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

The pathogenesis of the association of medullary sponge kidney and hyperparathyroidism from parathyroid adenoma remains obscure. This unusual case of medullary sponge kidney and secondary hyperparathyroidism due to renal-leak hypercalciuria gives insight into a possible mechanism for the occurrence of medullary sponge kidney with parathyroid adenoma. Suppressible hyperparathyroidism due to renal calcium wasting could represent an intermediate stage in the development of unsuppressible parathyroid hormone secretion. Thus, parathyroid adenoma occurring with medullary sponge kidney may represent a consequence of disordered renal calcium excretion rather than a primary abnormality.
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PMID:Medullary sponge kidney and renal-leak hypercalciuria. A link to the development of parathyroid adenoma? 43 Jun 89

Surgical exploration of the parathyroid glands was carried out in 84 patients who had recurrent kidney stones and serum calcium levels in the upper quartile and most of whom had hypercalciuria. Parathyroid adenoma(s) were found in 19 cases, hyperplasia in 39 cases, and normal parathyroid glands in 26 cases. Postoperatively, a clinical follow-up was carried out for 2 to 5 years. No relapse has occurred in the cases with adenoma(s) but did occur in 24% of the group with hyperplasia and in 48% of the group with normal glands. The histopathologic findings are described here, while the clinical results are given in another paper. The adenomas do not differ histologically from those giving rise to hypercalcemic hyperparathyroidism. The hyperplasia was of the chief cell type and was slight in most cases. The "normal" glands did not differ from other normal glands from euparathyroid subjects. There was no significant difference in weight and histopathologic appearance between the hyperplastic glands of patients who relapsed and those who did not. Nor did the normal glands of "cured" patients differ from those of patients with relapse. However, in both these groups, some histologic features seem to indicate a favorable outcome; in the group with hyperplasia, there were higher glandular and parencymal cell weight as well as predominance of light chief cells and small fibrotic areas. In the normal group, higher number of argyrophil cells and small fibrotic areas also seem to implicate a better prognosis.
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PMID:Parathyroid adenomas and glands in normocalcemic hyperparathyroidism. A light microscopic study. 93 8

Idiopathic hypercalciuria was noted in 10% of a series of 1635 subjects with renal lithiasis. Eight-day administration of thiazide diuretics as a test for the discovery of latent hyperparathyroidism in idiopathic hypercalciuria is described. In 6 cases diagnosed in this way, surgery disclosed the presence of a parathyroid adenoma. Resection was followed by persistent hypercalciuria and, in some instances, renal lithiasis activity. The pathogenesis of associations of these frequently observed diseases is examined.
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PMID:[Hypercalciuric and hyperparathyroid renal lithiasis]. 99 3

Eighty-four patients with recurrent kidney stones, serum calcium levels in the upper normal quartile, and most of whom with hypercalciuria had their parathyroids surgically explored. Parathyroid adenomata were found in 19 patients, hyperplasia in 39, and normal parathyroids in 26. Postoperatively there was a significant fall in serum calcium and urinary calcium excretion in all three groups. At clinical follow-up 2 to 5 years postoperatively there was no case of kidney stone recurrence among the adenoma patients. In the hyerplasia group there were recurrences tn 25 percent. The corresponding figure for the patients with normal parathyroids was 48 percent. The concept of normocalcemic primary hyperparathyroidism and the relationship between this syndrome and idiopathic hypercalciuria are discussed. Some prinicpal therapeutic measures are recommended.
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PMID:Normocalcemic hyperparathyroidism, kidney stones, and idiopathic hypercalciuria. 112 10

Serum ionized calcium was shown to be significantly elevated in a group of twenty-eight subjects with idiopathic hypercalciuria in whom the mean total serum calcium concentration was within normal limits. Measurement of parathyroid hormone levels confirmed that elevated values are suppressible by infusion of calcium. Ten subjects with simultaneous elevation of serum ionized calcium and parathormone levels above 3 S.D. of normal were referred for neck exploration, and a parathyroid adenoma was found and removed in nine. Significant decreases to normal values of serum ionized calcium and parathormone levels of urine and calcium excretion were documented some weeks following operation. The results conflict with both the alimentary calcium hyperabsorption theory and the renal calcium leak theory of the aetiology of idiopathic hypercalciuria, and support the possibility that idiopathic hypercalciuria in many cases represents an early or mild form of 'normocalcaemic' primary hyperparathyroidism.
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PMID:Serum ionized calcium and parathyroid hormone in renal stone disease. 125 1

