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Advanced CKD with insufficient urinary excretion of phosphorus is the main cause of hyperphosphatemia
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Friedman EA Consequences and management of hyperphosphatemia in patients with renal insufficiency Kidney Int Suppl 2005 Jun;(95):S1 7 [PMID: 15882307] Goodman WG Calcium and phosphorus metabolism in patients who have chronic kidney disease Med Clin North Am 2005 May;89(3):631 47 [PMID: 15755471] Tonelli M et al; Cholesterol And Recurrent Events Trial Investigators Relation between serum phosphate level and cardiovascular event rate in people with coronary disease Circulation 2005 Oct 25;112(17):2627 33 [PMID: 16246962]
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Table 21 12 Causes of hypomagnesemia
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Diminished absorption or intake Malabsorption, chronic diarrhea, laxative abuse Prolonged gastrointestinal suction Small bowel bypass Malnutrition Alcoholism Total parenteral alimentation with inadequate Mg2+ content Increased renal loss Diuretic therapy (loop diuretics, thiazide diuretics) Hyperaldosteronism, Gitelman s syndrome (a variant of Bartter s syndrome) Hyperparathyroidism, hyperthyroidism Hypercalcemia Volume expansion Tubulointerstitial diseases Transplant kidney Drugs (aminoglycoside, cetuximab, cisplatin, amphotericin B, pentamidine) Others Diabetes mellitus Post parathyroidectomy (hungry bone syndrome) Respiratory alkalosis Pregnancy
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DISORDERS OF MAGNESIUM CONCENTRATION
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The normal plasma concentration is 15 25 mEq/L, with about one-third bound to protein and two-thirds existing as free cation Excretion of magnesium ion is via the kidney Normally, about 3% of magnesium filtered by the glomerulus is excreted in urine Magnesium exerts physiologic effects on the nervous system resembling those of calcium Magnesium acts directly upon the myoneural junction Altered concentration of Mg2+ in the plasma usually provokes an associated alteration of Ca2+ Hypermagnesemia suppresses secretion of PTH with consequent hypocalcemia Severe and prolonged magnesium depletion impairs secretion of PTH with consequent hypocalcemia Hypomagnesemia may impair end-organ response to PTH as well
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mechanisms of magnesium wasting have been revealed in some hereditary disorders
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A Symptoms and Signs
Common symptoms are those of hypokalemia and hypocalcemia, with weakness and muscle cramps There is marked neuromuscular and central nervous system hyperirritability, with tremors, athetoid movements, jerking, nystagmus, and a positive Babinski response There may be hypertension, tachycardia, and ventricular arrhythmias Confusion and disorientation may be prominent features
ESSENTIALS OF DIAGNOSIS
Serum concentration of magnesium may not be decreased even in the presence of magnesium depletion Check urinary magnesium excretion if renal magnesium wasting is suspected Causes neurologic symptoms and arrhythmias Impairs release of PTH
B Laboratory Findings
Urinary excretion of magnesium exceeding 10 30 mg/d or a fractional excretion more than 2% indicates renal magnesium wasting In calculating fractional excretion of magnesium, since only 30% is protein bound, it follows that 70% of circulating magnesium is filtered by the glomerulus In addition to hypomagnesemia, hypocalcemia and hypokalemia are often present The ECG shows a prolonged QT interval, due to lengthening of the ST segment PTH secretion is often suppressed (see Hypocalcemia, above)
Causes of hypomagnesemia are listed in Table 21 12 Normomagnesemia does not exclude magnesium depletion because only 1% of total body magnesium is in the ECF Nearly 50% of hospitalized patients in whom serum electrolytes are ordered have unrecognized hypomagnesemia Up to 40% of patients with hypomagnesemia have hypokalemia, and up to 50% have hypocalcemia Hypomagnesemia and hypokalemia share many etiologies, including diuretics, diarrhea, alcoholism, aminoglycosides, and amphotericin B Renal potassium wasting also occurs from hypomagnesemia, and is refractory to potassium replacement until magnesium is repleted Hypomagnesemia also suppresses PTH release and causes endorgan resistance to it and to low 1,25-dihydroxyvitamin D3 levels This hypocalcemia is also refractory to calcium replacement until the magnesium is repleted In addition, molecular
Magnesium oxide, 250 500 mg orally once or twice daily, is useful for repleting stores in patients with chronic hypomagnesemia Treatment of symptomatic hypomagnesemia can include an infusion of 1 2 g of magnesium sulfate, followed by an infusion of 6 g magnesium sulfate in at least 1 L of fluids over 24 hours, repeated for up to 7 days to replete magnesium stores Magnesium sulfate may also be given intra-