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

Studies were performed on 12 patients with idiopathic hypercalciuria to evaluate the hypothesis that the acid load accompanying potassium acid phosphate would adversely affect renal calcium reabsorption and citrate excretion compared to the neutral form of the phosphate salt. During acute clearance studies, neutral phosphate (NP) led to a fall in FECa (2.2 +/- 0.6% to 0.8 +/- 0.1%, P less than 0.02) and no change in titratable acidity (TA) or net acid excretion (NAE). Acid phosphate (AP) did not reduce FECa acutely, and led to a rise in TA (22 +/- 4 to 62 +/- 6 muEq/min, P less than 0.02) and NAE (46 +/- 6 to 6 89 +/- 7 muEq/min, P less than 0.02). During chronic administration, AP resulted in higher urinary calcium excretion in both absorptive (187 +/- 29 vs. 141 +/- 18 mg/day, P less than 0.02) and renal hypercalciuric patients (233 +/- 24 vs. 173 +/- 190.02 mg/day, P less than 0.02). Also, TA and NAE were higher following AP, whereas citrate excretion was lower (375.4 +/- 64.6 vs. 633.4 +/- 28.8 mg/day, P less than 0.01). These data suggest that the reported ineffectiveness of AP in the therapy of nephrolithiasis may be related to the deleterious effects of the acid load on calcium and citrate metabolism.
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PMID:Differing effects of acid versus neutral phosphate therapy of hypercalciuria. 4 88

A patient with incomplete distal renal tubular acidosis (RTA) demonstrated hypercalciuria, potassium wasting and hyperreninemia. Indomethacin administration resulted in sustained improvement of these abnormalities. The results suggest that overproduction of prostaglandins contributes to hypercalciuria, potassium wasting and hyperreninemia in some patients with RTA and that indomethacin may be useful in treating patients with this disorder.
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PMID:Improvement of hypercalciuria, potassium wasting and hyperreninemia in incomplete distal renal tubular acidosis by indomethacin. 50 64

Urinary supersaturation in respect to brushite or calcium oxalate represents the main pathogenic factor in stone formation. Of the patients with calcium oxalate stones 30 to 40% present with hypercalciuria. Herein we determine and compare the effects and side effects in the treatment of hypercalciuria with sodium cellulose phosphate or Campanyl, a potassium versus calcium ion exchanger, and thiazides alone or in combination with an ion exchanger.
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PMID:Long-term treatment of hypercalciuria with thiazides, sodium or potassium cellulose phosphate, separately or in combination. 54 17

In a double-blind controlled clinical study, 71 patients with recurrent calcium oxalate stones were divided into three treatment groups: those who received potassium acid phosphate, those who received an inert placebo, and those who received a low calcium diet only. Follow-up periods averaged 2.9 years. Although the mean urinary calcium level of the patients who received phosphate was reduced 33 per cent, their renal stone disease did not diminish. Mean urinary phosphorus increased 88 per cent with phosphate treatment but did not correlate with the decrease in urinary calcium, or with treatment success. The data did not suggest that phosphorus and its metabolites retard calcium oxalate crystallization in urine. No evidence appeared for an association of hypercalciuria with severe stone disease, or with a specific clinical or chemical response to phosphate therapy. Patients whose urinary calcium level fell more than 25 percent when dietary calcium was reduced may have excessive gastrointestinal calcium absorption, which appears to be associated with improved chemical response to phosphate therapy.
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PMID:Recurrent nephrolithiasis: natural history and effect of phosphate therapy. A double-blind controlled study. 78 40

Despite the bewildering number of diuretics available to the physician, these drugs can be divided into 4 main groups, characterised by their site of action on sodium reabsorption in the kidney. Drugs acting on the ascending limb of the loop of Henle have a powerful but short acting diuretic effect; they include frusemide, ethacrynic acid and bumetanide. The benzothiadiazines and related compounds have a moderate diuretic action spread over a longer period, whilst the potassium-sparing diuretics, triamterene, amiloride and spironolactone, have only a weak diuretic effect but a marked ability to diminish urinary potassium excretion. The fourth group is made up of miscellaneous substances which function as vasodilator or osmotic agents. The pathogenesis of oedema formation in heart failure is outlined and a logical approach to treatment suggested. Duiretics are being increasingly used in the treatment of non-oedematous states, in particular hypertension, diabetes insipidus and hypercalciuria; their exact role in pregnancy and acute renal failure remains controversial. Side-effects can be related to their effect on electrolyte excretion and include hypokalaemia, hyponatraemia, hyperkalaemia and hyperuricaemia. The incidence of disturbed carbohydrate tolerance in previously normal individuals is low. Other less common side-effects are also discussed.
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PMID:Diuretics: mechanism of action and clinical application. 109 41

