Magnesium Metabolism in Chronic Renal Disease*

Randall, Russell E.

doi:10.1111/j.1749-6632.1969.tb13013.x

Cited by 21 publications

(10 citation statements)

References 40 publications

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“…However, the absorption of Mg in the jejunum has been demonstrated to be dependent on vitamin D, and that administration of 1‐25‐dihydroxyvitamin D 3 to patients with CRF resulted in an increased intestinal absorption of Mg (20). Furthermore, successful renal transplantation is able to restore the impaired Mg absorption in these patients (16). Therefore, deficient synthesis of the active metabolite of vitamin D by the kidneys may play a significant causative role in Mg malabsorption in CRF.…”

Section: Magnesium Homeostasismentioning

confidence: 99%

“…Early reports indicated that there were no significant differences in net Mg absorption between normal subjects and CRF patients (14,15). Randall (16) reported only slightly reduced absorption of Mg in chronic renal disease, whereas others found average net absorption rates ranging between 17% and 38% (17,18). Strictly controlled balance studies showed that the average net absorption of Mg in patients with CRF was significantly lower than the absorption in subjects with normal renal function (12), results that have been confirmed using radioisotope techniques, even when age was taken into consideration (19).…”

Section: Magnesium Homeostasismentioning

confidence: 99%

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Reviews: Clinical Implications of Disordered Magnesium Homeostasis in Chronic Renal Failure and Dialysis

Navarro‐González

Mora‐Fernández

García‐Pérez³

2009

Seminars in Dialysis

150

156

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Magnesium (Mg) is the fourth most abundant cation in the body, mainly located within bone and skeletal muscle. The normal total plasma Mg concentration varies in a narrow range, with approximately 60% present as free Mg ions, the biologically active form. The kidney plays a principal role in Mg balance. Approximately 70-80% of plasma Mg is ultrafilterable, and under normal circumstances, 95% of the filtered load of Mg is reabsorbed. As chronic renal failure (CRF) progresses, urinary Mg excretion may be insufficient to balance intestinal Mg absorption and dietary Mg intake becomes a major determinant of serum and total body Mg levels. Until severe reductions in glomerular filtration rate (<30 ml/min), serum Mg levels are usually normal; with lower rates of renal function, serum Mg is increased. Concerning dialysis patients, dialysate Mg plays a critical role in maintaining Mg homeostasis, with serum Mg being largely dependent on the concentration of the ion in the dialysis solution. Magnesium has been implicated in diverse consequences, both beneficial and deleterious, in patients with CRF and dialysis. Potential harmful effects of elevated Mg include altered nerve conduction velocity, increased pruritus, and alterations to osseous metabolism and parathyroid gland function (mineralization defects, contribution to osteomalacic renal osteodystrophy, and adynamic bone disease). Hypermagnesemia also may retard vascular calcification. Low Mg levels have been associated with impairment of myocardial contractility, intradialytic hemodynamic instability, and hypotension. In addition, low Mg has been also linked to carotid intima-media thickness, a marker of atherosclerotic vascular disease and a predictor of vascular events.

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Section: Magnesium Homeostasismentioning

confidence: 99%

Section: Magnesium Homeostasismentioning

confidence: 99%

Reviews: Clinical Implications of Disordered Magnesium Homeostasis in Chronic Renal Failure and Dialysis

Navarro‐González

Mora‐Fernández

García‐Pérez³

2009

Seminars in Dialysis

150

156

View full text Add to dashboard Cite

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“…Ammonia is toxic because it effectively removes a-ketoglutarate from the tricarboxylic acid cycle and can cause severe inhibition of respiration in the brain and nervous tissues. Renal tubular disorders have been known to cause hypomagnesemia [9]. This was probably the cause of hypomagnesemia in Aristolochia-poisoned goats and may have contributed to the nervous signs since nervous signs are known to occur in grass tetany in cattle [ 3 ] .…”

