Lower magnesium level associated with new-onset diabetes and pre-diabetes after kidney transplantation

Garg, Neetika; Weinberg, Janice; Ghai, Sandeep; Bradauskaite, Gitana; Nuhn, M; Gautam, Anju; Kumar, Nilay; Francis, Jean; Chen, Joline L.T.

doi:10.1007/s40620-014-0072-1

Cited by 28 publications

(20 citation statements)

References 39 publications

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“…In this study, tacrolimus was associated with PTDM, but the association disappeared when controlling for hypomagnesemia, suggesting that tacrolimus may increase the risk of PTDM, in part through the induction of hypomagnesemia. A smaller retrospective study revealed similar findings (77). A study in liver transplant recipients also suggested that early posttransplant hypomagnesemia was associated with increased PTDM (78).…”

Section: Role Of Immunosuppression Agentsmentioning

confidence: 60%

Post-Transplant Diabetes Mellitus: Causes, Treatment, and Impact on Outcomes

Shivaswamy

Boerner

Larsen³

2015

Endocrine Reviews

249

203

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and VA Nebraska-Western Iowa Health Care System (V.S.), Omaha, Nebraska 68105Post-transplant diabetes mellitus (PTDM) is a frequent consequence of solid organ transplantation. PTDM has been associated with greater mortality and increased infections in different transplant groups using different diagnostic criteria. An international consensus panel recommended a consistent set of guidelines in 2003 based on American Diabetes Association glucose criteria but did not exclude the immediate post-transplant hospitalization when many patients receive large doses of corticosteroids. Greater glucose monitoring during all hospitalizations has revealed significant glucose intolerance in the majority of recipients immediately after transplant. As a result, the international consensus panel reviewed its earlier guidelines and recommended delaying screening and diagnosis of PTDM until the recipient is on stable doses of immunosuppression after discharge from initial transplant hospitalization. The group cautioned that whereas hemoglobin A1C has been adopted as a diagnostic criterion by many, it is not reliable as the sole diabetes screening method during the first year after transplant. Risk factors for PTDM include many of the immunosuppressant medications themselves as well as those for type 2 diabetes. The provider managing diabetes and associated dyslipidemia and hypertension after transplant must be careful of the greater risk for drug-drug interactions and infections with immunosuppressant medications. Treatment goals and therapies must consider the greater risk for fluctuating and reduced kidney function, which can cause hypoglycemia. Research is actively focused on strategies to prevent PTDM, but until strategies are found, it is imperative that immunosuppression regimens are chosen based on their evidence to prolong graft survival, not to avoid PTDM. (Endocrine Reviews 37: 37-61, 2016)

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Section: Role Of Immunosuppression Agentsmentioning

confidence: 60%

Post-Transplant Diabetes Mellitus: Causes, Treatment, and Impact on Outcomes

Shivaswamy

Boerner

Larsen³

2015

Endocrine Reviews

249

203

View full text Add to dashboard Cite

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“…Those who have existing diabetes pretransplantation have a greater risk of having a CV related event compared to patients with posttransplant diabetes [22,61,68] and overall higher all cause mortality [69] . There are many risk factors for the development of posttransplant diabetes and these include increasing age [68] , ethnic background [67,70] (AfricanAmerican, Hispanic and South Asian), positive family history [71] , visceral adiposity [72] , hypomagnesaemia [73] , viral infections [61,74] (hepatitis C virus and Cytomegalovirus) and immunosup pression medications. Most of the commonly prescribed immunosuppressants exert negative effects on glucose metabolism leading to impaired insulin secretion and sensitivity [75] .…”

