Magnesium supplementation in Gitelman syndrome.

The metabolism of potassium and magnesium are closely linked (in situations where potassium and magnesium depletion coexist, magnesium restoration alone is sufficient to correct hypokalemia). Moreover, magnesium deficiency blunts the interplay between circulating calcium and the calciotropic hormones. Renal magnesium wasting, hypokalemia, alkalosis, hypocalciuria, and a tendency towards hypocalcemia characterize Gitelman syndrome.

Normal prostaglandinuria E2 in Gitelman's syndrome, the hypocalciuric variant of Bartter's syndrome.

In familial Bartter's syndrome, hyperprostaglandinuria is considered a constant feature and prostanoid synthetase inhibition often positively influences the disease course. The urinary calcium excretion distinguishes two clinically and biochemically different variants, namely, classic Bartter's syndrome (normocalciuric or hypercalciuric variant; urinary calcium to creatinine > or = 35.3 mg/mg 10(-3)) and Gitelman's syndrome (hypocalciuric variant; urinary calcium to creatinine < 35.

Genetic heterogeneity in tubular hypomagnesemia-hypokalemia with hypocalcuria (Gitelman's syndrome).

To better clarify the genetic inheritance of primary tubular hypomagnesemia-hypokalemia with hypocalciuria, or Gitelman's syndrome (GS), we studied eight families (10 patients aged 11 to 22 years; 16 parents; 9 siblings) in which at least one offspring had GS (plasma magnesium < 0.65 mmol/liter; plasma potassium < 3.6 mmol/liter; high magnesium and potassium fractional excretions; molar urinary calcium/creatinine < 0.

Renal tubular function in children and adolescents with Gitelman's syndrome, the hypocalciuric variant of Bartter's syndrome.

Renal tubular function was studied in 14 patients with Gitelman's syndrome and 14 control subjects. Apart from the biochemical hallmarks of Gitelman's syndrome, namely alkalaemia, hyperbicarbonataemia, hypokalaemia, hypomagnesaemia (with increased magnesium over creatinine ratio), increased urinary chloride over creatinine ratio, and low urinary calcium over creatinine, the patients were found to have hyperproteinaemia, hypochloraemia, high total plasma calcium concentration, reduced plasma ionized calcium concentration, and high urinary sodium excretion. A statistically significant negative linear relationship between plasma magnesium concentration and magnesium excretion corrected for glomerular filtration was observed in patients.

Evidence for disturbed regulation of calciotropic hormone metabolism in gitelman syndrome.

Little attention has been paid to interactions between circulating levels of calcium, PTH, and 1,25-dihydroxycholecalciferol [1,25(OH)2D] and bone mineral density in primary renal magnesium deficiency. Plasma and urinary electrolytes, and circulating levels of calciotropic hormones were studied in 13 untreated patients with primary renal tubular hypokalemic alkalosis with hypocalciuria and magnesium deficiency. The blood ionized calcium concentration was significantly lower in patients than in controls.