function deteriorates. Patients and Methods Study PopulationThe subjects were 65 patients (33 men and 32 women; aged 16 to 80 years old; mean age: 47Ϯ18 years; body mass index [BMI]: 22.2Ϯ4.1 kg/m 2 ; body weight: 58.2Ϯ14.2 kg) who were hospitalized with CKD at Nagoya City University Hospital. CKD was defined as the presence of kidney damage or a decreased glomerular filtration rate of Ͻ60 mL/min per 1.73 m 2 for Ն3 months, according to Kidney Disease Outcomes Quality Initiative CKD criteria. 10 Patients with diabetic nephropathy or nephrotic syndrome and those receiving antihypertensive agents or diuretics were excluded from the study. All of the participants were enrolled consecutively after informed cons...

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“…[4][5][6] Specifically, left ventricular hypertrophy, microalbuminuria, carotid intima-media thickening, cerebrovascular events and renal impairment are more prominent in nondippers than in dippers. [7][8][9][10][11][12] The b-thalassemia trait (b-TT) is one of the most prevalent genetic diseases in Mediterranean countries. 13 Several features are present in minor thalassemics, which may afford some protection against cardiovascular disease.…”

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confidence: 99%

Ambulatory blood pressure profile in hypertensive patients with β-thalassemia minor

Vyssoulis¹,

Karpanou

Sm³

et al. 2010

Hypertens Res

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b-thalassemia trait (b-TT) is a common genetic disorder in Mediterranean countries, including Greece. Previous studies have shown the protective effect of b-TT against myocardial infarction. However, the ambulatory blood pressure (BP) profile of such patients has not yet been investigated. Thus, the purpose of the present study was to investigate the ambulatory BP monitoring (ABPM) profile of hypertensives with b-TT, in comparison with all-cause anemic and non-anemic essential hypertensive patients. The study ultimately comprised of 8861 essential hypertensive, nondiabetic patients who were divided into three groups: group I (n¼191, with b-TT), group II (n¼655, anemic) and group III (n¼8015, nonanemic). All patients underwent full clinical, laboratory and echocardiographic evaluations, whereas all were subjected to ABPM. Anemia was defined as Hb o12 g per 100 ml for women and o13 g per 100 ml for men, whereas patients with b-TT were self-referred. The distribution of dipping patterns among the three groups was 61.3 vs. 41.2 vs. 45.8% (Po0.001), whereas for nondippers it was 20.4 vs. 31.5 vs. 27.7% (Po0.001), for extreme-dippers it was 15.7 vs. 15.0 vs. 17.5% (Po0.001) and for reverse dippers it was 2.6 vs. 12.4 vs. 9.0% (Po0.001). Furthermore, mean daytime systolic BP (SBP) among the three groups was 140.13 ± 7.79 vs. 142.02 ± 11.61 vs. 141.99 ± 9.87 mm Hg (P¼0.03), and mean nighttime SBP was 125.87 ± 10.4 vs. 131.13 ± 15.7 vs. 129.62±13.31 mm Hg (Po0.001). In the multiple regression analysis, after adjustments for age, body mass index and lipid levels, the differences among daytime and nighttime SBP remained significant at 140.18 ± 9.84 vs. 142.02 ± 9.85 vs. 141.99 ± 9.85 mm Hg (P¼0.04) and 125.99 ± 13.07 vs. 131.19 ± 13.08 vs. 129.61 ± 13.07 mm Hg (Po0.001), respectively. Hypertensive patients with b-TT present with a better 24-h BP profile in comparison with anemic and nonanemic hypertensives. Thus, b-TT may function protectively in their total cardiovascular risk profile.

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Circadian Blood Pressure Rhythm Is Disturbed by Nephrectomy

Cited by 43 publications

References 51 publications

Salt sensitivity and circadian rhythm of blood pressure: the keys to connect CKD with cardiovasucular events

Salt sensitivity and circadian rhythm of blood pressure: the keys to connect CKD with cardiovasucular events

Patients With Renal Dysfunction Require a Longer Duration Until Blood Pressure Dips During the Night

Ambulatory blood pressure profile in hypertensive patients with β-thalassemia minor

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