Section: Diabetes Mellitusmentioning

confidence: 99%

Cardiovascular risk factors following renal transplant

Neale

Smith

2015

WJT

118

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Kidney transplantation is the gold-standard treatment for many patients with end-stage renal disease. Renal transplant recipients (RTRs) remain at an increased risk of fatal and non-fatal cardiovascular (CV) events compared to the general population, although rates are lower than those patients on maintenance haemodialysis. Death with a functioning graft is most commonly due to cardiovascular disease (CVD) and therefore this remains an important therapeutic target to prevent graft failure. Conventional CV risk factors such as diabetes, hypertension and renal dysfunction remain a major influence on CVD in RTRs. However it is now recognised that the morbidity and mortality from CVD are not entirely accounted for by these traditional risk-factors. Immunosuppression medications exert a deleterious effect on many of these well-recognised contributors to CVD and are known to exacerbate the probability of developing diabetes, graft dysfunction and hypertension which can all lead on to CVD. Nontraditional CV risk factors such as inflammation and anaemia have been strongly linked to increased CV events in RTRs and should be considered alongside those which are classified as conventional. This review summarises what is known about risk-factors for CVD in RTRs and how, through identification of those which are modifiable, outcomes can be improved. The overall CV risk in RTRs is likely to be multifactorial and a complex interaction between the multiple traditional and non-traditional factors; further studies are required to determine how these may be modified to enhance survival and quality of life in this unique population. Core tip: Cardiovascular disease (CVD) is the leading cause of death and disability in patients following a renal transplant. Identification of risk factors for CVD and strategies for their improvement are required in order to prevent graft failure in this complex patient

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“…Magnesium entry into these tissues is regulated, at least in part, by the activity of the transient receptor potential melastatin 7 cation channel (TRPM7), a divalent ion transporter with a high affinity for magnesium. In populationbased studies, magnesium deficiency has been implicated in several disorders, such as diabetes (Garg et al, 2014), hypertension (Cunha et al, 2012), and CVD (Reffelmann et al, 2011). Although not currently considered to be a hallmark of CKD, abnormal serum magnesium has also been associated with increased cardiovascular events and mortality in endstage renal disease patients (Navarro-Gonzalez et al, 2009;Kanbay et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Magnesium Modifies the Impact of Calcitriol Treatment on Vascular Calcification in Experimental Chronic Kidney Disease

Zelt

McCabe

Svajger

et al. 2015

J Pharmacol Exp Ther

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Chronic kidney disease (CKD) patients are commonly treated with vitamin D analogs, such as calcitriol. Recent epidemiologic evidence revealed a significant interaction between vitamin D and magnesium, since an inverse relationship between vitamin D levels and mortality mainly occurs in patients with a high magnesium intake. The aim of the study was to assess the mechanisms involved by determining whether magnesium alone or combined with calcitriol treatments differentially impacts vascular calcification (VC) in male Sprague-Dawley rats with adenine-induced CKD. Treatment with moderate doses of calcitriol (80 mg/kg) suppressed parathyroid hormone to near or slightly below control levels. Given alone, this dose of calcitriol increased the prevalence of VC; however, when magnesium was given in combination, the severity of calcification was attenuated in the abdominal aorta (51% reduction), iliac (44%), and carotid arteries (46%) compared with CKD controls. The decreases in vascular calcium content were associated with a 20-50% increase in vascular magnesium. Calcitriol treatment alone significantly decreased TRPM7 protein (↓ to ∼11%), whereas the combination treatment increased both mRNA (1.7Â) and protein (6.8Â) expression compared with calcitriol alone. In summary, calcitriol increased VC in certain conditions, but magnesium prevented the reduction in TRPM7 and reduced the severity of VC, thereby increasing the bioavailable magnesium in the vascular microenvironment. These findings suggest that modifying the adverse effect profile of calcitriol with magnesium may be a plausible approach to benefiting the increasing number of CKD patients being prescribed calcitriol.

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Lower magnesium level associated with new-onset diabetes and pre-diabetes after kidney transplantation

Abstract: A lower magnesium level at 1 month after transplantation may be predictive of a subsequent diagnosis of glucose intolerance or diabetes in renal transplant recipients. Whether replenishing magnesium stores can prevent development of these disorders requires further investigation.

Cited by 28 publications

References 39 publications

Post-Transplant Diabetes Mellitus: Causes, Treatment, and Impact on Outcomes

Post-Transplant Diabetes Mellitus: Causes, Treatment, and Impact on Outcomes

Cardiovascular risk factors following renal transplant

Magnesium Modifies the Impact of Calcitriol Treatment on Vascular Calcification in Experimental Chronic Kidney Disease

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