On the basis of 3 infants with primary congenital hyperparathyroidism we discuss problems in the early diagnosis and interpretation of the results of laboratory findings. The lack of increased renal echogenicity and hypercalciuria, which is regularly present in idiopathic hypercalcaemia is emphasized. In contrast to secondary hyperparathyroidism caused by prolonged hypocalcaemia, e.g. in patients treated by longterm haemodialysis, the aetiology of primary hyperparathyroidism (pHPT) remained unclear although molecular genetic studies suggest that the development of parathyroid adenoma may be due to gene mutation in a cell. Congenital pHPT is a particularly rare condition usually due to diffuse hyperplasia of all parathyroid glands. Its inheritance is known to be autosomal. Three infants with congenital primary hyperparathyroidism were treated at the Child Health Centre in the years 1987-1988.
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PMID:Primary hyperparathyroidism in infants. Diagnostic and therapeutic difficulties. 203 3

The classical manifestations of primary hyperparathyroidism (hypercalcemia, hypophosphatemia, hypercalciuria, increased blood alkaline phosphatase level, and bone changes of the type of generalized osteoporosis) were found in approximately half of patients in a group of 23 who were examined. When Recklinghausen's disease is suspected, the patients must be subjected to a purposeful examination. The intraoperative diagnosis of parathyroid adenoma is difficult. In distinction from thyroid tissue, a lymph node, and adipose tissue a parathyroid adenoma almost always has a vascular pedicle, which makes verification of the diagnosis easier.
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PMID:[Diagnosis and treatment of parathyroid adenomas]. 206 59

Concomitance of hyperthyroidism and hyperparathyroidism is rare and only forty-nine well documented cases could be found in the literature. In the present study, only forty-three patients with adequate available clinical and laboratory data are reported. Hypercalcemia was found in all the patients and five of them (12%) had acute hyperparathyroidism. Two patients were also pregnant and had pancreatitis. Hypercalcuria was found in 73% and hypophosphatemia in 55% of the patients. Eleven patients (26%) had renal concretions. Skeletal roentgenograms showed abnormalities in 63% of the patients. Elevated serum level of alkaline phosphatase was present in 64% of the patients. However, there seemed to be no correlation with the severity of the skeletal lesions. Thyrotoxicosis commenced before that of Hyperparathyroidism in twenty-three patients (53%) whereas in the remaining twenty patients it was impossible to determine which disease began first. The etiologies of hyperparathyroidism as well as the differential diagnosis of parathyroid-related and nonparathyroid-related hypercalcemia are discussed. Microscopically, 74% of the patients had a single adenoma; 16% had hyperplasia of one to three parathyroid glands. One patient had an adenoma in combination with hyperplasia of one parathyroid gland, one had an adenoma and three hyperplastic glands, one had adenomas of two parathyroid glands in combination with hyperplasia of one parathyroid gland, and the other one had carcinoma of a parathyroid gland.2+ Finally, if a thyrotoxic patient still has hypercalcemia when becoming euthyroid after antithyroid therapy, coexisting hyperthyroidism should be considered and an operation should be performed as surgical treatment cured both diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary hyperparathyroidism and coexisting hyperthyroidism--review of the literature. 267 Jan 39

We report 2 cases of hypercalcaemia and hypercalciuria, with detectable levels of parathyroid hormone, which appeared to be precipitated by enteric fever. Extensive investigation of one case, including ultrasound, isotope scanning, angiography, computed tomographic scanning and surgical exploration, failed to detect a parathyroid adenoma. In both cases biochemical and hormonal abnormalities resolved several months after recovery of enteric fever. The mechanism of the proposed association is unexplained but it should be considered in any patient with hypercalcaemia and detectable parathyroid hormone levels, who is suffering from or has recently recovered from enteric fever. If such a patient is well, a period of several month's observation is recommended. We believe these two cases to be the first such reports of hypercalcaemia in association with enteric fever.
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PMID:Hypercalcaemia in association with enteric fever. 281 40

A 41-year-old man with acromegaly was suffering from chronic, progressive backache and aware of reduction in his body height. Endocrine studies revealed increased glucose non-suppressible serum growth hormone (GH) and serum prolactin (PRL). Pituitary microadenoma was detected by a computerized axial tomogram and subsequently resected by trans-sphenoidal adenomectomy. The tumor proved to be a mixed GH- and PRL-secreting adenoma by electron microscopy and immunoperoxidase staining. Concurrent investigation of backache and reduced height disclosed markedly reduced radiodensity of the spinal bones, bilateral nephrocalcinosis, and hypercalciuria, which were ascribed to renal tubular acidosis (RTA) demonstrated by reduced urinary excretion of acids and insufficient reduction of urinary pH following oral administration of ammonium chloride. From the analogy to certain endocrinopathies, it appears likely that enhanced calcium metabolism and resultant hypercalciuria due to excess GH and PRL have led to the development of RTA, which further enhanced calciuria. Such enhanced calcium metabolism and consequent hypercalicuria conceivably led to accelerated demineralization of the spine and resulted in the reduced height of this patient in his early forties.
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PMID:A case of active acromegaly with reduced height and type 1 renal tubular acidosis. 289 4


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