Predialysis and Postdialysis pH and Bicarbonate and Risk of All-Cause and Cardiovascular Mortality in Long-term Hemodialysis Patients

Yamamoto, Tadashi; Shoji, Shigeichi; Yamakawa, Tomoyuki; Wada, Atsushi; Suzuki, Kazutoshi; Iseki, Kunitoshi; Tsubakihara, Yoshiharu

doi:10.1053/j.ajkd.2015.04.014

Cited by 50 publications

(69 citation statements)

References 27 publications

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“…Further complicating the issue is a recent study [26] that questions the hypothesis that post-HD alkalosis was the mechanism contributing to the poor outcomes in the studies previously described. In this latter study, post-HD serum bicarbonate levels and post-HD pH had no association with all-cause or cardiovascular mortality.…”

Section: Discussionmentioning

confidence: 99%

Effect of Bicarbonate-Buffered Dialysate on Ventricular Arrhythmias in Hemodialysis Patients

et al. 2019

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Background: The etiology of sudden cardiac death in patients with end-stage renal disease (ESRD) on hemodialysis (HD) is largely unknown, though there is evidence to suggest that metabolic alkalosis induced by HD with a high-bicarbonate dialysate/prescription may play a role. Methods: We investigated the effects of metabolic alkalosis induced by HD with an acetate-containing bicarbonate-buffered dialysate on frequency of ventricular arrhythmia in 47 patients with ESRD on chronic HD using 48-h Holter monitoring in 3 phases: intra-HD, post-HD day 1, and post-HD day 2. Serum levels of bicarbonate, calcium, and potassium along with hemodynamics were measured pre-HD, post-HD, 20-h post-HD, and 44-h post-HD. Correlations were performed to verify the association between bicarbonate prescription and change in serum bicarbonate levels post-HD and to determine if the HD-induced change in serum bicarbonate level (metabolic alkalosis) had any direct association with ambient ventricular arrhythmia (premature ventricular contractions per hour) or indirect associations with ambient ventricular arrhythmia by affecting electrolytes or hemodynamics that are known to increase the risk of ventricular arrhythmia. Results: Mean pre-HD serum bicarbonate level was 21.3 mEq/L. Dialysate bicarbonate prescription (mean of 36.4 mEq/L) correlated with changes in serum bicarbonate levels immediately post-HD 26.7 mEq/L (r = 0.46, p < 0.01), 20-h post-HD 25.2 mEq/L (r = 0.38), and 44-h post-HD 23.2 mEq/L (r = 0.35, p = 0.01). No statistically significant correlations were found between the post-HD change in serum bicarbonate levels (metabolic alkalosis) with ambient ventricular arrhythmia, changes in serum calcium, potassium, or hemodynamics in any phase. Conclusions: High-bicarbonate dialysate prescription is associated with metabolic alkalosis following the HD procedure. A mild metabolic alkalosis induced by HD with an acetate-containing bicarbonate-buffered dialysate solution had no direct association with ambient ventricular arrhythmia on Holter monitoring and was not associated with changes in hemodynamics or changes in serum total calcium or potassium levels. This study helps to provide guidance for the safe use of high bicarbonate dialysate/prescription in patients with ESRD on HD.

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Section: Discussionmentioning

confidence: 99%

Effect of Bicarbonate-Buffered Dialysate on Ventricular Arrhythmias in Hemodialysis Patients

et al. 2019

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“…It is reasonable to speculate that patients with low levels of endogenous acid production are not eating well and many are malnourished, increasing their mortality risk. Although not discussed by Yamamoto et al, their Table 1 shows that patients with the highest predialysis pH ($7.40) and associated mortality risk actually had the lowest average PCO 2 values, 6 the opposite of what is expected in patients with higher serum bicarbonate levels. These data suggest abnormal hyperventilation in most alkalemic patients, often a sign of serious illness.…”

mentioning

confidence: 82%

“…[1][2][3][4][5] The terms acidosis and alkalosis have been used to characterize these findings, but very few complete acidbase measurements have been made in this group of patients. The study by Yamamoto et al 6 in this issue of AJKD is a welcome addition to the acid-base assessment of patients receiving intermittent HD. For the first time, we now have complete acid-base data (pH, PCO 2 , and bicarbonate) in a large cohort of patients, including not only predialysis but also postdialysis measurements.…”

