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

Seventy-seven patients with nephrocalcinosis as revealed by X-ray studies over a 10-year period are reviewed. A programmed clinical and metabolic study was performed on each case; the author's criteria included the different pathogenic factors considered in the etiologic definition of the disease. There were 22 cases with primary hyperparathyroidism, 19 with spongy kidney, nine with tubulointerstitial nephropathy, five with hyperoxaluria, five with distal renal tubular acidosis, four with esential hypomagnesemia, and three cases of miscellaneous etiology (vitamin D intoxication, Fanconi's syndrome, Bartter's disease). Ten other cases were classified as idiopathic nephrocalcinosis since no definite cause could be found. The clinical characteristics (symptoms, associated diseases, diet and medication intake, family history) and the biochemical findings are analysed for each group. The physiopathologic mechanisms, comparisons between each etiologic group, treatment, clinical course, and prognosis are commented on. The conclusion drawn is that nephrocalcinosis is a clinical syndrome of various etiologies which in most cases arises from an underlying metabolic disease.
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PMID:[Nephrocalcinosis as a clinical syndrome. Study of 77 cases (author's transl)]. 52 25

Cysts of the parathyroid glands are uncommon, and functioning parathyroid cysts that cause primary hyperparathyroidism are rare. A 63-year-old man had primary hyperparathyroidism because of cystic hyperplasia of all four parathyroid glands. He also had squamous cell carcinoma of the soft palate, chronic renal failure, hypertension, type-4 renal tubular acidosis, a hyperplastic thyroid adenoma, and hyporeninemic hypoaldosteronism. To our knowledge, this is the first patient to be described with hyperparathyroidism due to multiple parathyroid cysts. The finding of cystic involvement of all four glands supports the theory that at least some parathyroid cysts are either a result of a common embryologic defect or of retention of parathyoid secretions rather than of cystic infarction of parathyroid adenomas.
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PMID:Hyperparathyroidism due to primary cystic parathyroid hyperplasia. 65 52

The diangosis, clinical manifestations and management of 11 children with nephrocalcinosis encountered in a 20-year period are presented. Renal tubular acidosis, primary hyperoxaluria, primary hyperparathyroidism, exogenous hyperadrenocorticism and idiopathic hypercalcemia of infancy were the principal causes of nephrocalcinosis in this series. In the presence of normal or near-normal renal function, a 55 per cent or better cure rate can be expected. Children with significantly diminished renal function have a poor prognosis and should be considered for renal transplantation.
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PMID:Nephrocalcinosis in infancy and childhood. 109 88

An increase in the average calcium oxalate content and decrease in average calcium phosphate content of stones received for analysis has been noted in a 9-year study. These changes appear to be due to a progressive increase in the number of patients with noninfected upper urinary tract stone and to the gradual elimination of phosphatic stones as a result of improved diagnosis and treatment. Some of the conditions associated with calcium phosphate stones are examined, particularly primary hyperparathyroidism, renal tubular acidosis, and medullary sponge kidney. These results further emphasize the importance of calcium oxalate in idiopathic stone disease and the need for a fuller understanding of the factors influencing calcium oxalate crystallization.
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PMID:Changes in the composition of urinary tract stones. 118 36

Shortly after diagnosis of primary hyperparathyroidism, a patient had serum hyperosmolality, polyuria, isosthenuria, profound potassium depletion, and elevated plasma antidiuretic hormone levels, all consistent with nephrogenic diabetes insipidus. After parathyroidectomy, serum calcium and serum osmolality levels fell concurrently. Profound potassium deficits did not recur. We propose that (1) hypercalcemia produced a concentrating defect and polyuria; (2) renal tubular acidosis and polyuria combined to produce severe potassium depletion; (3) hypokalemia potentiated the nephrogenic diabetes insipidus caused by hypercalcemia; and (4) postoperative disappearance of the diabetes insipidus confirmed its reversible, purely metabolic causes.
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PMID:Primary hyperparathyroidism and coexisting nephrogenic diabetes insipidus: rapid postoperative correction. 188 51

