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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of high sodium intake on bone mineral content of rats fed a normal (0.6% Ca) or a low (0.02% Ca) calcium diet was studied. Rats on a normal calcium diet given 1.8% sodium chloride to drink showed persistent and significant hypercalciuria and subnormal bone mineral content. Total calcium content of femur was significantly lower after 4 months (p < 0.02) and 12 months (p < 0.001). In rats maintained on a low calcium diet (0.02% Ca), a high sodium diet for 8 weeks caused a significant loss of calcium in bone similar to that seen in animals fed a normal calcium diet for 4 months. We conclude that high sodium intake reduces bone mineral content, especially if the diet is low in calcium.
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PMID:The effect of high sodium intake on bone mineral content in rats fed a normal calcium or a low calcium diet. 829 46

The effects of dietary sodium and potassium, given as salts of chloride or bicarbonate, on theophylline-induced hypercalciuria in the rat were investigated. In experiment 1, rats fed diets containing 0.3 mmol/g diet NaCl, KCl, NaHCO3, or KHCO3 exhibited a calciuria of NaCl > KCl > controls = NaHCO3 = KHCO3. This study indicated that cation effects were dependent on the accompanying anion, however the dose of added salt was inadequate to produce a consistent, significant salt effect. A second experiment was run in which animals were given salts at 0.4 mmol/g diet; the salt-induced pattern of calciuria was similar. After one week of salt pretreatment, rats were given diets containing theophylline (7.72 mumol/g diet), which induced calciuria all groups regardless of salt pretreatment. Urinary volume and urinary phosphate changes were parallel to each other and not to the changes in urinary calcium induced by salt or theophylline. Changes in urinary excretion of prostaglandin E2 were directly proportional to changes in urinary calcium. In the rat, pretreatment with sodium bicarbonate or sodium chloride reduces the extent of theophylline-induced diuresis, but does not reduce theophylline-induced hypercalciuria. Further, potassium chloride increases and potassium bicarbonate does not reduce urinary calcium excretion. Theophylline-induced calciuria is correlated with prostaglandin E2 excretion rates.
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PMID:Effect of diets high in sodium and potassium on the magnitude of theophylline-induced hypercalciuria in the rat. 840 66

Severe hyperkalemia resistant to treatment with sodium chloride (NaCl) supplements plus cation exchange resins can be found in pseudohypoaldosteronism type I. In a patient with the multiple target organ variant of this condition, hyperkalemia persisted at dangerous levels (8.5 mmol/l) despite large doses of NaCl (50 mmol/kg per day) and cation exchange resins (6 g/kg per day). Hypercalciuria was also present. The total volume of fluids and supplements required was not tolerated orally. Indomethacin (2 mg/kg per day) and later hydrochlorothiazide (2 mg/kg per day) were tried to further correct imbalance. Plasma potassium (K) and Na levels, the urinary Na/K ratio, transtubular potassium gradient (TTKG), and urinary calcium/creatinine (Ca/Cr) ratio were used to evaluate the effect of hydrochlorothiazide. Under treatment, plasma Na was stable (137-144 mmol/l), K levels decreased from 8.5 to 5 mmol/l, urinary Na/K from 90 to 24, and TTKG increased from 0.3 to 1.8. Ca/Cr decreased from 3.5 to 1.5 mmol/mmol. The dosage of cation exchange resins was decreased, oral fluids were tolerated, and the patient's general condition improved. Hence: hydroclorothiazide can be useful in the treatment of severe hyperkalemia and hypercalciuria of pseudohypoaldosteronism type I.
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PMID:Effect of hydrochlorothiazide in pseudohypoaldosteronism with hypercalciuria and severe hyperkalemia. 886 53

This baby boy was born after a pregnancy complicated by severe polyhydramnios at a gestational age of 28 weeks. Analysis of the amniotic fluid had shown a high chloride content, but normal concentrations of sodium, potassium, and calcium. After birth he displayed extreme polyuria, severe renal sodium and chloride loss, and marked hypercalciuria. Five weeks after birth, his sodium chloride loss turned into renal potassium loss, along with a marked decrease in urine output. All these features are characteristic of the neonatal variant of Bartter syndrome. He was discharged after 11 weeks with oral supplements of sodium chloride, potassium gluconate, and 500 ml of fluid. The follow-up for a period of 6 years showed a surprising evolution: he has no hypokalemic alkalosis, no polyuria, and no hypercalciuria; growth and development are within the normal ranges and, at the time of writing, he is a healthy boy needing no medication and with no medical problems whatsoever.
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PMID:Neonatal Bartter syndrome: spontaneous resolution of all signs and symptoms. 963 34

