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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients with nephrolithiasis were found to have both medullary sponge kidney (MSK) and primary hyperparathyroidism. In all cases, urine calcium excretion returned to normal after parathyroidectomy. The passage of stones was abolished for more than 20 years in one case and for more than 12 years in another. The available data suggest that many patients with MSK are asymptomatic and that the risk of stone formation is increased by an associated metabolic abnormality such as hypercalciuria or hyperparathyroidism.
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PMID:Primary hyperparathyroidism. A cause of hypercalciuria and renal stones in patients with medullary sponge kidney. 57 83

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
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PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

The tubular reabsorption of calcium is increased in primary hyperparathyroidism as compared to control subjects and patients with resorptive hypercalciuria. The mean percentage of filtered calcium being reabsorbed by the renal tubules is decreased in primary hyperparathyroidism and hypercalciuria. This might point towards a maximal tubular transport capacity being exceeded in some cases of primary hyperparathyroidism whereas a relative hypoparathyroidism with decreased stimulation of tubular calcium reabsorption might be involved in hypercalciuria.
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PMID:[Renal calcium excretion in primary hyperparathyroidism and idiopathic hypercalciuria (author's transl)]. 105 87

The seventh case in the world literature of primary hyperparathyroidism in a neonate is reported. This is the fifth case in which an autopsy was performed. The clinical and anatomic findings in all seven cases are reviewed and compared. Neonates with primary hyperparathyroidism show diffuse hyperplasia of the parathyroid glands. The bones show disturbed osteogenesis, bone resorption, and widespread fibrosis of the marrow cavities. Bony cysts are not appreciated. Pathologic fractures are common. Marked hypercalciuria or hyperphosphaturia is usually not observed, perhaps because the immature renal tubules fail to respond to the influence of excess parathormone. Aminoaciduria and anemia are commonly observed. The prognosis is grave, and the etiology of this syndrome remains unexplained.
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PMID:Primary neonatal hyperparathyroidism. Report of a case and review of the literature. 110 78

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

The physicochemical factors involved in the formation of calcium-containing renal stones have been elucidated previously and some of the techniques for their quantitation are currently available. Accordingly, urinary activity product ratio (state of saturation), formation product ratio (limit of metastability), and crystal growth of brushite and calcium oxalate in 24-hr urine samples were compared between a control group without stones and stone-forming groups composed of patients with absorptive hypercalciuria, normocalciuric nephrolithiasis, and primary hyperparathyroidism. The activity product ratios of brushite and calcium oxalate were significantly elevated in stone-forming groups, largely because of the high renal excretion of calcium. The formation product ratios were reduced in most stone-forming groups, and the crystal growth was increased in the group with primary hyperparathyroidism. Thus, the physicochemical environment of urine in stone-forming groups was favorable to the nucleation of the nidi of brushite and calcium oxalate; in primary hyperparathyroidism, it may be conducive to the subsequent growth of nidi as well.
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PMID:Nucleation and growth of brushite and calcium oxalate in urine of stone-formers. 127 73

Bone mineral density (BMD) of the 3rd lumbar spine was measured by dual photon absorptiometry (DPA) in 8 patients with primary hyperparathyroidism (PHP) and 39 patients with idiopathic urolithiasis (IU). Of the patients, 15 were classified into idiopathic hypercalciuria (IH) which were further classified into 2 types of IH--renal hypercalciuria (RH) and absorptive hypercalciuria (AH)--by Ca restriction and load test. BMD of the IH patients tended to be lower than patients with normocalciuria, but significantly higher than the PHP patients. BMD of the RH patients was significantly lower than the AH patients. In conclusion, DPA may be a simple method for classifying the types of idiopathic hypercalciuria.
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PMID:[Bone mineral densitometry by dual photon absorptiometry in patients with urolithiasis--on the possibility of the differential diagnosis of idiopathic hypercalciuria]. 177 98

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

Hypercalciuria is one of the main causes of recurrent generation of urinary calcium-containing calculi. 107 patients with recurrent calcium nephrolithiasis were examined and results presented. Concentrations of potassium, sodium, chlorides, calcium, phosphorus, uric acid and creatinine were investigated in serum and urine, as well as indices of acid-base balance in arterial blood. pH-metry, "preliminary" and oral calcium tolerance test were also carried out. The microcomputer data analysis established that the diagnosis of primary hyperparathyroidism may be identified in case of increased serum calcium level before and after calcium load test, the same of parathyroid, and increased urinary cAMP excretion. Renal hypercalciuria is characterized by low blood calcium level in both periods of the oral test, high basal calciuria, increased urinary cAMP excretion and its slight decrease after the oral calcium load test, by a tendency to lower serum magnesium levels in high magnesuria. The patients with absorptive hypercalciuria had an upper normal or increased blood calcium level, a significant calcemic and calciuric "response" to the calcium load, reduction in urinary cAMP elimination and more severe decrease (close to 0) of these indices after oral calcium load and normal magnesium levels in blood and urine. On a base of the "preliminary" test data the patients with relapsing calcium nephrolithiasis and metabolic disorders may be differed from those without calcium and phosphorus metabolic deteriorations. The "preliminary" test defines indications for the oral calcium tolerance test, automatic diagnosis and computer data storage facilitate physician to work and to solve problems of the patients' survey.
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PMID:[The comprehensive examination of patients with recurrent calcium nephrolithiasis]. 185 97


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