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 possibility that hypercalciuria could cause calcium stone formation through a mechanism other than by increasing urinary saturation of stone-forming calcium salts was explored. The effect of increasing calcium concentration on the inhibitor activity against the spontaneous precipitation of calcium oxalate was examined in whole urine (in the presence of naturally occurring inhibitors) and in synthetic media (with added inhibitors). In 11 patients with calcium nephrolithiasis, the induced hypercalciuria from calcium supplementation (600 mg/day) caused a significant fall in the urinary inhibitory activity against calcium oxalate precipitation, as shown by a decline in the formation product ratio from 12.6 +/- 1.1 SEM to 9.6 +/- 1.4 (P less than 0.005). In order to more fully explore this observation, the effect of increasing calcium concentration on the inhibitory activities of citrate (2 mM), chondroitin sulfate (0.05 mg/liter) and a heterogeneous group of naturally-occurring urinary inhibitors (1.0 mg/liter) against calcium oxalate precipitation was examined in vitro in synthetic solutions. The inhibitory actions of both citrate and chondroitin sulfate were significantly attenuated by increasing calcium concentration from 0.25 mM to 6.0 mM (P less than 0.01). However, raising the calcium concentration in synthetic media containing a mixture of partially purified urinary inhibitors produced a significant rise in the urinary inhibitory activity of this macromolecular mixture (P less than 0.01). We conclude that hypercalciuria can attenuate the inhibitory activities of citrate and chondroitin sulfate against calcium oxalate precipitation while at the same time accentuating the inhibitory activity of naturally-occurring urinary inhibitors.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Modulation by calcium of the inhibitor activity of naturally occurring urinary inhibitors. 313 70

Calcium hydrogen phosphate (CaHPO4) was considered as one of the main factors governing renal calculus formation. The degree of saturation with respect to this phase was therefore calculated in urines of 36 hypercalciuric children (20 absorptive, 16 renal subtype) with isolated hematuria, 10 renal stone patients, and 30 healthy controls. The effects of low calcium diet and hydrochlorothiazide treatment were also investigated in the patient groups. The results were compared to the widely used indicator of hypercalciuria (Ca/Cr ratio). Urines of both the hypercalciuric and the normocalciuric renal stone patients were saturated on basal conditions. On low calcium diet, 12 children of the absorptive hypercalciuric, 13 of the renal hypercalciuric and 7 of the renal stone-forming children had their urines in the saturated zone - irrespective of the evolution of Ca/Cr ratio. Thiazide normalized the activity product of CaHPO4 in all groups. The use of the Ca/Cr ratio as the sole parameter in the investigation of children with isolated hematuria and hypercalciuria or calcium nephrolithiasis seems to be insufficient; simultaneous determinations of the state of saturation of urines is recommended. This technique should also allow a quantitative assessment of the various therapeutic regimens recommended.
 ...
PMID:Data on the degree of saturation of urine with respect to calcium hydrogen phosphate in hypercalciuric children and renal stone formers. 325 61

Calcitriol was compared with placebo in the treatment of postmenopausal osteoporosis in a double-blind, randomized, parallel clinical trial of 24 months' duration. Adjustment was made in dietary calcium to maximize the dose of calcitriol. The study was completed by 15 patients who received placebo and 12 patients who received calcitriol. The calcitriol group had positive slopes (compared with negative slopes for the placebo group) for total body calcium, bone mineral content of the radius, bone mineral density of the lumbar spine, and radiographic absorptiometry of the middle phalanges. The difference between the two groups was statistically significant for each of these measurements. The fracture rate in the treatment group was 250 per 1,000 patient-years as compared with 333 for the placebo group. The mean dose of calcitriol was 0.8 micrograms per day. Hypercalcemia, hypercalciuria, and perhaps nephrolithiasis were observed as complications of treatment. Calcitriol increased bone mineral density by decreasing bone resorption, but not by increasing bone formation. Future studies should concentrate on treatment with oral calcitriol in lower doses. It would also be of interest to examine parenteral administration of calcitriol. It is possible that bone formation can be increased by achieving higher serum levels of the drug, whereas complications may be avoided by using a non-oral route of administration.
 ...
PMID:Calcitriol in the treatment of postmenopausal osteoporosis. 327 69