Nearly 50 years after its initial description by Dr. F. Albright, the term idiopathic hypercalciuria (IH) is still in use. The exact mechanism of hypercalciuria is still unknown despite extensive pathophysiologic investigations; recent advances represent the focus of this review. A precise definition of true IH is proposed, taking into account the various nutritional conditions influencing calcium excretion. The potential pathogenic mechanisms are discussed, and the limits of the classical Pak's pathophysiological classification are recalled. The evidence supporting the role of an increased intestinal calcium absorption, a defect in renal tubular calcium reabsorption, or an increased bone loss as a primary mechanism in IH are successively examined. Since overall available human data indicates that all three mechanisms may be found in IH, the hypothesis that a broader disorder encompassing all these various abnormalities may be involved in IH is discussed. Three global hypotheses to account for IH physiopathology are examined: a diffuse defect in fatty acid content of cell membranes, an increased expression of the vitamin D receptor of the 25(OH) vitamin D 1 alpha-hydroxylase, or of the calcium sensor receptor and a monocyte disease. Finally, the available clinical data justifying the therapeutic approaches are reviewed, and guidelines for dietary recommendations regarding calcium and also animal protein, sodium chloride, alcohol, carbohydrate, phosphate, and potassium intakes are proposed, and drug therapy indications are discussed.
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PMID:Pathophysiology and treatment of idiopathic hypercalciuria. 972 2

Pregnancies with fetuses affected with the Bartter syndrome, an autosomal recessive disorder of hyperreninism and hyperaldosteronism, are complicated by early onset of polyhydramnios which results in preterm deliveries. We have assessed biochemical changes in amniotic fluid and the mother's blood with a view to early diagnosis. Aldosterone levels of both amniotic fluid and the mother's blood were found to be increased at 27 weeks of gestation, while electrolyte levels did not differ significantly from those reported earlier for controls. After birth the baby suffered from polyuria with hyponatremia, hypomagnesemia and hypercalciuria which could be controlled by treatment with sodium chloride and magnesium. Elevated aldosterone thus might be a useful marker for early diagnostic purposes.
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PMID:Elevated aldosterone in amniotic fluid and maternal blood has diagnostic potential in pregnancies complicated with a fetus of Bartter syndrome. 1626 Aug 79

Congenital chloride diarrhea is due to mutations in the intestinal Cl(-)/HCO(3)(-) exchange (SLC26A3) which results in sodium chloride and fluid depletion leading to hypochloremic and hypokalemic metabolic alkalosis. Although treatment with sodium and potassium chloride offers protection from renal involvement in childhood, the long-term renal outcome remains unclear. Here we describe two cases of congenital chloride diarrhea-associated end-stage renal disease with transplantation. Further, we show that there is a high incidence of mild chronic kidney disease in 35 other patients with congenital chloride diarrhea. The main feature of the renal injury was nephrocalcinosis, without hypercalciuria or nephrolithiasis with small sized kidneys and commensurately reduced glomerular filtration rates. This suggests that diarrhea-related sodium chloride and volume depletion, the first signs of non-optimal salt substitution, promote urine supersaturation and crystal precipitation. The poor compliance with salt substitution along with long-lasting hypochloremic and hypokalemic metabolic alkalosis is likely to induce progressive calcification and renal failure. Both our patients developed nephrocalcinosis in the transplanted kidneys suggesting that this complication is a consequence of intestinal SLC26A3 deficiency. Interestingly, the transporter is expressed in the distal nephron but the recurrence of nephrocalcinosis in the transplanted kidney suggests that it does not play a significant renal role in this syndrome.
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PMID:The impact of sodium chloride and volume depletion in the chronic kidney disease of congenital chloride diarrhea. 1882

