Hypertension in renal parenchymal disease: Why is it so resistant to treatment?

Campese, Vito M.; Mitra, Noémi; Sandee, Duanpen

doi:10.1038/sj.ki.5000177

Cited by 115 publications

(94 citation statements)

References 71 publications

(63 reference statements)

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“…27 In particular, tubulointerstitial injuries are generally considered to lead to microvascular damage and renal ischemia, resulting in resistant hypertension. 28 Male sex was an independent variable for postoperative hypertension. Compared with premenopausal women, male sex is known as a risk factor of arteriosclerosis and hypertension.…”

Section: Discussionmentioning

confidence: 99%

Renal Resistive Index Predicts Postoperative Blood Pressure Outcome in Primary Aldosteronism

et al. 2016

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Section: Discussionmentioning

confidence: 99%

Renal Resistive Index Predicts Postoperative Blood Pressure Outcome in Primary Aldosteronism

et al. 2016

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“…aTRH may result in microalbuminuria through prolonged increases in glomerular pressure and subsequent renal damage (19). Furthermore, sodium retention and excessive activation of the renin-angiotensin-aldosterone system have been linked to uncontrolled BP in individuals with CKD (20,21). Also, albuminuria is thought to be preceded by systemic endothelial dysfunction (22).…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Apparent Treatment-Resistant Hypertension among Individuals with CKD

Tanner

Calhoun²,

Bell³

et al. 2013

Clinical Journal of the American Society of Nephrology

140

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SummaryBackground and objectives Apparent treatment-resistant hypertension is defined as systolic/diastolic BP$140/ 90 mmHg with concurrent use of three or more antihypertensive medication classes or use of four or more antihypertensive medication classes regardless of BP level.Design, setting, participants, & measurements The prevalence of apparent treatment-resistant hypertension among Reasons for Geographic and Racial Differences in Stroke study participants treated for hypertension (n=10,700) was determined by level of estimated GFR and albumin-to-creatinine ratio, and correlates of apparent treatment-resistant hypertension among those participants with CKD were evaluated. CKD was defined as an albumin-to-creatinine ratio$30 mg/g or estimated GFR,60 ml/min per 1.73 m 2 .Results The prevalence of apparent treatment-resistant hypertension was 15.8%, 24.9%, and 33.4% for those participants with estimated GFR$60, 45-59, and ,45 ml/min per 1.73 m 2 , respectively, and 12.1%, 20.8%, 27.7%, and 48.3% for albumin-to-creatinine ratio,10, 10-29, 30-299, and $300 mg/g, respectively. The multivariableadjusted prevalence ratios (95% confidence intervals) for apparent treatment-resistant hypertension were 1.25 (1.11 to 1.41) and 1.20 (1.04 to 1.37) for estimated GFR levels of 45-59 and ,45 ml/min per 1.73 m 2 , respectively, versus $60 ml/min per 1.73 m 2 and 1.54 (1.39 to 1.71), 1.76 (1.57 to 1.97), and 2.44 (2.12 to 2.81) for albumin-tocreatinine ratio levels of 10-29, 30-299, and $300 mg/g, respectively, versus albumin-to-creatinine ratio,10 mg/g. After multivariable adjustment, men, black race, larger waist circumference, diabetes, history of myocardial infarction or stroke, statin use, and lower estimated GFR and higher albumin-to-creatinine ratio levels were associated with apparent treatment-resistant hypertension among individuals with CKD.Conclusions This study highlights the high prevalence of apparent treatment-resistant hypertension among individuals with CKD.

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“…Indeed, in renal disease, nondipping is the rule, with a prevalence between 74% and 82%. [25][26][27][28][29] Crosssectional observations have demonstrated that nondippers have more severe morphological 30 and functional 31,32 changes than dippers. Fukuda et al 31 studied subjects with biopsy-proven glomerulopathy and found that creatinine clearance (Cl Cr ) was significantly negatively related to the night/day ratios of both sodium excretion and MAP, whereas Farmer et al 32 have shown that the prevalence of nondipping increases with plasma creatinine concentration in patients with chronic renal insufficiency.…”

Section: Nocturnal Blood Pressure Dipping and Sodium Excretionmentioning

confidence: 99%

Nocturnal Sodium Excretion, Blood Pressure Dipping, and Sodium Sensitivity

2006

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M ore than 30 years ago, Guyton 1 described pressurenatriuresis: increasing arterial blood pressure promotes sodium excretion, decreasing blood volume and lowering blood pressure, whereas when blood pressure falls, sodium excretion decreases, and blood volume and blood pressure increase. 1,2 The linchpin of the model of Guyton et al 3 is the concept of feedback gain. Gain is the degree to which a feedback system can correct a perturbation, that is, the amount of correction of a deviation divided by the residual degree of deviation. When a control system corrects a perturbation minimally, its feedback gain is near 0. When it corrects it completely, its gain is infinite. As emphasized by Guyton et al,3 in integrated systems with infinite and finite gain components, the infinite gain function ultimately dominates. There are myriad blood pressure control systems, for example, arterial baroreceptors and chemoreceptors, the central nervous system ischemic response, the renin-angiotensin system, and capillary fluid shift, but all are ultimately trumped by pressure-natriuresis. In the experiments by Guyton et al, 3 pressure-natriuresis had near infinite gain over a wide range of urinary sodium excretion, such that the set point of blood pressure regulation was not affected by sodium intake over a period of several days or a few weeks.This pressure-natriuresis model describes a steady-state relationship. At short time intervals, blood pressure and sodium excretion may not be closely linked, but the body will always eventually bring the system back into balance. In this review, we wish to draw attention to differences in the relationship of blood pressure to sodium excretion during day and night and to how nighttime pressure-natriuresis and sodium sensitivity of blood pressure interact. We will suggest that these features of pressure-natriuresis have implications both for the clinical management of hypertension and research into the genetic underpinnings of the disease. Diurnal Rhythm of Sodium Excretion in Normotensive and Hypertensive SubjectsIn healthy people, sodium excretion reaches a maximum during the day and a minimum at night during sleep, and it has long been thought that blood pressure is the primary determinant of nighttime sodium excretion. 4 -7 Centonza et al 8 performed ambulatory blood pressure monitoring over a 26-hour period in normotensive subjects for whom sodium intake was fixed at a moderate amount (170 mmol/day). All of the subjects demonstrated a nocturnal dip in blood pressure with a concomitant dip in sodium excretion. Moreover, there were significant positive correlations between blood pressure and sodium excretion during the night and over 24 hours, as well as during periods of quiet supine wakefulness and postprandial sitting. No similar relationship was apparent when subjects carried out daily activities in the standing position. The authors concluded that the pressure-natriuresis relationship is blunted during upright posture, possibly because of the activation of neurohumoral systems. 8 St...

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Hypertension in renal parenchymal disease: Why is it so resistant to treatment?

Cited by 115 publications

References 71 publications

Renal Resistive Index Predicts Postoperative Blood Pressure Outcome in Primary Aldosteronism

Renal Resistive Index Predicts Postoperative Blood Pressure Outcome in Primary Aldosteronism

Prevalence of Apparent Treatment-Resistant Hypertension among Individuals with CKD

Nocturnal Sodium Excretion, Blood Pressure Dipping, and Sodium Sensitivity

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