Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of acute and chronic metabolic acidosis on serum immunoreactive parathyroid hormone (iPTH) were studied. Acute metabolic acidosis induced by administration of ammonium chloride (NH4Cl) produced a barely detectable increase in serum iPTH. Chronic NH4Cl administration produced a marked elevation of serum iPTH that was well correlated with the magnitude of acid-induced hypercalciuria but not with the degree of acidosis. Acetazolamide administration produced an equivalent degree of acidosis, but hypercalciuria was minimal and iPTH increased only marginally. Methionine administration caused moderate hypercalciuria and a significant but moderate increase in iPTH. Chronic NH4Cl-induced acidosis produced no hypercalciuria when dietary sodium intake was rigidly restricted, and under these conditions serum iPTH remained normal. When sodium intake was suddenly increased while maintaining the acid load, hypercalciuria appeared and was followed by progressive rise in serum iPTH equivalent to that observed during chronic NH4Cl-induced acidosis in subjects consuming salt ad lib. These results indicate that chronic acidosis elevates iPTH mainly by producing hypercalciuria and that acidosis itself is not a primary stimulus to PTH secretion.
 ...
PMID:Effect of acute and chronic metabolic acidosis on serum immunoreactive parathyroid hormone in man. 120 55

Only about 20% of renal stone cases have an unquestionable cause such as hyperparathyroidism, renal tubular acidosis etc. explaining their stone formation. About 20-40% are believed to result from idiopathic hypercalciuria. The purpose of the present investigation was to study the renal excretion of calcium, magnesium, sodium and phosphate in 47 consecutive men with recurring renal stone formation without a demonstrable underlining metabolic disease and, for comparison, 43 normal men. The results are related to previous hypotheses on renal stone formation. No difference in urinary calcium (either concentration or excretion) per day is found between the two groups. Consequently the concept of idiopathic hypercalciuria is questioned. The Mg/Ca ratio in urine is found lower in the stone patients than in the controls, suggesting that the Mg/Ca ratio might be of importance in stone formation.
 ...
PMID:The urinary excretion and serum concentration of calcium, magnesium, sodium and phosphate in male patients with recurring renal stone formation. 120 81

In 19 adult patients, with renal stones containing calcium and hypercalciuria, urinary calcium and magnesium excretion and urinary calcium/magnesium ratio was investigated before and during 4 days of treatment with sodium cellulose phosphate. Urinary magnesium excretion fell following sodium cellulose phosphate therapy in all but 1 patient investigated: in 9 patients by less than 50% and in 10 by more than 50% of the pretreatment values. In the latter group of patients urinary calcium/magnesium ratio increased significantly from the mean values ( +/- SD) 3.2 +/- 1.1 to 6.77 +/- 6.9. In 6 patients serum magnesium absorption is suggested, and routine serum and urinary magnesium analysis with the early treatment of magnesium deficiency in patients treated with sodium cellulose phosphate are recommended.
 ...
PMID:Sodium cellulose phosphate-induced increment in urinary calcium/magnesium ratio. 123 99

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.
 ...
PMID:Diuretic agents. Mechanisms of action and clinical uses. 126 95

1. Urinary excretion of prostaglandin E2 is increased in patients with idiopathic hypercalciuria, but in order to conclude that hyperprostaglandinuria is a primary phenomenon, it must be demonstrated that high levels of urinary prostaglandin E2 can be dissociated from other factors, such as urine volume and natriuresis, and from the hypercalciuria itself. 2. We studied 10 patients with idiopathic hypercalciuria and 10 control subjects on high and low calcium diets providing daily calcium intakes of 30-35 mmol and 7.5-10 mmol, respectively, and similar sodium intakes. In addition, patients with idiopathic hypercalciuria and control subjects were studied during water restriction and water diuresis. 3. Urinary prostaglandin E2 excretion was more than twice as high in patients with idiopathic hypercalciuria than in control subjects on the low and high calcium diets as well as during water restriction and water diuresis (P less than 0.01). 4. Urinary prostaglandin E2 excretion was not affected by changes in urinary calcium excretion in patients with idiopathic hypercalciuria and in control subjects. Patients with idiopathic hypercalciuria on the low calcium diet and control subjects on the high calcium diet had similar levels of calciuria and natriuresis, yet urinary prostaglandin E2 excretion (mean +/- SEM) was 11.62 +/- 1.71 nmol/day in the patients with idiopathic hypercalciuria and 3.26 +/- 0.48 nmol/day in the control subjects (P = 0.0006). 5. These results indicate that increased urinary prostaglandin E2 excretion is a cardinal characteristic of patients with idiopathic hypercalciuria.
 ...
PMID:Increased urinary excretion of prostaglandin E2 in patients with idiopathic hypercalciuria is a primary phenomenon. 132 25

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.
 ...
PMID:[The neonatal form of Bartter's syndrome: current findings in etiology and physiopathology]. 141 86

