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      Metabolic Acidosis in Peritoneal Dialysis Patients: The Role of Residual Renal Function

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          Background: Metabolic acidosis (MA) is common in chronic renal insufficiency (CRI) patients, and its pattern changes as renal function deteriorates. Although the prevalence of acidosis in peritoneal dialysis has been reported to be rather high, the causes of it have not been well studied. The present study was performed to examine the prevalence of metabolic acidosis in our continuous ambulatory peritoneal dialysis (CAPD) patients and its possible causes. Methods: In this cross-sectional study, we analyzed data from patients who received maintenance CAPD in our hospital and had been on dialysis for at least one month. Patients’ demographic features, medications, and intercurrent medical conditions were recorded. Data including blood biochemistry, dialysis adequacy, and nutrition were collected. A serum bicarbonate concentration of less than 23 mmol/l was defined as having acidosis. The normal value of the serum anion gap (AG) was defined as 12 ± 4 mmol/l. Results: A total of 154 patients (76 males and 78 females) with age of 60.04 ± 13.92 years and the time on dialysis of 16.83 ± 21.59 months were included in this study. Sixty-six patients (43%) had a serum bicarbonate of less than 23 mmol/l, among whom 12 patients (8%) were identified as having MA with increased AG, 54 (35%) were identified as having MA with normal AG. Patients who had better residual renal function (RRF) had a significantly lower serum bicarbonate level despite their higher total KT/V<sub>urea</sub> as compared to those with lower RRF. In addition, patients with MA and normal AG had the highest RRF and highest total KT/V<sub>urea</sub>. All patients with MA and increased AG had significantly lower values of dietary protein intake (DPI) as compared to their values of normalized protein nitrogen appearance (nPNA), and had higher serum urea and phosphate levels as compared with those patients without MA. Conclusion: Our study suggested that CAPD patients with better RRF were more susceptible to metabolic acidosis, which was characterized by normal anion gap and hyperchloremia. Thus, we speculate that renal loss of bicarbonate may to a large extent be responsible for the occurrence of MA in these patients.

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          Most cited references 13

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          Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease.

          Low serum albumin is a strong risk factor for mortality, but its association with low serum bicarbonate and inflammation in the setting of mild to moderately decreased kidney function is uncertain. We analyzed data from 15594 subjects over the age of 20 who participated in the Third National Health and Nutrition Examination Survey (NHANES III). Glomerular filtration rate (GFR) in mL/min/1.73 m2 was estimated by the abbreviated Modification of Diet in Renal Disease (MDRD) equation using appropriately calibrated serum creatinine. The age-adjusted prevalence of hypoalbuminemia (serum albumin or= 0.22 mg/dL was 36%, 44%, 69%, and 81%, respectively, both P trend 1 g/g, dietary protein intake, dietary caloric intake, serum bicarbonate, CRP, and GFR category were all significant predictors of hypoalbuminemia on univariate analysis. On simultaneously adjusting for the above variables, hypertension, diabetes, GFR, and dietary protein and caloric intake were no longer significant independent predictors of hypoalbuminemia. The adjusted odds ratio (OR) of serum bicarbonate (by quartile) for hypoalbuminemia was 1.0 for serum bicarbonate >28 mEq/L (reference), 1.25 for 26-28 mEq/L, 1.51 for 23-25 mEq/L, and 1.54 for 1.0 mg/dL. Elevated CRP and low serum bicarbonate are independently associated with hypoalbuminemia, explaining much of the high prevalence of hypoalbuminemia in chronic kidney disease.
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            Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure.

            Metabolic acidosis, a common condition in patients with renal failure, may be linked to protein-energy malnutrition (PEM) and inflammation, together also known as malnutrition-inflammation complex syndrome (MICS). Methods of serum bicarbonate measurement may misrepresent the true bicarbonate level, since the total serum carbon dioxide measurement usually overestimates the serum bicarbonate concentration. Moreover, the air transportation of blood samples to distant laboratories may lead to erroneous readings. In patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD), a significant number of endocrine, musculoskeletal, and metabolic abnormalities are believed to result from acidemia. Metabolic acidosis may be related to PEM and MICS due to an increased protein catabolism, decreased protein synthesis, endocrine abnormalities including insulin resistance, decreased serum leptin level, and inflammation among individuals with renal failure. Evidence suggests that the catabolic effects of metabolic acidosis may result from an increased activity of the adenosine triphosphate (ATP)-dependent ubiquitin-proteasome and branched-chain keto acid dehydrogenase. In contrast to the metabolic studies, many epidemiologic studies in maintenance dialysis patients have indicated a paradoxically inverse association between mildly decreased serum bicarbonate and improved markers of protein-energy nutritional state. Hence metabolic acidosis may be considered as yet another element of the reverse epidemiology in ESRD patients. Interventional studies have yielded inconsistent results in CKD and ESRD patients, although in peritoneal dialysis patients, mitigating acidemia appears to more consistently improve nutritional status and reduce hospitalizations. Large-scale, prospective randomized interventional studies are needed to ascertain the potential benefits of correcting acidemia in malnourished and/or inflamed CKD and maintenance hemodialysis patients. Until then, all attempts should be made to adhere to the National Kidney Foundation Kidney Disease and Dialysis Outcome Quality Initiative guidelines to maintain a serum bicarbonate level in ESRD patients of at least 22 mEq/L.
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              Metabolic acidosis and skeletal muscle adaptation to low protein diets in chronic uremia.

              To maintain nitrogen equilibrium when prescribed a low protein diet (LPD), metabolic adaptations occur involving a reduction protein turnover, principally decreased muscle protein degradation. Studies suggest that in patients with chronic renal failure (CRF) uncomplicated by metabolic acidosis (MA), these adaptive responses are intact. Because MA stimulates muscle proteolysis, this study examined the hypothesis that in CRF complicated by MA, the adaptation to LPD may be impaired, inducing a nitrogen wasting state. Six adults with CRF (mean GFR: 12.8 +/- 1.5 ml/min) and MA (mean serum bicarbonate: 17.0 +/- 1.0 mM/liter) receiving an unrestricted diet (protein intake: 1.2 g/kg body wt/day) were converted to an isocaloric LPD (protein: 0.6 g/kg body wt/day). Two weeks later total urinary nitrogen losses decreased, but skeletal muscle protein catabolism (SMPC), assessed from the urinary 3-methyl histidine:creatinine ratio, increased, demonstrating impairment in the adaptive down-regulation of SMPC. The LPD was continued for a further two weeks and MA was corrected with oral sodium bicarbonate (mean serum bicarbonate: 24.3 +/- 1.2 mM/liter). Correcting MA decreased SMPC to a level below that measured prior to protein restriction. The decreased SMPC was paralleled by further decreases in urinary nitrogen losses, confirming that MA impaired nitrogen utilization. It is concluded that MA can override the expected metabolic adaptive response to a LPD. The associated impairment of nitrogen utilization not only diminishes the efficacy of the diet, but also accelerates the loss of lean body mass.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                December 2005
                19 December 2005
                : 23
                : 6
                : 459-465
                Institute of Nephrology, First Hospital, Peking University, Beijing, China
                88989 Blood Purif 2005;23:459–465
                © 2005 S. Karger AG, Basel

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                Figures: 2, Tables: 3, References: 28, Pages: 7
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/88989
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