A patient with pseudoxanthoma elasticum was documented to be hyperphosphatemic and mildly hypercalcemic for six years. Complications included metastatic calcification, absorptive hypercalciuria, and renal insufficiency. The 1,25-dihydroxyvitamin D value was elevated, despite normal serum parathyroid hormone values, high serum phosphate levels, and renal insufficiency. Either increased dietary calcium or prednisone seemed to suppress the 1,25-dihydroxyvitamin D value. Nephrolithiasis or abnormalities suggestive of pseudoxanthoma elasticum occurred in the patient's father, daughter, and several siblings, suggesting a distinct familial syndrome in which connective tissue changes are accompanied by abnormalities of phosphorus and vitamin D metabolism that may resemble those in the syndrome of familial tumoral calcinosis. Nine similar cases were described before 1970.
 ...
PMID:Heritable syndrome of pseudoxanthoma elasticum with abnormal phosphorus and vitamin D metabolism. 333 71

Despite the frequency and morbidity of nephrolithiasis in autosomal dominant polycystic kidney disease (ADPKD), this association has not been subject to a detailed study. One hundred fifty-one of 751 ADPKD patients seen at the Mayo Clinic between 1976 and 1986 had nephrolithiasis. Seventy-four had passed calculi or had stones surgically removed. Stone analysis was available in 30 patients: uric acid, calcium oxalate, calcium phosphate, and struvite were present in 56.6%, 46.6%, 20%, and 10%, respectively. Calculi were observed in 71 of 79 patients with excretory urograms available for review. Faintly opaque and bull's eye stones, probably containing uric acid, were present in 12.7% and 14.1% of these patients, respectively. Precaliceal tubular ectasia was observed in 15.5%. Ninety-seven patients had preserved renal function (serum creatinine less than 1.5 mg/dL) at the initial evaluation. Six were excluded because they had other known causes of stone disease. The most common metabolic abnormality in the remaining 91 patients was hypocitric aciduria (ten of 15 patients with measurements). The urine pH in the first voided morning specimens (5.66 +/- 0.05) was significantly lower than that of an unselected control population (5.92 +/- 0.03, P less than 0.001). Hyperuricosuria, hyperoxaluria, and hypercalciuria were observed in six of 32 (18.8%), six of 31 (19.4%), and three of 39 (9.7%) patients with preserved renal function. The composition of the stones, the frequency of hypocitric aciduria, and the low urine pH (possibly related to the defect in excretion of ammonia described in ADPKD), suggest that metabolic, along with mechanical, factors are responsible for the frequent occurrence of nephrolithiasis in this disease.
 ...
PMID:The association of nephrolithiasis and autosomal dominant polycystic kidney disease. 335 68

Urinary glycosaminoglycans are thought to be macromolecular inhibitors of calcium stone formation. The 24-hour excretion of urinary glycosaminoglycans was measured quantitatively in 24 normal subjects and 206 patients with different etiologies of stone disease. In both groups a positive correlation was found between urinary glycosaminoglycans and total urinary volume and urinary sulfate. In normal subjects total urinary volume was r equals 0.716, p less than 0.001 and urinary sulfate was r equals 0.813, p less than 0.001, while in patients with stones these values were r equals 0.338, p less than 0.001 and r equals 0.326, p less than 0.001, respectively. The only significant difference in excretion of urinary glycosaminoglycans between the groups was found in the subgroup of patients with type I absorptive hypercalciuria. The type I absorptive hypercalciuria value of 33.4 +/- 14.9 mg. per day in patients with stones was significantly higher than the 25.8 +/- 8.3 mg. per day detected in normal subjects (p less than 0.05). Urinary glycosaminoglycan excretion in all other subgroups of nephrolithiasis as well as in a combined group of all patients with stones showed no significant difference when compared to that of normal subjects. Thus, no major quantitative relationship could be demonstrated between urinary glycosaminoglycan excretion and calcium stone formation in this study.
 ...
PMID:Urinary glycosaminoglycans in normal subjects and patients with stones. 175 Aug 87