Section: Discussionmentioning

confidence: 99%

The Toxicity of Aristolochia bracteata in Goats

1983

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Abstract. Diarrhea, dyspnea, tympany, arching of the back, loss of condition, and loss of hair from the back were the prominent signs when Aristolochia bracteata was given orally to goats. The main lesions were hemorrhages in the lungs, heart, and kidneys, fatty change and congestion in the liver, mucoid abomasitis and enteritis and straw-colored fluid in serous cavities. An increase in aspartate aminotransferase activity, ammonia and urea concentrations and a decrease in the concentrations of total protein and magnesium were detected in the serum.Aristolochia bructeatu is a member of the family Aristolochiaceae and is used in Kenya, Tanzania, Ethiopia, and Sudan for the treatment of infections with nematodes [4, 141. The present study was designed to study in detail the clinical and biochemical changes, and lesions in Nubian goats dosed with A. bracteata. Materials and MethodsEight six-to twelve-month-old Nubian goats of either sex were used throughout the experiment. They were fed on lucerne and water ad libitum. The goats were divided into four groups. The fresh leaves of A . bracteata were chopped, suspended in water, and given by stomach tube at the rate of 5.0 g/kg/day to two goats (group I), 1 .O g/kg/day to two goats (group II), and 0.5 g/kg/day to two goats (group HI). The two goats in group IV were untreated controls. Daily dosing was continued until the goats died or were killed in extremis. The total plant leaves given to each goat is found in table I.All goats were bled from the jugular vein before dosing commenced and at two-day intervals thereafter for serum analysis and hematology. Blood samples were allowed to clot, serum was separated and stored at -20°C until analyzed. Serum samples were examined for the activities of asparate aminotransferase and alanine aminotransferase [lo]. Tissues were fixed in 10% formal-saline and 6-pm parafin sections were stained with C',

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“…Previously no standard has been available by which to test such a possibility but the suggested model should enable renal wasting of magnesium to be recognized with greater precision. Of nine patients in whom such wasting was inferred (Randall, 1969), only six had values of T,,M,/GFR below 0.625 mmol/l when the data were plotted as in Fig. 4.…”

Section: Fig 5 Comparison Of Changes In Tubular Reabsorption Of Calmentioning

confidence: 99%

“…The kidney is the principal agent of magnesium conservation and so is important in the prevention of magnesium depletion (Heaton, 1969). Conversely, when conservation is defective, excessive renal excretion of magnesium can be a cause of magnesium depletion (Randall, 1969; Bar, Wilson & Mazzaferri, 1975). Although this dual role of the kidney is generally acknowledged, there are few quantitative descriptions of its behaviour in these two situations.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Cellulose Phosphate on Plasma and Urinary Magnesium at Different Levels of Parathyroid Function in Man

1976

Clinical Science

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1. Previously published data obtained by magnesium infusion in man were found to conform to a Tm/glomerular filtration rate (GFR) model on the assumption of 80% diffusibility of plasma magnesium. The lower limit of Tm,Mg/GFR was 625 mumol/l. 2. Previously published data concerning the effect of cellulose phosphate on magnesium metabolism in normal subjects, patients with latent hypoparathyroidism and patients with primary hyperparathyroidism were found to conform to the same model, with the same limit for Tm,Mg/GFR for all three levels of parathyroid function. 3. The threshold for magnesium excretion is sharper with less 'splay' than for phosphate, but as for phosophate it is close to the normal blood concentration. 4. Because of the geometrical relationship between different methods of presentation of data, at a constant value for Tm,Mg/GFR changes in magnesium load or in GFR automatically produce changes in fractional magnesium clearance. This is the explanation for the increase in fractional magnesium clearance which occurs which with diminishing renal function. 5. Renal conservation of magnesium is a passive consequence of the fall in plasma magnesium. There was no evidence of augmented tubular reabsorption of magnesium in response to magnesium deprivation in any of the three groups of subjects. 6. The tubular reabsorption of magnesium was not altered detectably by a moderate deficiency or excess of parathyroid hormore. Changes in parathyroid hormone secretion are probably not concerned in normal magnesium homeostasis.

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Magnesium Metabolism in Chronic Renal Disease*

Cited by 21 publications

References 40 publications

Reviews: Clinical Implications of Disordered Magnesium Homeostasis in Chronic Renal Failure and Dialysis

Reviews: Clinical Implications of Disordered Magnesium Homeostasis in Chronic Renal Failure and Dialysis

The Toxicity of Aristolochia bracteata in Goats

The Effect of Cellulose Phosphate on Plasma and Urinary Magnesium at Different Levels of Parathyroid Function in Man

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