Bartter's syndrome is a constellation of symptoms characterized by hyper-reninemic hypokalemia, metabolic alkalosis, elevated renin and aldosterone, low or normal blood pressure, and hyperplasia of the juxtaglomerular apparatus. So far, five gene mutations in proteins regulating the sodium chloride transport in the thick ascending limb of Henle's loop have been described. However, the molecular mechanisms underlying the presentation of hypomagnesemia in some of these patients remains unclear. Claudins are a family of transmembranous proteins within the tight junctions that have been shown to be important for the paracellular movement of ions. Mutations in claudin-16 have been identified in patients with familial hypomagnesemia with hypercalciuria and nephrocalcinosis. To test the hypothesis that mutations in claudin genes may be involved in the altered magnesium and calcium transport in Bartter's syndrome, we began to examine the genes of claudins known to be present in renal tubules in four pediatric patients with Bartter's syndrome. All four patients were African Americans with hypomagnesemia and hypercalciuria. In this study, we did not find any mutation in the coding regions of claudin-2, -3, -4, -7, -8, -10, -11, or -16 genes in these patients. However, all patients had a single nucleotide substitution of C for T at the position of 451 of claudin-8 gene sequence that changes amino acid residue from serine to proline at the position of 151 in the second extracellular domain of claudin-8 protein. The significance of this known single nucleotide polymorphism remains to be determined.
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PMID:Analysis of claudin genes in pediatric patients with Bartter's syndrome. 1953 97

Hypomagnesemia is defined as a serum magnesium level less than 1.8 mg/dL (< 0.74 mmol/L). Hypomagnesemia may result from inadequate magnesium intake, increased gastrointestinal or renal losses, or redistribution from extracellular to intracellular space. Increased renal magnesium loss can result from genetic or acquired renal disorders. Most patients with hypomagnesemia are asymptomatic and symptoms usually do not arise until the serum magnesium concentration falls below 1.2 mg/dL. One of the most life-threatening effects of hypomagnesemia is ventricular arrhythmia. The first step to determine the likely cause of the hypomagnesemia is to measure fractional excretion of magnesium and urinary calcium-creatinine ratio. The renal response to magnesium deficiency due to increased gastrointestinal loss is to lower fractional excretion of magnesium to less than 2%. A fractional excretion above 2% in a subject with normal kidney function indicates renal magnesium wasting. Barter syndrome and loop diuretics which inhibit sodium chloride transport in the ascending loop of Henle are associated with hypokalemia, metabolic alkalosis, renal magnesium wasting, hypomagnesemia, and hypercalciuria. Gitelman syndrome and thiazide diuretics which inhibit sodium chloride cotransporter in the distal convoluted tubule are associated with hypokalemia, metabolic alkalosis, renal magnesium wasting, hypomagnesemia, and hypocalciuria. Familial renal magnesium wasting is associated with hypercalciuria, nephrocalcinosis, and nephrolithiasis. Asymptomatic patients should be treated with oral magnesium supplements. Parenteral magnesium should be reserved for symptomatic patients with severe magnesium deficiency (< 1.2 mg/dL). Establishment of adequate renal function is required before administering any magnesium supplementation.
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PMID:Hypomagnesemia: an evidence-based approach to clinical cases. 2008 Dec 99

The sodium chloride cotransporter (NCC) is the primary target of thiazides diuretics, drugs used commonly for long-term hypertension therapy. Thiazides also completely reverse the signs of familial hyperkalemic hypertension (FHHt), suggesting that the primary defect in FHHt is increased NCC activity. To test whether increased NCC abundance alone is sufficient to generate the FHHt phenotype, we generated NCC transgenic mice; surprisingly, these mice did not display an FHHt-like phenotype. Systolic blood pressures of NCC transgenic mice did not differ from those of wild-type mice, even after dietary salt loading. NCC transgenic mice also did not display hyperkalemia or hypercalciuria, even when challenged with dietary electrolyte manipulation. Administration of fludrocortisone to NCC transgenic mice, to stimulate NCC, resulted in an increase in systolic blood pressure equivalent to that of wild-type mice (approximately 20 mm Hg). Although total NCC abundance was increased in the transgenic animals, phosphorylated (activated) NCC was not, suggesting that the defect in FHHt involves either activation of ion transport pathways other than NCC, or else direct activation of NCC, in addition to an increase in NCC abundance.
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PMID:Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension. 2189 37


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