Calcium loading tests were performed in 21 children with hypercalciuria, haematuria and/or nephrolithiasis and 10 control subjects. Comparisons of 24-h calcium excretion before and after loading were evaluated rather than fasting urinary calcium to urinary creatinine ratio. The differences in calcium excretion before and after loading clearly distinguished absorptive from renal hypercalciuria. A difference higher than 0.035 mmol/kg indicated absorptive hypercalciuria in 6 of 21 patients, whereas in the remaining 15 much lower differences indicated renal hypercalciuria. Resorptive hypercalciuria caused by low serum values of 25-hydroxyvitamin D was considered in 6 of the 15 patients with renal hypercalciuria. These patients had low values of phosphate reabsorption (TmP/GFR) and could be clearly separated by high values of calcium reabsorption (TmCa/GFR), in contrast to patients with renal hypercalciuria who had normal values of TmP/GFR and low values of TmCa/GFR. The correct treatment and prevention of nephrolithiasis caused by hypercalciuria in children should be based on accurate diagnosis; this can be achieved by using the calcium loading test described in this report.
 ...
PMID:The diagnosis of hypercalciuria in children. 339 95

In seven patients with severe idiopathic hypercalciuria and recurrent calcium oxalate nephrolithiasis, we have determined the effects on mineral balance of chronic treatment with chlorthalidone or trichlormethiazide, drugs that are widely used to lower urine calcium losses and reduce stone recurrence. Each person excreted above 350 mg of calcium daily while untreated, and was studied twice, before and after three to six months of treatment. Compared to pretreatment, the drugs reduced intestinal calcium absorption; but they reduced urine calcium loss even more, so calcium retention increased. Phosphate retention also increased. Serum levels of calcitriol, parathyroid hormone, calcium, phosphate, and magnesium were unchanged. At least in patients of this type, chlorthalidone and trichlormethiazide seem ideal treatments, that lower urine calcium yet increase calcium and phosphate retention. Whether patients with less severe hypercalciuria respond this way is unknown.
 ...
PMID:Chlorthalidone promotes mineral retention in patients with idiopathic hypercalciuria. 340 13

Thirty-six patients with recurrent calcium oxalate nephrolithiasis were selected from the stone clinic. Fourteen were normocalcemic and had normal daily urinary calcium excretion. Among 22 patients with idiopathic hypercalciuria, 10 received thiazide diuretics for the prevention of new stone formation. Single-voided urine samples were collected at the outpatient clinic and 24-hour urine at the patients' homes. In hypercalciuric patients, irrespective of thiazide diuretic therapy, the mean value of the calcium/creatinine concentration ratios of postprandial single-voided urine specimens had a meaningful correlation with the man value of 24-hour urinary calcium excretion rates. Also in hypercalciuric patients with thiazide diuretics, a negative correlation was observed between the calcium/creatinine concentration ratio and the index for urinary saturation with calcium oxalate of a postprandial single-voided urine sample. Thus, in the hypercalciuric stone formers, 24-hour urinary calcium excretion rates and the degree of urinary saturation with calcium oxalate can be estimated from the calcium/creatinine concentration ratios of single-voided urinary samples.
 ...
PMID:Significance of the calcium to creatinine concentration ratio of a single-voided urine specimen in patients with hypercalciuric urolithiasis. 345 77

A 35-year-old white male with rheumatoid arthritis who had developed hypercalcemia, hypercalciuria, and nephrolithiasis was found to be abnormally sensitive to vitamin D as a result of lack of regulation of circulating 1,25-dihydroxyvitamin D (1,25-(OH)2D). An increase in daily intake of vitamin D from 10 micrograms (400 units) per day to 50 micrograms (2000 units) per day produced an abnormal elevation in serum 1,25-(OH)2D, hypercalcemia, and hypercalciuria which were corrected by prednisone. Serum 25-hydroxyvitamin D initially was abnormally low, and increased with vitamin D to values which were in the low normal range. There were significant positive correlations between serum 1,25-(OH)2D (p less than .05) and serum calcium and between serum 1,25-(OH)2D and urinary calcium (p less than .05). Serum immunoreactive parathyroid hormone, initially in the lower range of normal, decreased further during hypercalcemia. A radiograph of the chest, gallium scan, and serum angiotensin-converting enzyme activity were normal. No granulomas or evidence of lymphoma were found in biopsies of the liver and of several lymph nodes. It is concluded that the abnormal calcium metabolism in this patient resulted from increased circulating 1,25-(OH)2D and that the defect in vitamin D metabolism was not related to sarcoidosis, other granulomatous disease, Hodgkin's disease, or lymphoma. The relationship, if any, of the abnormal metabolism of vitamin D and calcium to rheumatoid arthritis remains to be established.
 ...
PMID:Abnormal calcium metabolism caused by increased circulating 1,25-dihydroxyvitamin D in a patient with rheumatoid arthritis. 350 40


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