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

Tubular proteinuria is generally accepted as the critical effect following long-term, low-level exposure to cadmium as seen in an industrial environment. This effect may not be of immediate importance to the health of the individual, but the significance, in terms of long-term morbidity and mortality, of the renal tubular defect of which it is an indicator is not fully understood, and certain sequelae may have remained unrecognized due to inadequate follow-up.Follow-up studies have been performed in nine of 12 workers who were initially investigated in 1962. In six of the men exposures ranged from 28 to 45 years to cadmium sulfide dust and for shorter periods in the earlier years to cadmium oxide fume and dust. These six men had tubular proteinuria when first seen, and this has persisted in the five survivors. All six men had hypercalciuria, and two of them became recurrent stone formers. One man whose urinary calcium excretion later fell to a low level more recently developed vitamin D resistant osteomalacia. In addition, each of the six men had exhibited some, but not all, of a variety of biochemical abnormalities related to other proximal renal tubular defects, and the worker who developed osteomalacia had additional evidence of a distal tubular defect. The five survivors also have evidence of slowly progressive deterioration in glomerular function.Follow-up of this small group has shown that renal tubular dysfunction in cadmium workers may continue symptom-free for long intervals, but in a proportion of cases serious clinical effects may develop after a number of years.
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PMID:Renal tubular dysfunction and abnormalities of calcium metabolism in cadmium workers. 48 32

A 36-year-old woman suffered from bone pain, muscle weakness, and renal stones after prolonged ingestion of antacids for esophageal reflux. Investigation disclosed hypophosphatemia, hypercalciuria, and osteomalacia by bone biopsy. All symptoms and abnormal laboratory findings reversed with a regimen of oral phosphate supplementation and cessation of antacid intake.
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PMID:Antacid-induced osteomalacia and nephrolithiasis. 64 54

The calcium tolerance test is of diagnostic importance only in osteomalacia, which it helps to identify before bone biopsy when the static phosphocalcic parameters are not a deciding factor. However, the test does not make it possible to distinguish an osteoporosis from a cortisone osteopathy or an idiopathic hypercalciuria. In the first two diseases, the rates of urinary calcium elimination are comparable to that of normal individuals. It seems that the rate of urinary elimination of I.V. administered calcium is, approximately, all the more elevated as the level of iPTH is low; and, when the level of iPTH is low, the osteoid tissue seems less calcified than normally.
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PMID:[The provoked hypercalciuria test. Significance and limitations]. 74 25

The elimination of calcium, phosphorus, hydroxyproline and nitrogen was studied in 127 patients with inflammatory joint diseases and )6 healthy controls for 4 days. On the third day, 186 mg of calcium was administered intravenously. Provoked hypercalciuria tests were made in 35 males, 116 females with rheumatiod arthritis (RA), 18 males with ankylosing spondylitis (ASp), 8 postinfectious arthritis (PA) and 18 healthy controls (C). In 120 patients comparison was made between the ratios of eliminated P/hydroxyproline, Ca/hydroxyproline and P/Ca with regards to the results obtained in healthy controls. The kinetics of 47Ca were studied in 7 males with ASp and 4 C. The ratios Ca/P in serum and P/Ca in urine were studied in the same patients and compared with 21 C. The results show that the bone symptomatology of PA manifests itself by elimination of elevated amounts of all of the indicators studied, especially phosphorus. In RA there may be considerable oscillations of flow of urine due to the perspiration of patients. RA differs from decompensated coxarthrosis and gonarthrosis in that the patients eliminate significantly less calcium and phosphorus. Corticosteroids stimulate the elimination of hydroxyproline. Younger patients with RA (25-44) show changes compatible with osteoporosis, older females (45-64) display changes similar to those seen in osteomalacia, the oldest female patient (65-84) appear to have insufficient binding capacity for calcium. The hyposthesis is proposed that at the disease onset RA is characterized by an extremely marked syndrome of osteopathy. ASp is characterized by significantly reduced elimination of hydraxyproline, higher metabolic pool of calcium, lower elimination of calcium in urine and faeces and lower accretion to bone.
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PMID:[Calcium, phosphorus, hydroxyproline and nitrogen in inflammatory joint diseases]. 84 46

We have studied a family in which nine members present hyperchloremic acidosis with normal plasma creatinine and good ability to acidify urine. Renal functions, other than bicarbonate wasting, are normal, which identifies the condition as a pure form of proximal renal tubular acidosis. The acidosis persists into adult life and appears to be inherited as an autosomal dominant trait. All affected members are asymptomatic and the only peculiar finding is a decrease in stature. No hypercalciuria was detected, and no evidence of rickets or osteomalacia was found by x-ray studies. We consider these findings characteristic of a familial trait different from that in previously reported cases of renal tubular acidosis.
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PMID:Familial proximal renal tubular acidosis. A distinct clinical entity. 88 46

Total parenteral nutrition (TPN) for a prolonged period of time can be associated with bone pain and osteomalacia. We performed a study on the phosphorus/calcium metabolism and serum levels of osteocalcin (BGP), a protein proposed as constituting the bone turnover index in 31 patients receiving TPN (age 57 +/- 14 years, 22 males and 9 females) diagnosed as suffering from pathology of the digestive tract or geno-urinary pathology. The duration of the TPN was from 9.1 +/- 6.6 days (range 2-31 days). We observed and increase of FA (178 +/- 101 U/l), with a significant decrease of BGP (2.2 +/- 2.0 ng/ml vs. 3.7 +/- 1.3 ng/ml in controls; p less than 0.001). Serum levels of phosphorus and calcium corrected according to proteins were within normal limits. Hypercalciuria was detected in the urine (328 +/- 278 mg/24 hours), and phosphaturia (607 +/- 522 mg/24 hours). Based on the BGP results, we can conclude that patients subjected to TPN for a short period of time undergo a decrease in bone turnover.
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PMID:[Effect of total parenteral nutrition on bone metabolism]. 139 Nov 9

Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a new autosomal form of hypophosphatemic rickets, recently described. This disease is characterized, and differs from other forms of hereditary hypophosphatemic rickets and/or osteomalacia by increased serum levels of 1,25-dihydroxyvitamin D, hypercalciuria and complete remission of the disease on phosphate therapy alone. However, only another probable Israeli kindred, and seemingly a few sporadic cases from Europe, North America and Japan have been reported in the literature. We describe here a new kindred of Jewish Yemenite origin (unrelated to other Israeli families) with typical HHRH. Two additional members of this family suffer from a milder asymptomatic form of the disease, which presents as absorptive hypercalciuria without signs or symptoms of bone disease. It seems to us that HHRH is underdiagnosed, due to its similarity to other hypophosphatemic syndromes in clinical, radiological and most biochemical parameters. Therefore, it is recommended that urinary calcium excretion and serum 1,25-dihydroxyvitamin D concentrations be measured in every patient with hypophosphatemic rickets/and or osteomalacia before the initiation of any therapy. The correct diagnosis of HHRN is of immense therapeutic implications. Phosphate therapy alone could cause a complete remission in HHRH, while the addition of active vitamin D metabolites, as is recommended in hypophosphatemic vitamin D resistant rickets, could cause deterioration in the patient's condition.
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PMID:A new kindred with hereditary hypophosphatemic rickets with hypercalciuria: implications for correct diagnosis and treatment. 143 10

We characterized the bone disease of transilial biopsy specimens from children with hereditary hypophosphatemic rickets with hypercalciuria (HHRH) and genetically related asymptomatic hypercalciuric subjects. All HHRH patients showed irregular mineralization fronts, markedly elevated osteoid surface and seam width, increased number of osteoid lamellae, and prolonged mineralization lag time. These findings are consistent with a mineralization defect and indicate unambiguously that the bone disease in HHRH is osteomalacia. The only abnormality seen in the asymptomatic hypercalciuric subjects was slightly extended osteoid surface. Parametric and nonparametric statistical analyses performed on a pooled sample of HHRH patients and asymptomatic hypercalciuric subjects revealed a very high inverse correlation and a tight linear relationship between serum phosphorus and osteoid parameters. Serum 1,25-dihydroxyvitamin D, which is low in other forms of hereditary hypophosphatemia and osteomalacia, is elevated in HHRH and correlated positively with osteoid parameters and the mineralization lag time. Serum alkaline phosphatase showed similar relationships. These results as well as the clinical, biochemical, and radiological remission of bone disease consequent to phosphate therapy strongly suggest that in HHRH 1) hypophosphatemia alone is sufficient to cause osteomalacia; and 2) the elevation of 1,25-dihydroxyvitamin D reflects the degree of the primary renal phosphate leak, but is not involved in the pathogenesis of the bone disease.
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PMID:Osteomalacia in hereditary hypophosphatemic rickets with hypercalciuria: a correlative clinical-histomorphometric study. 198 23

We present what we believe is the first case of rickets following prolonged treatment with aluminum containing antacids that bind phosphate, in an 18-year-old mentally retarded boy with cerebral palsy and spastic quadriplegia. As expected, serum calcitriol was increased and urinary phosphate excretion was very low. However, in contrast to all published cases of antacid induced hypophosphatemic osteomalacia in adults, despite a substantial increase in bone resorption reflected by urinary total hydroxyproline excretion, urinary calcium excretion was low rather than high, and significant hypocalcemia occurred after antacids were ceased and a phosphate salt administered. We suggest that the skeleton was so under-mineralized because of growth during prolonged phosphate deficiency, possibly augmented by anticonvulsant administration and immobilization, that increased bone resorption did not release enough calcium to cause hypercalciuria, or to prevent hypocalcemia during resumption of normal mineralization.
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PMID:Hypophosphatemic rickets with hypocalciuria following long-term treatment with aluminum-containing antacid. 179 81

A total of 2484 newly detected metabolic bone diseases during the past 17 years comprised 79.67% cases of osteoporoses and 20.33% of osteomalacia. The group of osteoporoses included 325 patients (16.43%) with the primary form of the disease, in 1654 patients (83.57%) a cause of decalcification of bones (secondary form) was found. With advancing time the number of secondary osteoporoses rises steadily, while the number of primary cases remains at the same level. In the aetiology of demineralization a major part was played by lactose intolerance, maldigestion and malabsorption, idiopathic, hypercalciuria, diabetes and steroids. The female: male ratio in primary osteoporoses was 4.71:1 and in secondary osteoporoses 2.35:1. Primary osteomalacia was recorded in 113 patients (22.38%) and secondary in 392 (77.62%). Here too with advancing time the number of secondary forms is increasing. The largest groups are hepatic and renal affections, smaller ones malabsorption and antiepileptic drugs. The female: male ratio in primary osteomalacia is 2.13:1 and in secondary osteomalacia 2.26:1. With the development of knowledge on the aetiopathogenesis of bone demineralizations we expect in future a further increase of secondary forms of the disease at the expanse of primary ones.
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PMID:[Secondary osteopenia]. 228 20


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