Primary hypomagnesemia

Prolonged nasogastric suction Malabsorption syndromes Extensive bowel resection Acute and chronic diarrhea Intestinal and biliary fistulas Protein-calorie malnutrition Acute hemorrhagic pancreatitis Primary hypomagnesemia (neonatal)... 

Diuretic phase of acute tubular necrosis Postobstructive nephropathy Renal tubular acidosis Post-renal transplantation Primary hypomagnesemia Phosphate depletion... 

Genetically determined variations in the distribution of lithium between plasma and erythrocytes have been found in sheep (Schless et. al. 1975). Likewise, depressive patients react differently to lithium treatment, with heredity a probable contributory factor, as has been shown investigations conducted in twins. A hereditary recessive primary hypomagnesemia that is accompanied by a low level of calcium in the blood leads to tetany. This is presumably caused by a nonfunctional magnesium resorption in the intestine (Lombeck and Bremer... 

Further genes involved in other conditions responsible for renal stone development among many others could be identified e.g. osteopetrosis with tubular acidosis type 1 (xanthinoxidase), hyperoxaluria typel (alanine-glyoxylate-aminotrans-ferase), adenine-phosphoribosyltransferase deficiency (ATRTase), distal tubular acidosis and primary hypomagnesemia. 

Fhtients with hypomagnesemia (low magnesium plasma levels) are at increased risk for digitalis toxicity. If low magnesium levels are detected, die primary care provider may prescribe magnesium replacement dierapy. 

The primary endpoint for monitoring treatment of fluid and electrolyte disorders is the correction of the abnormal serum electrolyte. The frequency depends on the presence of symptoms and degree of abnormality. In general, monitoring is initially performed at frequent intervals and, as homeostasis is restored, subsequently performed at less frequent intervals. AH electrolytes should be monitored since individual electrolyte abnormalities typically coexist with another abnormality (e.g., hypomagnesemia with hypokalemia and hypocalcemia, or hyperphosphatemia with hypocalcemia). Patients should be monitored for resolution of clinical manifestations of electrolyte disturbances and for treatment-related complications. 

Tacrolimus may induce tubular dysfunction characterized as an increased excretion of urinary enzymes, decreased urinary concentrating ability, increased fractional excretion of magnesium in the presence of hypomagnesemia, hyperkalemia, hyperuricemia and fubular acidosis [12,260,645,647,705,736,737. In vitro sfudies showed fhat TAC inhibit Na/K - ATPase in rat microdissected cortical collecting duct and medullary thick ascending limb [738], and that high TAC doses added to primary human proximal tubules cultures decreased cell proliferation after 72 hours of incubation... 

Decreased 1,25 0H)2D Renal failure Hyperphosphatemia Hypomagnesemia Hypoparathyroidism Pseudohypoparathyroidism Vitamin D-dependent rickets, type I Hypercalcemia of malignancy Increased l,25(OH)2D Granulomatous diseases Primary hyperparathyroidism Lymphoma... 

Patients with persistent or recurrent VF or PVT following antiarrhythmic administration should be assessed for underlying electrolyte abnormalities as a cause for their refractory arrhythmia. The primary electrolyte abnormalities associated with refractory ventricular arrhythmias include hyperkalemia, hypokalemia, and hypomagnesemia. 

Hypocalcemia is the result of alterations in the effect of parathyroid hormone and vitamin D on the bone, gut, and kidney (see Fig. 49-9). The primary causes of hypocalcemia are postoperative hypoparathyroidism and vitamin D deficiency. Other causes include magnesium deficiency, thyroid surgery, medications, hypoalbuminemia, blood transfusions, peripheral blood progenitor cell harvesting, tumor lysis syndrome, and mutations in the calcium-sensing receptor. " Parathyroid hormone concentrations are elevated in conditions of hypocalcemia, with the exception of hypoparathyroidism and hypomagnesemia (Fig. 49-11). ... 

Liebscher and Liebscher 2000, Meij etal. 2002). Meanwhile, four primary hereditary hypomagnesemia disorders have been identified (i) hypomagnesemia with secondary hypocalcemia (HSH) (ii) familial hypermagnesemia, hypercalciuria and neph-rocalcinesis (HHN) and (iii) dominant hypo-magnesemia/hypocalciuria and (iv) recessive hypomagnesemia (Meij et al. 2002). 

The primary treatment for hypomagnesemia is oral supplementation and increased dietary intake of foods containing magnesium. Table 8-1 lists suggested dietary interventions. 

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