Dialysate Sodium Levels, Ambulatory Aortic Blood Pressure and Arterial Stiffness in Hemodialysis Patients.
Increased aortic blood-pressure(BP) and arterial stiffness are associated with higher cardiovascular risk in hemodialysis. Previous works showed that lower dialysate sodium is associated with lower brachial-BP; data on aortic-BP and arterial stiffness are limited. This study aimed to investigate the effects of different dialysate sodium concentrations on 72-h aortic-BP and arterial stiffness parameters in hemodialysis patients.
This analysis is part of a prospective, non-randomized interventional study. Twenty-five hemodialysis patients underwent a set of three periods of different dialysate sodium concentrations; six sessions with dialysate sodium of 137meq/L, followed consecutively by six sessions with 139meq/L and, finally, six sessions with 141meq/L. At the start of the sixth hemodialysis session on each sodium concentration, 72-h ABPM (Mobil-O-Graph) was performed to evaluate aortic-BP and arterial stiffness indices during the overall 72-h, different 24-h, day-time and night-time periods.
Mean 72-h aortic SBP/DBP were higher with increasing dialysate sodium concentrations (137meq/L: 114.2±15.3/77.0±11.8mmHg vs 139meq/L: 115.4±17.3/77.9±14.0mmHg vs 141meq/L: 120.5±18.4/80.5±14.7mmHg, p=0.002/p=0.057, respectively). Wave-reflections parameters (AIx, AIx(75), AP) were not significantly different between the three dialysate sodium concentrations. Ambulatory PWV was significantly higher with increasing dialysate sodium concentrations (137meq/L: 8.5±1.7m/s vs 139meq/L: 8.6±1.6m/s vs 141meq/L: 8.8±1.6m/s, p<0.001). In generalized linear-mixed-models including 72-h brachial SBP as random covariate, the adjusted marginal-means of 72-h PWV were not significantly different between-groups.
This study showed that lower dialysate sodium concentrations are associated with significant decreases in ambulatory aortic BP and PWV. This study showed that higher dialysate sodium concentrations are associated with significant increases in ambulatory aortic BP and PWV. These findings further support the need for modification of dialysate sodium concentration in hemodialysis.
Bratsiakou A
,Theodorakopoulou M
,Iatridi F
,Sarafidis P
,Davoulos C
,Goumenos DS
,Papachristou E
,Papasotiriou M
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Low dialysate sodium levels for chronic haemodialysis.
Cardiovascular (CV) disease is the leading cause of death in dialysis patients and is strongly associated with fluid overload and hypertension. It is plausible that low dialysate sodium ion concentration [Na+] may decrease total body sodium content, thereby reducing fluid overload and hypertension and ultimately reducing CV morbidity and death. This is an update of a review first published in 2019.
This review evaluated the harms and benefits of using a low (< 138 mM) dialysate [Na+] for maintenance haemodialysis (HD) patients.
We searched the Cochrane Kidney and Transplant Register of Studies up to 1 October 2024 through contact with the Information Specialist using search terms relevant to this review. Studies in the Register are identified through searches of CENTRAL, MEDLINE, and EMBASE, conference proceedings, the International Clinical Trials Registry Platform (ICTRP) Search Portal and ClinicalTrials.gov.
Randomised controlled trials (RCTs), both parallel and cross-over, of low (< 138 mM) versus neutral (138 to 140 mM) or high (> 140 mM) dialysate [Na+] for maintenance HD patients were included.
Two authors independently screened studies for inclusion and extracted data. Statistical analyses were performed using the random-effects model, and results expressed as risk ratios (RR) for dichotomous outcomes, and mean differences (MD) or standardised MD (SMD) for continuous outcomes, with 95% confidence intervals (CI). Confidence in the evidence was assessed using Grades of Recommendation, Assessment, Development and Evaluation (GRADE).
We included 17 studies randomising 509 patients, with data available for 452 patients after dropouts. All but three studies evaluated a fixed concentration of low dialysate [Na+], with one using profiled dialysate [Na+] and two using individualised dialysate [Na+]. Five were parallel group studies, and 12 were cross-over studies. Of the latter, only six used a washout between intervention and control periods. Most studies were short-term with a median (interquartile range) follow-up of 4 (4 to 16) weeks. Two were of a single HD session and two of a single week's HD. Seven studies were conducted prior to 2000, and six reported the use of obsolete HD practices. Other than for indirectness arising from older studies, risks of bias in the included studies were generally low. Compared to neutral or high dialysate [Na+] (≥ 138 mM), low dialysate [Na+] (< 138 mM) reduces interdialytic weight gain (14 studies, 515 participants: MD -0.36 kg, 95% CI -0.50 to -0.22; high certainty evidence) and antihypertensive medication use (5 studies, 241 participants: SMD -0.37, 95% CI -0.64 to -0.1; high certainty evidence), and probably reduces left ventricular mass index (2 studies, 143 participants: MD -7.65 g/m2, 95% CI -14.48 to -0.83; moderate certainty evidence), predialysis mean arterial pressure (MAP) (5 studies, 232 participants: MD -3.39 mm Hg, 95% CI -5.17 to -1.61; moderate certainty evidence), postdialysis MAP (5 studies, 226 participants: MD -3.17 mm Hg, 95% CI -4.68 to 1.67; moderate certainty evidence), predialysis serum [Na+] (11 studies, 435 participants: MD -1.26 mM, 95% CI -1.81 to -0.72; moderate certainty evidence) and postdialysis serum [Na+] (6 studies, 188 participants: MD -3.09 mM, 95% CI -4.29 to -1.88; moderate certainty evidence). Compared to neutral or high dialysate [Na+], low dialysate [Na+] probably increases intradialytic hypotension events (13 studies, 15,764 HD sessions: RR 1.58, 95% 1.25 to 2.01; moderate certainty evidence) and intradialytic cramps (10 studies, 14,559 HD sessions: RR 1.84, 95% 1.29 to 2.64; moderate certainty evidence). Effect size for important outcomes were generally greater with low dialysate [Na+] compared to high compared with neutral dialysate [Na+], although formal hypothesis testing identifies that the difference was only certain for postdialysis serum [Na+]. Compared to neutral or high dialysate [Na+], it is uncertain whether low dialysate [Na+] affects intradialytic or interdialytic MAP, and dietary salt intake. It is also uncertain whether low dialysate [Na+] changed extracellular fluid status, venous tone, arterial vascular resistance, left ventricular volumes, or fatigue. Studies did not examine CV or all-cause death, CV events, or hospitalisation.
