Do diuretics cause magnesium deficiency?

Davies, D. L.; Fraser, Robert

doi:10.1111/j.1365-2125.1993.tb05883.x

Cited by 27 publications

(10 citation statements)

References 104 publications

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“…In contrast, insulin resistance has been proposed to explain the reduced TRPM6 activity and hypomagnesemia in T2DM (94). Until now, it has been widely accepted that Na + and Mg 2+ transport in the DCT go hand in hand, since reduced NCC activity causes hypomagnesemia as shown in patients with Gitelman syndrome and in users of thiazide diuretics (105,106 Reports on diabetic retinopathy suggest that insulin regulates the potassium channel Kir4.1 in the retina (107,108). Given that Kir4.1 is also an important regulator of Na + and Mg 2+ transport in DCT, and patients with mutations in Kir4.1 develop hypomagnesemia and hypokalemia, future studies should include regulation of Kir4.1 in T2DM patients (109,110).…”

Section: Diabetes-dct Paradoxmentioning

confidence: 99%

Hypomagnesemia in Type 2 Diabetes: A Vicious Circle?

et al. 2015

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Over the past decades, hypomagnesemia (serum Mg 2+ <0.7 mmol/L) has been strongly associated with type 2 diabetes mellitus (T2DM concentrations. This Perspective provides a systematic overview of the molecular mechanisms underlying the effects of Mg 2+ on insulin secretion and insulin signaling. In addition to providing a review of current knowledge, we provide novel directions for future research and identify previously neglected contributors to hypomagnesemia in T2DM.Globally, over 300 million people suffer from type 2 diabetes mellitus (T2DM), and the prevalence is predicted to rise to over 600 million over the next decades (1). T2DM is characterized by a combination of insulin deficiency and insulin resistance. The general pathophysiological concept is that hyperglycemia emerges when endogenous insulin secretion can no longer match the increased demand owing to insulin resistance (2).Since the 1940s, it has been reported that T2DM is associated with hypomagnesemia (3,4). Low serum magnesium (Mg 2+ ) levels have been reported in large cohorts of patients with T2DM (5). In T2DM, the prevalence of hypomagnesemia ranges between 14 and 48% compared with between 2.5 and 15% in healthy control subjects (4). Hypomagnesemia is associated with a more rapid, and permanent, decline in renal function in patients with T2DM (6). In addition, epidemiological studies consistently show an inverse relationship between dietary Mg 2+ intake and risk of developing T2DM (7). Several patient studies have shown beneficial effects of Mg 2+ supplementation on glucose metabolism and insulin sensitivity (8-10). Recently, Rodríguez-Morán et al. (11) published an excellent overview of the clinical studies addressing the role of Mg 2+ in T2DM. In our review, we will focus on the molecular mechanisms underlying these clinical observations. Mg 2+ is an essential ion for human health, as it is involved in virtually every mechanism in the cell, including energy homeostasis, protein synthesis, and DNA stability (12). Considering these divergent functions, it can be appreciated that serum Mg 2+ levels are tightly regulated between 0.7 and 1.05 mmol/L in healthy individuals. However, impaired intestinal Mg 2+ absorption or renal Mg 2+ wasting can lead to hypomagnesemia. A wide range of genetic and environmental factors can affect the Mg 2+ -deficient state, which have previously been extensively reviewed (12).In this review, we address the following questions that are central to the role of hypomagnesemia in T2DM: 1) Does Mg 2+ regulate insulin secretion? 2) How does Mg 2+ affect insulin resistance? 3) How does insulin regulate Mg 2+ homeostasis? Taken together, these questions will aid the understanding of whether hypomagnesemia is a causative factor for or a consequence of T2DM.

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Section: Diabetes-dct Paradoxmentioning

confidence: 99%

Hypomagnesemia in Type 2 Diabetes: A Vicious Circle?

et al. 2015

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“…Concurrent changes in neurohumoral control mechanisms such as the renin-angiotensin system and sympathetic nervous system, dietary factors, medication effects including diuretics, digitalis, and renal function make prediction of Mg status imprecise [4][5][6][7][8][9]13,[21][22][23][24][25][26][27][28][29]. Since Mg deficiency is known to contribute to hypokalemia [4][5][6][7]21] well as cardiac arrhythmias [4,5,[8][9][10][11][12]21], and sudden death [5,11,12]; clinical questions regarding Mg status frequently arise.…”

Section: Introductionmentioning

confidence: 99%

Magnesium supplementation in patients with congestive heart failure.

Costello

Moser-Veillon

DiBianco

1997

Journal of the American College of Nutrition

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Supplementation with 10.4 mmol oral magnesium daily for 3 months did not significantly alter blood levels or magnesium retention; however, patients demonstrated lower retention of magnesium after supplementation. Differences in magnesium retention was not related to basal magnesium intake, blood levels or excretion. Unfortunately, even an intensive effort at characterizing magnesium status did not identify a clinical indicator of utility for differentiating patients with congestive heart failure before, during, and after 3 months of magnesium supplementation.

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“…A large body of evidence indicates that hypomagnesemia after cyclosporine treatment is caused by enhanced urinary excretion [5,18) and perhaps even by intracellular uptake of the ion [18]. Apart from cyclosporine, diabetes mellitus [lo, 161 and the use of benzothiadiazines or high-ceiling diuretics [9] are expected to enhance hypomagnesemia after renal transplantation. In this study, hypomagnesemia was more pronounced among patients with diabetes mellitus.…”

Section: Discussionmentioning

confidence: 99%

Permanently reduced plasma ionized magnesium among renal transplant recipients on cyclosporine

et al. 1999

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Hypomagnesemia is common after kidney transplantation. Until recently, only the determination of total plasma magnesium was possible, whereas the assessment of ionized magnesium has since become practicable. One hundred and nine renal transplant patients on cyclosporine with allografts functioning stably for more than 6 months and plasma creatinine levels of less than 200 pmolil entered the study. Total and ionized circulating magnesium were assessed among these 109 patients, as well as among 15 renal transplant patients not on cyclosporine and 21 healthy volunteers. Cyclosporine patients showed significantly lower total and ionized circulating magnesium values than the two control groups. Plasma total and ionized magnesium levels were also significantly lower among cyclosporine patients treated concurrently with insulin or oral hypoglycemic agents than among those who were not. No correlation was noted between time after transplantation and plasma magnesium with respect to patients on cyclosporine. In conclusion, the study demonstrates that a large subset of renal transplant patients treated with cyclosporine have permanent deficiencies of ionized and total magnesium. The tendency towards hypomagnesemia is also more pronounced among patients with diabetes mellitus.

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Do diuretics cause magnesium deficiency?

Cited by 27 publications

References 104 publications

Hypomagnesemia in Type 2 Diabetes: A Vicious Circle?

Hypomagnesemia in Type 2 Diabetes: A Vicious Circle?

Magnesium supplementation in patients with congestive heart failure.

Permanently reduced plasma ionized magnesium among renal transplant recipients on cyclosporine

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