The relationship between the degree of metabolic acidosis and calcium phosphate stone formation was studied. Furthermore, the reasons why renal tubular acidosis (RTA) and primary hyperparathyroidism (PHPT) dominantly occur in women, and female stone formers more often produce calcium phosphate stone are discussed. Blood was slightly more acidotic in women than in men in both the urolithiasis and the control groups. Likewise, blood was significantly more acidotic and urinary pH significantly higher in patients with PHPT. Patients with RTA had severe metabolic acidosis, and urinary pH was highest among all groups. Calcium phosphate concentration was significantly higher in women than in men, and was also higher in patients with PHPT than in those with urolithiasis. All patients with RTA had pure calcium phosphate stones. The reasons why females are more acidotic and have more calcium phosphate in stones are suspected to be related to progesterone and urinary tract infection.
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PMID:Relationship between metabolic acidosis and calcium phosphate urinary stone formation in women. 193 25

Plasma osteocalcin levels were measured by radioimmunoassay in 70 consecutive patients with recurrent calcium (sterile) nephrolithiasis during diagnostic evaluation for the cause of the disease. Nephrogenous cyclic adenosine 3,5'-monophosphate levels also were measured in most of the subjects. Included in the sampling, as determined by standard diagnostic criteria, were 12 patients with absorptive hypercalciuria type I, 15 with absorptive hypercalciuria type II, 22 with renal leak hypercalciuria, 11 with normocalciuria, 6 with primary hyperparathyroidism, 3 with renal tubular acidosis and 1 with Paget's disease, as well as 12 control subjects. The observed plasma osteocalcin levels (ng. per ml. mean +/- standard error) were absorptive hypercalciuria I 2.6 +/- 0.20, absorptive hypercalciuria II 3.1 +/- 0.21, renal hypercalciuria 8.7 +/- 0.45, normocalciuric nephrolithiasis 3.3 +/- 0.25, primary hyperparathyroidism 13.2 +/- 0.91, renal tubular acidosis (range) 5.2 to 10.6, Paget's disease 18.0 and control 3.1 +/- 0.20. There were significant differences between the plasma osteocalcin levels of renal hypercalciuria versus primary hyperparathyroidism and renal hypercalciuria/primary hyperparathyroidism versus any other group. There was good correlation between plasma osteocalcin and cyclic adenosine 3,5'-monophosphate data (correlation coefficient 0.72, p less than 0.005). Plasma osteocalcin levels are a potential differential diagnostic tool for patients with stone disease. The diagnostic value compares favorably with that of cyclic adenosine 3,5'-monophosphate, with the advantage that the determination of plasma osteocalcin requires only a single test.
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PMID:Plasma osteocalcin levels in stone disease. A potential aid in the differential diagnosis of calcium nephrolithiasis. 282 25

Medullary sponge kidney (MSK), parathyroid adenoma, renal cell carcinoma, and renal-leak hypercalciuria coincided in 1 female patient. Renal-leak hypercalciuria was not corrected by removal of a parathyroid adenoma. Since the patient had renal tubular acidosis (RTA), alkali treatment was conducted and resulted in the correction of hypercalciuria. Renal cell carcinoma eventually developed and MSK was confirmed histologically. This case suggests that MSK and primary hyperparathyroidism occurred independently.
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PMID:Medullary sponge kidney and hyperparathyroidism. 334 Nov 5

Investigation of a patient with hypercalcaemia, hypophosphataemia, and nephrocalcinosis failed to lead to a clear diagnosis. Neither primary hyperparathyroidism nor primary incomplete renal tubular acidosis could explain all the biochemical features, and it seems that more than one fundamental abnormality may have been present.
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PMID:Hypercalcaemia, hypophosphataemia, and inability to excrete hydrogen ions. 463 53

Two cases of primary hyperparathyroidism due to single parathyroid adenomas presented with the additional feature of hyperchloremic acidosis. The defect in urinary acidification responsible was not of the distal or gradient-limited type since both patients could lower urine pH adequately. However, there was a defect of bicarbonate reabsorption, an abnormality referred to as the proximal or rate-limited type of renal tubular acidosis. It is suggested that this defect represents an exaggeration of the physiological effect of parathormone on bicarbonate reabsorption and may be responsible for the frequent finding of hyperchloremia in association with primary hyperparathyroidism as well as for the urinary bicarbonate-wasting associated with a variety of causes of secondary hyperparathyroidism.
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PMID:Primary hyperparathyroidism and proximal renal tubular acidosis: report of two cases. 501 29


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