A 52 year old man with a long history of marked hypertension, peptic ulcer disease, nephrocalcinosis and intermittent hypercalcemia was referred to be evaluated for primary aldosteronism suspected on the basis of low plasma renin activity, hypokalemia and blood pressure responsive to spironolactone. Aldosterone excretion, however, was extremely low. Alkaluria, high urinary sodium excretion and hypercalciuria were observed. The patient admitted to chronic ingestion of large amounts of baking soda. Upon cessation of alkali abuse, his blood pressure fell dramatically; orthostatic hypotension, concomitant azotemia, hemoconcentration, hyperkalemia and weight loss occurred. Despite dramatic elevation in plasma renin activity, urinary aldosterone excretion remained low during this period. Adrenal glucocorticoid secretion was intact. All abnormalities of sodium, potassium and aldosterone subsequently returned to normal. A 10 day challenge with oral sodium bicarbonate was associated with a rise in blood pressure, but serum calcium remained normal. The patient remains normotensive 15 months after discontinuing alkali abuse.
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PMID:Hypertension corrected by discontinuing chronic sodium bicarbonate ingestion. Subsequent transient hypoaldosteronism. 111 72

Diuretics act primarily by blocking reabsorption of sodium at four major sites in the nephron. Clinically useful agents that block sodium reabsorption effectively in the proximal tubule are lacking. Furosemide (Lasix), ethacrynic acid (Edecrin), and possibly organomercurial agents are effective in the ascending limb of Henle's loop. Thiazides are the major agents acting in the early distal tubule. In the late distal tubule and collecting duct, spironolactone (Aldactone) and triamterene (Dyrenium) are useful, especially in combination with diuretics which act more proximally. In treating edematous states, initial therapy with thiazides is effective in most patients who do not exhibit moderate or severe renal insufficiency, severe hyperaldosteronism with excessive distal reabsorption of sodium in exchange for potassium, or excessive sodium reabsorption in the proximal tubule or ascending limb. Nonedematous states in which diuretic therapy is useful include hypertension, hypercalcemia, hypercalciuria, diabetes insipidus, and acute renal failure.
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PMID:Diuretic agents. Mechanisms of action and clinical uses. 126 95

I. Time has come to distinguish "Bartter syndrome" from "Bartter disease". The latter is an autosomal recessive renal tubulopathy which manifests itself mostly during infancy and childhood. II. Bartter disease is caused neither by a primary renal potassium loss nor by a primary renal hyperprostaglandinism. All evidence is in favor of a defect in the chloride pump located at the thick ascending limb of Henle's loop. III. The most severe expression of Bartter disease is its neonatal form which is characterized by polyhydramnios, premature delivery and a life threatening sodium chloride loss during the early weeks of life. It takes several weeks before sodium wasting turns into renal potassium wasting. IV. Polyhydramnios not associated with echographically detectable fetal malformation is highly suggestive of Bartter disease. Prenatal diagnosis is based on the combination of fetal polyuria and elevated chloride in the amniotic fluid. V. In this setting the administration of indomethacin is useless and even dangerous from the 32nd week of gestation on. Similarly, indomethacin should not be given to the newborn Bartter patient for the first weeks and months of life. Treatment at that stage consist mainly of the administration of large amounts of fluid and sodium chloride. VI. Indomethacin can be used as soon as children with Bartter disease stop growing normally and preferably after the age of 18 months when kidney maturation is established. The daily dose should not exceed 2.5 mg/kg body weight. VII. Hypercalciuria is part of (the neonatal form of) Bartter disease and it is so severe that nephrocalcinosis seems to be the rule. This hypercalciuria is the direct consequence of the chloride reabsorption defect in Henle's loop. Research is needed to find an adequate solution to this problem.
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PMID:[The neonatal form of Bartter's syndrome: current findings in etiology and physiopathology]. 141 86

Oxalic acid seems to play a far greater role in the formation of calcium oxalate stone than calcium. Three grams of calcium lactate and 3 g of sodium potassium citrate were administered to 46 urolithiasis patients, whose stones were mainly composed of calcium oxalate. Urinary oxalate level was reduced significantly without raising urinary calcium level by the administration of the two drugs for two weeks. The reduction of urinary oxalic acid was particularly remarkable in patients without hypercalciuria. The mechanism of action of these drugs was discussed.
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PMID:Reduction of urinary oxalate by combined calcium and citrate administration without increase in urinary calcium oxalate stone formers. 154 Oct 59

The main risk factors for calcium urolithiasis that are clinically detectable are low diuresis, hypercalciuria, hyperruricuria, alkaline urinary pH, hyperoxaluria, hypomagnesuria, hypocitraturia. They should be evaluated, all the more precisely that the disease is active, under both the urological and metabolic points of view, using 24 hour urine collection made at home on a free diet with a dietary record. In the majority of the cases the calcic urolithiasis is idiopathic, i.e. not related to a cause of secondary hypercalciuria like primary hyperparathyroidism, or to a hyperroxaluria either primary or of digestive or toxic origin. Its treatment if mainly dietary with high fluid intake (diuresis greater than 2 1/24 h), normoclacic diet (800-1000h mh/24 h) with meat but not dairy product restriction, oxalate salts, carbohydrate and alcohol restriction. These dietary recommendations should be controlled by measuring the above cited parameters in the 24 hour urine samples and by measuring urea excretion which should not exceed 0.33 g/kg of body weight. When diet fails, drugs may be added mainly allopurinol, thiazides and potassium citrate.
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PMID:[Physiopathology, exploration and treatment of calcium lithiasis]. 178 95


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