Interaction between hypertension and other cardiovascular risk factors in survival of hemodialyzed patients

Kimura, Genjiro; Tomita, Jun; Nakamura, Satoko; Uzu, Takashi; Inenaga, Takashi

doi:10.1016/0895-7061(96)00152-5

Cited by 33 publications

(19 citation statements)

References 20 publications

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“…Several factors may contribute to the development of cardiovascular events, including hypertension, anemia, hyperparathyroidism, glucose intolerance, electrolyte disturbances, acidosis and hyperlipidemia [11, 12]. LVH is present in >70% of patients with ESRD [13]and is an important factor for the development of cardiovascular events.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II Type 1 Receptor Antagonist, Losartan, Causes Regression of Left Ventricular Hypertrophy in End-Stage Renal Disease

Shibasaki

Masaki

Nishiue

et al. 2002

Nephron

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Left ventricular hypertrophy (LVH) commonly occurs in patients with end-stage renal disease (ESRD) and is an independent risk factor for cardiovascular events. Angiotensin II type 1 receptor (AT1-R) antagonists may be able to reverse LVH independent to the hypotensive effect in the ESRD setting. Thirty chronically hemodialyzed uremic patients with hypertension were randomly assigned to receive the AT1-R antagonist losartan (n = 10), the angiotensin-converting enzyme (ACD) inhibitor enalapril (n = 10), or calcium antagonist amlodipine (n = 10). Left ventricular mass (LVM) index was measured by echocardiography before and 6 months after treatment. The baseline demographic and clinical characteristics did not differ between the three groups. The mean baseline LVM index also did not differ in the three groups. After 6 months of treatment, losartan treatment significantly reduced the LVM index (–24.7 ± 3.2%) than amlodipine (–10.5 ± 5.2%) or enalapril (–11.2 ± 4.1%) therapy. All three groups had a similar decrease in the mean blood pressure with treatment. The plasma angiotensin II concentration increased 5-fold with losartan treatment. In contrast, the plasma angiotension II concentration did not change with enalapril and only increased 2-fold with amlodipine. Thus, the present study indicates that losartan more effectively regresses LVH in patients with ESRD than do enalapril and amlodipine despite a comparable depressor effect between the three drugs.

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Section: Discussionmentioning

confidence: 99%

Angiotensin II Type 1 Receptor Antagonist, Losartan, Causes Regression of Left Ventricular Hypertrophy in End-Stage Renal Disease

Shibasaki

Masaki

Nishiue

et al. 2002

Nephron

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“…[98][99][100][101] It is important to understand the precise mechanisms underlying the increase in cardiovascular events as renal function deteriorates and the capacity to excrete sodium into the urine is impaired, even in mild degree. 13,17,102 As discussed above, the incidence of stroke is increased in both saltsensitive hypertension and CKD.…”

Section: Pathophysiology Of the Cardiorenal Connectionmentioning

confidence: 99%

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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“…Recent studies have reported that this is due to an increasing prevalence of cardiac complications in this population [16]. Sudden cardiac death is the most common form of death in dialysis patients, accounting for 20% to 30% of all deaths in this cohort [17].…”

Section: Discussionmentioning

confidence: 93%

Parameters of Cardiac Electrical Instability in Chronic Haemodialysis Patients

Abdel-Galeel¹

2015

AJIM

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Interaction between hypertension and other cardiovascular risk factors in survival of hemodialyzed patients

Cited by 33 publications

References 20 publications

Angiotensin II Type 1 Receptor Antagonist, Losartan, Causes Regression of Left Ventricular Hypertrophy in End-Stage Renal Disease

Angiotensin II Type 1 Receptor Antagonist, Losartan, Causes Regression of Left Ventricular Hypertrophy in End-Stage Renal Disease

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

Parameters of Cardiac Electrical Instability in Chronic Haemodialysis Patients

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