mentioning

confidence: 99%

Acid-Base Status and Mortality Risk in Hemodialysis Patients

Gennari

2015

American Journal of Kidney Diseases

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“…As already reported [2], metabolic acidosis was improved more strongly in A(-)D relative to that in A(+)D hemodialysis in this study because of the higher bicarbonate concentration in A(-)D (Tables 2 and 4 (ii) those with post-dialysis pH < 7.40 exhibited a significantly higher risk of all-cause mortality (HR, 1.22; 95% CI, 1.00-1.49), and (iii) pre-and post-dialysis bicarbonate levels were not associated with all-cause and CV mortality, which suggested predialysis pH might be the most appropriate reference for acute correction of metabolic acidosis in hemodialysis patients [19]. As shown in Table 5, even with 2 weeks of A(-)D, including 35 mEq/L bicarbonate, the mean predialysis pH was 7.370, which did not exceed a pH of 7.40, and the mean post-dialysis pH was 7.470, which is >7.40 and clearly suggested that A(+)D is safe from the standpoint of mortality on the basis of the relationship between pH and mortality data in Japanese hemodialysis patients.…”

Section: St A(+)d 1st A(-)d After 2 Weeks Of A(+)d 7th A(-)d After 2mentioning

confidence: 96%

The Effects of Acetate-Free Citrate-Containing Dialysate on Calcium Metabolism and Fatigue in Patients on Maintenance Hemodialysis

Yamada¹,

Inaba²,

Shoji³

et al. 2017

AJCEM

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Abstract:Although the significance of acetate-free citrate with 3.0 mEq/L Ca-containing-dialysate (A(−)D) has been reported, its effective Ca level and the overtreatment needed to correct metabolic acidosis on the basis of serum whole parathyroid hormone (wPTH) and arterial pH have not been evaluated in detail. Furthermore, recent reports have suggested the beneficial effect of citrate on fatigue, which is a significant risk for cardiovascular disease. Thirty-two hemodialysis patients receiving acetate with 2.75 mEq/L Ca-containing dialysate (A(+)D) participated in the present A(+)D to A(-)D one-arm switch study over 4 weeks. Predialysis wPTH increased significantly from 85.1 ± 59.0 pg/mL during hemodialysis A(+)D to 106.8 ± 78.8 pg/mL (p = 0.0015) after 2 weeks of A(-)D treatment. Predialysis arterial pH and bicarbonate levels significantly increased from 7.335 ± 0.037 to 7.370 ± 0.035 (p < 0.0001) and from 19.6 ± 2.1 mEq/L to 21.3 ± 1.7 mEq/L (p = 0.0001), respectively, whereas post-dialysis arterial pH and bicarbonate levels significantly increased from 7.447 ± 0.022 to 7.473 ± 0.027 (p < 0.0001) and from 25.2 ± 1.0 mEq/L to 28.1 ± 1.0 mEq/L (p < 0.0001). When all patients were divided into two equal-sized groups by fatigue score, the improvement in the fatigue score was significantly greater in the high group (∆1.8 ± 3.7) than in the low group (∆-0.8 ± 2.3) (p = 0.0252). This study demonstrated that the effective Ca level might be significantly lower in A(−)D than in A(+)D and metabolic acidosis was improved more strongly in A(-)D relative to that in A(+)D because of the higher bicarbonate concentration in A(-)D. Furthermore, A(-)D had a beneficial effect on intradialytic hemodynamics and fatigue sensation.

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Predialysis and Postdialysis pH and Bicarbonate and Risk of All-Cause and Cardiovascular Mortality in Long-term Hemodialysis Patients

Cited by 50 publications

References 27 publications

Effect of Bicarbonate-Buffered Dialysate on Ventricular Arrhythmias in Hemodialysis Patients

Effect of Bicarbonate-Buffered Dialysate on Ventricular Arrhythmias in Hemodialysis Patients

Acid-Base Status and Mortality Risk in Hemodialysis Patients

The Effects of Acetate-Free Citrate-Containing Dialysate on Calcium Metabolism and Fatigue in Patients on Maintenance Hemodialysis

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