Correction of Metabolic Acidosis on Serum Albumin and Protein Catabolism in Hemodialysis Patients

Movilli, Ezio; Viola, Battista Fabio; Camerini, Corrado; Mazzola, Giuseppe; Cancarini, Giovanni

doi:10.1053/j.jrn.2008.08.012

Cited by 22 publications

(14 citation statements)

References 18 publications

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“…During the AFHD period, not only less hypotensive and malaise tendencies, but also slight but statistically insignificant increases in serum creatinine, and hemoglobin were noted (Table 5), resulting in a decrease in the epoetin dose needed (data not shown). These results suggest that avoidance of acetate use and correction of acidosis have beneficial effects on nutritional and metabolic parameters (11) and protein catabolism (12,13).…”

Section: Discussionmentioning

confidence: 76%

“…In this study, we measured pre and post‐dialysis arterial bicarbonate in nine patients, which showed a marked potential to correct acidosis in AFHD to within the K/DOQI target range of the pre‐dialysis arterial bicarbonate level: 22 mEq/L (BHD: pre 21.0 ± 1.72 mEq/L, post 24.7 ± 0.41, AFHD: pre 25.3 ± 2.54, post 31.2 ± 1.20). The correction of acidosis in hemodialysis patients has beneficial effects on nutritional and metabolic parameters (11), protein catabolism (12,13), and also hemodynamic effects (14). Gabutti et al.…”

Section: Discussionmentioning

confidence: 99%

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Comparison of Acetate‐Free Citrate Hemodialysis and Bicarbonate Hemodialysis Regarding the Effect of Intra‐Dialysis Hypotension and Post‐Dialysis Malaise

Daimon¹,

Dan²,

Kawano

2011

Ther Apher Dial

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Compared with acetate dialysate, bicarbonate dialysate has shown beneficial effects in reducing the morbidity associated with dialysis, but a small amount of acetate in bicarbonate dialysate may evoke hypotension or malaise. Acetate-free citrate hemodialysis (AFHD) may avoid these problems. In 44 hemodialysis patients bicarbonate hemodialysis (BHD) was conducted for three months, followed by a switch to AFHD for three months, and a further switch to bicarbonate hemodialysis (ReBHD). In BHD, AFHD and ReBHD, intra-dialysis hypotension and post-dialysis malaise were determined (hypotension: intra-dialysis systolic blood pressure (SBP) was expressed as a percentage of SBP at the start of hemodialysis, malaise was assessed by a self-reported 0 to 3 scale, 0: absence of malaise, 3: unbearable malaise). Compared with BHD, AFHD patients complained of less malaise but the intra-dialysis blood pressure change did not differ significantly (malaise: BHD 0.73 ± 0.76 vs. AFHD 0.32 ± 0.47, P < 0.0001, end hemodialysis SBP: BHD 93.6 ± 8.9 vs. AFHD 93.8 ± 10.1, P = NS). After switching to ReBHD from AFHD, the malaise score increased (AFHD 0.32 ± 0.47 vs. ReBHD 0.77 ± 0.89, P < 0.0001) and the intra-dialysis blood pressure dropped markedly (end hemodialysis SBP: AFHD 93.8 ± 10.1 vs. ReBHD 87.3 ± 10.5, P < 0.0001). Malaise was very severe in five patients who could not continue ReBHD. After ten days under ReBHD, ReBHD was changed to AFHD again in all patients. Although the exact mechanisms are not known, AFHD may be preferable to BHD to prevent hemodialysis-induced hypotension and malaise.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Comparison of Acetate‐Free Citrate Hemodialysis and Bicarbonate Hemodialysis Regarding the Effect of Intra‐Dialysis Hypotension and Post‐Dialysis Malaise

Daimon¹,

Dan²,

Kawano

2011

Ther Apher Dial

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“…In another experiment, Movilli and colleagues studied hemodialysis patients with metabolic acidosis before and after they were treated with supplements of sodium bicarbonate (NaHCO 3 ). After 3 months, correction of the metabolic acidosis was associated with significant improvements in the serum albumin concentration [13]. The NaHCO 3 treatment also decreased protein catabolism but only in patients who did not have high levels of circulating cytokines (i.e., inflammation).…”

