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      Serum Sulphate Levels in Hemodialysis Patients

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          Abstract

          Objective

          Sulphur, similar to phosphorus, is easily attached to organic compounds. The inadequate elimination of sulphate may cause high sulphate concentrations in hemodialysis (HD) patients because sulphate is low in free form in plasma. Although we are well aware of the accumulation of phosphorus in chronic dialysis patients, we do not have an adequate knowledge database about the sulphur compounds. This study was designed to determine the level of sulphate in hemodialysis patients.

          Materials and Methods

          Ninety-four prevalent HD patients and 33 patients without renal failure were included in the study. The serum inorganic sulphate levels were measured by turbidimetric technique. Moreover, the serum level of urea, creatinine, albumin, calcium, phosphorus, and parathyroid hormone concentrations was simultaneously recorded.

          Results

          Mean levels of plasma sulphate were significantly higher (0.56 ± 0.17 mM vs 0.31 ± 0.13 mM, p < 0.001) in HD patients. Serum sulphate level correlated with patient's age, serum albumin, serum BUN and creatinine, and serum phosphorus level in HD patients. Serum sulphate levels were not associated with serum parathyroid hormone levels.

          Conclusion

          Serum sulphate levels were approximately twofold higher in HD patients than in the normal control group. Inorganic sulphate does not seem to accumulate in long-term dialysis patients, and mild increased serum levels of sulphate has no poor clinical outcome in these patients.

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          Most cited references22

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          The clinical chemistry of inorganic sulfate.

          Michael Cole, J Evrovski (2000)
          Although inorganic sulfate is an essential and ubiquitous anion in human biology, it is infrequently assayed in clinical chemistry today. Serum sulfate is difficult to measure accurately without resorting to physicochemical methods, such as ion chromatography, although many other techniques have been described. It is strongly influenced by a variety of physiological factors, including age, diet, pregnancy, and drug ingestion. Urinary excretion is the principal mechanism of disposal for the excess sulfate produced by sulfur amino acid oxidation, and the kidney is the primary site of regulation. In renal failure, sulfoesters accumulate and hypersulfatemia contributes directly to the unmeasured anion gap characteristic of the condition. In contrast, sulfate in urine is readily assayed by a number of means, particularly nephelometry after precipitation as a barium salt. Sulfate is most commonly assayed today as part of the clinical workup for nephrolithiasis, because sulfate is a major contributor to the ionic strength of urine and alters the equilibrium constants governing saturation and precipitation of calcium salts. Total sulfate deficiency has hitherto not been described, although genetic defects in sulfate transporters have been associated recently with congenital osteochondrodystrophies that may be lethal. New insights into sulfate transport and its hormonal regulation may lead to new clinical applications of sulfate analysis in the future.
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            Elevated levels of serum sulfite in patients with chronic renal failure.

            H Kajiyama, Y Nojima, H Mitsuhashi … (2000)
            Sulfite, a well known air pollutant, is toxic for humans, especially those with sulfite hypersensitivity. Sulfite is also generated endogenously, during normal metabolism of sulfur-containing amino acids. Mammalian tissues contain the enzyme sulfite oxidase, which detoxifies both endogenous and exogenous sulfite by oxidation to sulfate. Deficiency of sulfite oxidase in humans is fatal, demonstrating its physiologic importance. Nevertheless, information about serum and tissue levels of sulfite in normal and pathologic conditions is limited. Using a sensitive HPLC assay, it is shown here that sera from patients with chronic renal failure (CRF) contain significantly higher amounts of sulfite than those from healthy subjects. Mean +/- SD of serum sulfite in healthy subjects (n = 20) was 1.55 +/- 0.54 microM, whereas those in patients under maintenance hemodialysis (HD patients; n = 44) and CRF patients before introducing dialysis therapy (pre-HD patients; n = 33) were 3. 23 +/- 1.02 microM (P < 0.01) and 3.80 +/- 3.32 microM (P < 0.01), respectively. Among pre-HD patients, serum sulfite was positively correlated with serum creatinine (r = 0.714, P < 0.0001), and negatively with serum albumin (r = -0.407, P = 0.0188), hematocrit (r = -0.524, P = 0.0017), and total cholesterol (r = -0.375, P = 0. 0318). There was no significant association between sulfite and patient age, gender, or leukocyte counts. Multiple regression analysis revealed serum creatinine as the sole independent predictor of serum sulfite levels. Each HD treatment was associated with approximately 27% reduction in serum sulfite levels, suggesting the presence of a dialyzable form in serum. Thus, these results indicate that reduced glomerular filtration is a factor that determines serum sulfite levels. Chronic elevation in serum sulfite levels might contribute to tissue or organ dysfunction in patients with CRF.
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              Effect of a chronic acid load as sulfate or sulfur amino acids on bone metabolism in adult rats.