During the past 5 years, we have identified idiopathic hypercalciuria in five of seven patients referred for evaluation of renal glycosuria between 1985 and 1991. The children, all boys, ranged in age from 6 to 12 years. Endocrine function was normal, and none of the patients had hyperparathyroidism, hypercalcemia, renal tubular acidosis, or other secondary causes of hypercalciuria. The calcium/creatinine ratio in a fasting urine specimen was elevated in all five children who had hypercalciuria, with a mean value (+/- SD) of 0.34 +/- 0.06 (normal, < 0.2). In one child who had renal colic with spontaneous passage of gravel-like material, the idiopathic hypercalciuria persisted after 1 week on a diet containing 2000 mg of sodium and 300 mg of calcium. On the basis of studies that examined the site along the nephron responsible for hypercalciuria in rats with streptozocin-induced diabetes, we speculate that in children with renal glycosuria, there is defective reabsorption of glucose and calcium in the straight portion of the proximal tubule or in the collecting duct. It is likely that a similar mechanism accounts for the idiopathic hypercalciuria in children with diabetes mellitus.
 ...
PMID:Hypercalciuria in children with renal glycosuria: evidence of dual renal tubular reabsorptive defects. 841 May 29

Dual-energy x-ray absorptiometry and single-photon absorptiometry were used to determine bone density at the lumbar spine and radial shaft in 62 patients with absorptive hypercalciuria, 27 patients with fasting hypercalciuria, and 31 nonhypercalciuric stone formers. Lumbar bone density was significantly lower in patients with absorptive (-10%) as well as in those with fasting hypercalciuria (-12%), with 74 and 92% of patients displaying values below the normal mean, whereas only 48% of the nonhypercalciuric stone formers had bone density values below the normal mean. In contrast, radial bone density was similar in all three groups of renal stone formers investigated. The comparison of urinary chemistry in patients with absorptive hypercalciuria and low normal bone density compared to those with high normal bone density showed a significantly increased 24 h urinary calcium excretion on random diet and a trend toward a higher 24 h urinary uric acid excretion and a higher body mass index in patients with low normal bone density. Moreover, among the patients with absorptive hypercalciuria we found a statistically significant correlation between the spinal bone density and the 24 h sodium and sulfate excretion and the urinary pH. These results gave evidence for an additional role of environmental factors (sodium and animal proteins) in the pathogenesis of bone loss in absorptive hypercalciuria. In conclusion, our data suggest an osteopenia of trabecular-rich bone tissues in patients with fasting and absorptive hypercalciurias.
 ...
PMID:Reduced vertebral bone density in hypercalciuric nephrolithiasis. 148 24

Forty-two patients with calcium calculi were selected based on calciuria > 0.1 mmol/kg/d on an uncontrolled diet. To measure excretion of sodium, calcium, phosphates and hydroxyproline, a 24-hr urine sample was collected on the 4th day of a milk product-free diet, a fasting urine specimen was collected on the morning of the 5th day and another sample was taken 4 hr after the oral administration of calcium. On the 5th day, plasma levels of calcium, phosphates, intact parathyroid hormone (PTH), calcidiol and calcitriol were determined on an empty stomach and after administration of a calcium load. The results, compared to those of healthy subjects evaluated under the same conditions, enabled classification of the stone-formers as having dietary hypercalciuria (n = 18), when calciuria returned to normal on a low calcium diet, and idiopathic hypercalciuria (n = 24), when the urinary calcium level remained high. Patients with idiopathic hypercalciuria were then classified, according to Pak's criteria, as having absorptive hypercalciuria (n = 8), when the fasting calciuric levels was normal, renal hypercalciuria (n = 1), when fasting hypercalciuria with elevated circulating PTH was controlled by a calcium load, or undetermined hypercalciuria (n = 15) for those individuals with fasting hypercalciuria and normal plasma PTH levels. In addition, vertebral density was measured tomodensitometrically and expressed as a percentage of the normal as a function of sex and age based on a regression line calculated with the results of 239 normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Vertebral density of hypercalciuric lithiasis. Its relation to calcium-protein intake and vitamin D metabolism]. 148 31

In order to clarify the pathogenesis of hypercalciuria, the response to extrinsic human parathyroid hormone (h-PTH) was studied the 21 patients with calcium containing urinary stone(s) and 5 normal controls (NO). The stone patients were classified into 3 groups from the result of the oral calcium loading test, i.e. Non-hypercalciura (NH, n = 8) and absorptive hypercalciuria (AH, n = 8) and renal hypercalciuria (RH, n = 5). Only in the AH group, urinary excretion of calcium (u-Ca) was strongly correlated to that of sodium (u-Na) in pre-load of h-PTH, and both increments were also correlated in post-load of h-PTH. As of this fact the increase in Na excretion seems to be responsible for a cause of hypercalciuria in the AH group. There was a significant correlation between the value of %TRP in pre-load of h-PTH and the rate of urinary phosphorus (P) increment between pre-load and post-load of h-PTH in the NO and NH groups. However, this relationship was not found in the AH and RH groups. These findings indicate that there is response disorder of P to h-PTH. In addition, serum P was low, plasma 1,25 (OH)2D was high, N-c-AMP was low in the AH group, whereas both serum P and %TRP were low in the RH group in pre-load of h-PTH. These findings are compatible with the primary renal P leak.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[The pathogenesis of hypercalciuria from the aspect of the response to human parathyroid hormone in Ca containing stone formers]. 150 27


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>