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      Posttransplantation Hypomagnesemia as a Predictor of Better Graft Function after Transplantation

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          Abstract

          Background: Hypomagnesemia is frequently seen after transplantation and is particularly associated with the use of calcineurin inhibitors (CNIs). Methods: We conducted a retrospective, single-center analysis (2000–2013, N = 726) to explore the relationship between hypomagnesemia and long-term allograft outcome in kidney transplant recipients. For this study, a median serum magnesium (Mg) level of all measured Mg levels from 1 month to 1 year after renal transplantation was calculated. Results: For every increase in Mg by 0.1 mg/dL, the GFR decreased by 1.1 mL/min at 3 years posttransplant ( p < 0.01) and by 1.5 mL/min at 5 years posttransplant. A median blood Mg level of ≥1.7 was found to be an independent predictor of a GFR <60 mL/min at 3 years posttransplant. The odds of having a GFR <60 mL/min 3 years posttransplant was almost 2-fold higher in the high Mg group than in the low Mg group. Conclusions: Hypomagnesemia from 1 to 12 months after renal transplantation is associated with a better allograft function up to 5 years posttransplant. This relationship was found to hold true after accounting for baseline allograft function and the presence of slow graft function.

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          Chronic kidney disease: effects on the cardiovascular system.

           Mark L. Lipman,  E Schiffrin,  Johannes Mann (2007)
          Accelerated cardiovascular disease is a frequent complication of renal disease. Chronic kidney disease promotes hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. Furthermore, diabetic nephropathy is the leading cause of renal failure in developed countries. Together, hypertension, dyslipidemia, and diabetes are major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Inflammatory mediators are often elevated and the renin-angiotensin system is frequently activated in chronic kidney disease, which likely contributes through enhanced production of reactive oxygen species to the accelerated atherosclerosis observed in chronic kidney disease. Promoters of calcification are increased and inhibitors of calcification are reduced, which favors metastatic vascular calcification, an important participant in vascular injury associated with end-stage renal disease. Accelerated atherosclerosis will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Consequently, subjects with chronic renal failure are exposed to increased morbidity and mortality as a result of cardiovascular events. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with chronic kidney disease.
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            Magnesium intake and incidence of metabolic syndrome among young adults.

             David R Jacobs,  M Daviglus,  Linda Van Horn … (2006)
            Studies suggest that magnesium intake may be inversely related to risk of hypertension and type 2 diabetes mellitus and that higher intake of magnesium may decrease blood triglycerides and increase high-density lipoprotein (HDL) cholesterol levels. However, the longitudinal association of magnesium intake and incidence of metabolic syndrome has not been investigated. We prospectively examined the relations between magnesium intake and incident metabolic syndrome and its components among 4637 Americans, aged 18 to 30 years, who were free from metabolic syndrome and diabetes at baseline. Metabolic syndrome was diagnosed according to the National Cholesterol Education Program/Adult Treatment Panel III definition. Diet was assessed by an interviewer-administered quantitative food frequency questionnaire, and magnesium intake was derived from the nutrient database developed by the Minnesota Nutrition Coordinating Center. During the 15 years of follow-up, 608 incident cases of the metabolic syndrome were identified. Magnesium intake was inversely associated with incidence of metabolic syndrome after adjustment for major lifestyle and dietary variables and baseline status of each component of the metabolic syndrome. Compared with those in the lowest quartile of magnesium intake, multivariable-adjusted hazard ratio of metabolic syndrome for participants in the highest quartile was 0.69 (95% confidence interval [CI], 0.52 to 0.91; P for trend <0.01). The inverse associations were not materially modified by gender and race. Magnesium intake was also inversely related to individual component of the metabolic syndrome and fasting insulin levels. Our findings suggest that young adults with higher magnesium intake have lower risk of development of metabolic syndrome.
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              Dietary calcium and magnesium, major food sources, and risk of type 2 diabetes in U.S. black women.

               Supriya Krishnan,  Lynn Rosenberg,  Frank Hu … (2006)
              Inverse associations between magnesium and calcium intakes and risk of type 2 diabetes have been reported for studies in predominantly white populations. We examined magnesium, calcium, and major food sources in relation to type 2 diabetes in African-American women. This is a prospective cohort study including 41,186 participants of the Black Women's Health Study without a history of diabetes who completed validated food frequency questionnaires at baseline. During 8 years of follow-up (1995-2003), we documented 1,964 newly diagnosed cases of type 2 diabetes. The multivariate-adjusted hazard ratio of type 2 diabetes for the highest compared with the lowest quintile of intake was 0.69 (95% CI 0.59-0.81; P trend <0.0001) for dietary magnesium and 0.86 (0.74-1.00; P trend = 0.01) for dietary calcium. After mutual adjustment, the association for calcium disappeared (hazard ratio 1.04 [95% CI 0.88-1.24]; P trend = 0.88), whereas the association for magnesium remained. Daily consumption of low-fat dairy (0.87 [0.76-1.00]; P trend = 0.04) and whole grains (0.69 [0.60-0.79]; P trend <0.0001) were associated with a lower risk of type 2 diabetes compared with a consumption less than once a week. After mutual adjustment, the hazard ratio was 0.81 (0.68-0.97; P trend = 0.02) for magnesium and 0.73 (0.63-0.85; P trend <0.0001) for whole grains. These findings indicate that a diet high in magnesium-rich foods, particularly whole grains, is associated with a substantially lower risk of type 2 diabetes in U.S. black women.
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                Author and article information

                Journal
                Journal ID (publisher-id): KBR
                Journal ID (nlm-ta): Kidney Blood Press Res
                Journal ID (doi): 10.1159/issn.1420-4096
                Title: Kidney and Blood Pressure Research
                Publisher: S. Karger AG
                ISSN (Print): 1420-4096
                ISSN (Electronic): 1423-0143
                Publication date Subscription-year: 2020
                Publication date (Print): December 2020
                Publication date (Electronic): 05 November 2020
                Volume: 45
                Issue: 6
                Pages: 982-995
                Affiliations
                aSheba Medical Center, Nephrology Department, Tel Aviv University, Tel Aviv, Israel
                bDepartment of Internal Medicine “T”, Tel Aviv Souraski Medical Center, Tel Aviv University, Tel Aviv, Israel
                cDivision of Pulmonary and Critical Care Medicine, Oregon Health and Science University, Portland, Oregon, USA
                dRenal Division, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
                eTransplant Research Center, Renal Division, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
                Author notes
                *Tammy Hod, Sheba Medical Center, Nephrology Department, Derech sheba 2, Ramat Gan 52621 (Israel), tamar.hod@sheba.health.gov.il
                Article
                Publisher ID: 510797 Other ID: Kidney Blood Press Res 2020;45:982–995
                DOI: 10.1159/000510797
                PubMed ID: 33152728
                Copyright statement: © 2020 The Author(s) Published by S. Karger AG, Basel
                License:

                This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 1, Tables: 5, Pages: 14
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/510797
                Categories
                Subject: Research Article

                Data availability:

                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology

                Keywords: Hypomagnesemia, Calcineurin inhibitors, Renal allograft function

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