              James S. Whiting, H Draper (1981)
              Diets containing an acid load as either sulfur amino acids (SAA) or inorganic sulfate were fed to 45Ca-labeled adult male rats for 10 months. Radioisotope excretion and bone composition data (femur, tibia, mandibles) were compared with those for rats fed a control (15% soy protein) diet. Rats fed the SAA supplement (1.28% cystine plus 0.19% methionine) exhibited a significant reduction in femoral weight and A:R ratio and a tendency toward lower specific gravity, dry weight, fat-free weight and calcium content. Femoral radioautographs indicated a reduction in metaphyseal bone density in six of eight animals. We have postulated that the osteopenia produced by feeding excess free SAA may be due to decreased bone formation caused by a reaction between homocysteine and the aldehyde groups of collagen, as in genetic homo-cystinuric osteoporosis. Sulfate feeding (1.42% of the diet) produced a significant increase in 45Ca excretion, indicative of enhanced bone resorption, lasting about 2 months. There was a tendency for bone mass measurements to be lower than controls after 10 months, but the differences were not significant. Two of eight sulfate-fed rats showed radiographic evidence of osteopenia. No evidence of osteopenia was seen in the controls or in rats previously fed a high protein diet containing the same concentration of SAA.
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                Author and article information

                Contributors
                Ibrahim Yildirim:
                ORCID: https://orcid.org/0000-0003-4064-1753
                Journal
                Journal ID (nlm-ta): Int J Nephrol
                Journal ID (iso-abbrev): Int J Nephrol
                Journal ID (publisher-id): IJN
                Title: International Journal of Nephrology
                Publisher: Hindawi
                ISSN (Print): 2090-214X
                ISSN (Electronic): 2090-2158
                Publication date Collection: 2019
                Publication date (Electronic): 1 December 2019
                Volume: 2019
                Electronic Location Identifier: 1063514
                Affiliations
                1University of Health Sciences, Department of Internal Medicine, Division of Nephrology, Ankara, Turkey
                2Bulent Ecevit University Medical School, Department of Internal Medicine, Zonguldak, Turkey
                3Bulent Ecevit University Medical School, Department of Medical Biochemistry, Zonguldak, Turkey
                4Zonguldak Atatürk State Hospital, Department of Nephrology, Zonguldak, Turkey
                5Samsun Educational and Research Hospital, Department of Nephrology, Samsun, Turkey
                Author notes

                Academic Editor: Jaime Uribarri

                Author information
                https://orcid.org/0000-0003-4064-1753
                https://orcid.org/0000-0003-3307-7234
                Article
                DOI: 10.1155/2019/1063514
                PMC ID: 6913331
                SO-VID: dcb32c45-df27-4c25-86f9-ae4a1a0a820f
                Copyright © Copyright © 2019 Ibrahim Yildirim et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 4 July 2019
                Date revision received : 7 October 2019
                Date accepted : 15 October 2019
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Nephrology
                Data availability:
                ScienceOpen disciplines: Nephrology

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