Low dialysate [Na+] reduces intradialytic weight gain and probably blood pressure, which are effects directionally associated with improved outcomes. However, the intervention probably increases intradialytic hypotension and probably reduces serum [Na+], effects that are associated with an increased risk of death. The effect of the intervention on overall patient health and well-being is unknown. Further evidence is needed in the form of longer-term studies in contemporary settings, evaluating end-organ effects in small-scale mechanistic studies using optimal methods, and clinical outcomes in large-scale multicentre RCTs.
Marshall MR
,Wang MY
,Vandal AC
,Dunlop JL
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《Cochrane Database of Systematic Reviews》
Study of the association of markers of central and peripheral arterial stiffness with renal function in patients with arterial hypertension, diabetes mellitus and chronic kidney disease.
Increased aortic or central arterial stiffness (CAS) is a major factor in cardiovascular morbidity and mortality in patients with vascular risk factors. Decreased glomerular filtration rate (GFR) and increased urinary albumin excretion (uALB) are associated with lethal and non-lethal cardiovas-cular events. The pathophysiological mechanisms of this association are not fully defined. The aim of this study was: 1.- To analyse the CAS, comparing several markers, in subjects with arterial hypertension (HTN), diabetes mellitus (DM), chronic kidney disease (CKD) and their combination. 2.- To study the possible association of CAS with renal dysfunction (decrease in GFR and increase in uALB).
A total of 286 subjects were included, divided into several groups: Control (n:38); HTN (n:51); DM without CKD (n:26); CKD without DM (n:77); CKD with DM (n:94). Several indices obtained by applanation tonometry were used to determine the CAS: carotid-femoral pulse velocity (VPc-f); central pulse pressure (cPP); augmentation index standardised to a cardiac frequency of 75 L/min (IA75); peripheral/aortic arterial stiffness gradient (ASGp-a). As a marker of peripheral arterial resistance, the carotid-radial pulse velocity (PVc-r) was determined. The ASGp-a was calculated from the PVc-r/PVc-f ratio. The subendocardial viability index (iBuckberg) was obtained from the aortic pulse wave. Multiple regression, binary logistic regression, and multinomial regression were used to study the association between arterial stiffness markers and renal function.
The adjusted values of the PVc-f [(median (interquartile range) (m/s)] were significantly higher in subjects with DM [(9 (1.2)], CKD [(9.4 (0.7)] and DM with CKD [(10.9 (0.7)] than in the control group [(8.2 (1.3)] and group with HTN [(8.3 (0.9)], (p: 0.001). Patients with DM with CKD had higher PVc-f values than all other groups (p: 0.001). The ASGp-a of the patients was significantly lower than that of the controls, and the group with DM with CKD had significantly lower values than the other groups. The cPP in the DM with CKD group was significantly higher than in the other groups. All patients had an AI75 higher than the control group. When all aortic stiffness markers were introduced together in the regression, PV c-f was the only one that, after multivariate adjustment, was independently and inversely associated with GFR (β; -4, p: 0.001) and predicted the presence of GFR decrease (<60 mL/min/1.73 m2), [(OR (95%CI): 1.50 (1.17-1.92; p: 0.001]. The PVc-f was the only index directly associated with albuminuria (β: 0.15, p: 0.02) and predicted the existence of abnormal albuminuria (>30 mg/g), [(OR; 1.66 (1.25-2.20), p: 0.001)]. The PVc-f was also associated with the iBuckberg (β: -2.73, p: 0.01). Multinomial regression confirmed that PVc-f is a significant determinant of GFR and uALB. On the other hand, the increase in PVc-f and the presence of DM contribute significantly to the magnitude of albuminuria.
Aortic stiffness increases in the presence of vascular risk factors such as hypertension, DM and CKD. This increase is greater when DM and CKD coexist. Increased aortic stiffness is inversely associated with GFR and directly with uALB, and is predictive of decreased GFR and abnormal uALB. The VPc-f is the parameter of aortic stiffness that is most consistently associated with renal dysfunction. Increased aortic stiffness could be one of the pathomechanisms linking renal dysfunction to cardiovascular events.
Perelló Martínez J
,Michán Doña A
,Santamaría Olmo R
,Hidalgo Santiago JC
,Gálvez Moral J
,Gómez-Fernández P
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