Section: Mechanisms Stimulating Protein Catabolismmentioning

confidence: 99%

Mechanisms stimulating muscle wasting in chronic kidney disease: the roles of the ubiquitin-proteasome system and myostatin

Thomas

2013

Clin Exp Nephrol

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Catabolic conditions including chronic kidney disease (CKD), cancer, and diabetes cause muscle atrophy. The loss of muscle mass worsens the burden of disease because it is associated with increased morbidity and mortality. To avoid these problems or to develop treatment strategies, the mechanisms leading to muscle wasting must be identified. Specific mechanisms uncovered in CKD generally occur in other catabolic conditions. These include stimulation of protein degradation in muscle arising from activation of caspase-3 and the ubiquitin-proteasome system (UPS). These proteases act in a coordinated fashion with caspase-3 initially cleaving the complex structure of proteins in muscle yielding fragments that are substrates which are degraded by the UPS. Fortunately, the UPS exhibits remarkable specificity for proteins to be degraded because it is the major intracellular proteolytic system. Without a high level of specificity cellular functions would be disrupted. The specificity is accomplished by complex reactions that depend on recognition of a protein substrate by specific E3 ubiquitin ligases. In muscle, the specific ligases are Atrogin-1 and MuRF1 and their expression has characteristics of a biomarker of accelerated muscle proteolysis. Specific complications of CKD (metabolic acidosis, insulin resistance, inflammation, and angiotensin II) activate caspase-3 and the UPS through mechanisms that include glucocorticoids and impaired insulin or IGF-1 signaling. Mediators activate myostatin which functions as a negative growth factor in muscle. In models of cancer or CKD, strategies that block myostatin prevent muscle wasting suggesting that therapies which block myostatin could prevent muscle wasting in catabolic conditions.

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“…Pre-dialysis acidosis is deleterious due to its catabolic and pro-inflammatory effects, tightly linked to mortality [26]. Reducing acidosis in dialysis patients improves nutritional status and is associated with fewer hospitalizations, increased serum albumin, less muscle protein catabolism, better insulin sensitivity and sensitivity of parathyroid glands to serum calcium, and bone turnover [27-31]. K-DOQI guidelines have advocated a mid-week pre-HD serum (HCO 3 – ) of >22 mmol/L [32].…”

Section: Acid-base Electrolyte and Volume Derangements In Esrdmentioning

confidence: 99%

Acid-Base and Electrolyte Managements in Chronic Kidney Disease and End-Stage Renal Disease: Case-Based Discussion

et al. 2018

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Acid-base and electrolyte alterations are common in patients with chronic kidney disease (CKD) and end-stage kidney failure (ESRD). The alterations become more complex as CKD advances to ESRD, leading to morbidity and mortality. Three cases are presented illustrating some key prototypic features in CKD and ESRD. Each is accompanied by discussion of pathophysiology, diagnosis, and treatment options. Newer investigational results are integrated into the existing body of knowledge. Although rigorous assessment of various dialysis prescriptions is scanty, in its current state, instituting a well thought-out, multi-pronged management plan to minimize CKD/ESRD and dialysis-related electrolyte and acid-base disruptions is appropriate. There is a pressing need for prospective interventional trials in the future.

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Correction of Metabolic Acidosis on Serum Albumin and Protein Catabolism in Hemodialysis Patients

Cited by 22 publications

References 18 publications

Comparison of Acetate‐Free Citrate Hemodialysis and Bicarbonate Hemodialysis Regarding the Effect of Intra‐Dialysis Hypotension and Post‐Dialysis Malaise

Comparison of Acetate‐Free Citrate Hemodialysis and Bicarbonate Hemodialysis Regarding the Effect of Intra‐Dialysis Hypotension and Post‐Dialysis Malaise

Mechanisms stimulating muscle wasting in chronic kidney disease: the roles of the ubiquitin-proteasome system and myostatin

Acid-Base and Electrolyte Managements in Chronic Kidney Disease and End-Stage Renal Disease: Case-Based Discussion

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