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)

A 25-year-old woman with persistent nephrogenic diabetes insipidus (NDI) following parathyroidectomy for primary hyperparathyroidism is described. NDI is a well recognized complication of primary hyperparathyroidism, generally imputed to hypercalcemia, and promptly reversible after correcting it. In our case, the impaired concentrating ability of the renal tubule was irreversible after the removal of the parathyroid adenoma and the correction of the hypercalcemia, presumptively due to the morphological irreversible changes in the kidney. In addition, hypercalciuria persisted and was the cause of a compensatory hyperparathyroidism. Treatment with thiazide diuretic was effective to decrease relative hypercalciuria, thus reversing the compensatory hyperparathyroidism.
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PMID:A case with persistent nephrogenic diabetes insipidus following parathyroidectomy for hyperparathyroidism. 322 2

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

Due to a hypercalcaemia and changeably appearing hypercalciuria 13 patients with relapsing urolithiasis were under suspicion of a primary hyperparathyroidism. After selective sounding and withdrawal of blood from the cervical veins in all cases the determination of parathormones was performed and always an increased activity of parathormones was found. The exploration of the cervical region carried out could in 11 performed operations in 8 cases prove an adenoma and in 3 cases a hyperplasia as cause of hyperparathyroidism. A localization of the suspected adenoma was in 5 cases possible in combination with the angiography of the thyroid gland. By equally high activity in 3 cases no clear evidence was possible. An improvement of the diagnostics of localization might be achieved by supraselective sounding of the veins. On principle the authors recommend to perform a selective determination of parathormones before operation, which in case of need is to be supplemented by a selective angiography of the thyroid gland.
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PMID:[Diagnosis of primary hyperparathyroidism by selective determination of parathyroid hormones]. 403 77

A 26-year-old woman was admitted to the Institute of Endocrinology in Bucharest for evaluation of primary hyperparathyroidism (P-HPT). Anamnesis revealed a 10-year history of nephrolithiasis; peptic ulcer, chronic pancreatitis, cholelithiasis. Eight months previously, she had given birth to a child who had neonatal hypocalcaemic tetany. Investigations revealed the presence of moderate hypercalcaemia, hypercalciuria, hypo-phosphoremia; serum chloride level was above 100 mEq/1, and the chloride phosphate ratio was greater than 33. X-ray films of the abdomen revealed the presence of nephrolithiasis and right nephrocalcinosis. Selenium methyonine scanning, ultrasonography and computerized tomography were negative. On surgical exploration a 2-3 cm parathyroid adenoma was removed from between the trachea and the esophagus.
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PMID:Primary hyperparathyroidism. Report of a clinical case without bone lesions. 404 20

The availability of accurate and inexpensive methods for measuring serum calcium levels has resulted in a rapid increase in the number of diagnoses of primary hyperparathyroidism, notably in its asymptomatic hypercalcemic forms. In addition, the development of a radioimmunoassay of the parathyroid hormone and, more recently, measurements of nephrogenous cyclic AMP during fasting and after calcium loading have led to the recognition of clinical variants of the disease, such as intermittent or borderline hypercalcemia and pure hypercalciuria with normal calcemia. The degree of hypercalcemia in stable primary hyperparathyroidism depends on renal tubular reabsorption of calcium rather than on bone resorption. The poor correlation observed between calcium tubular reabsorption rate and magnitude of parathyroid hormone hypersecretion suggests that as yet undetermined factors interfere with the effects of parathyroid hormone on renal tubules and probably account for the fluctuations in calcemia reported during serial determinations in patients. The sigmoid relationship between parathyroid hormone release and extracellular calcium concentrations has been analyzed from recent in vitro studies with dispersed parathyroid cells. In primary hyperplasia of the parathyroid glands hypersecretion of parathyroid hormone seems to depend principally upon the increase in tissue mass with normal sensitivity to calcium at cellular levels, whereas in adenoma the primary abnormality responsible for hypersecretion of parathyroid hormone would be an alteration in cell sensitivity to calcium, as indicated by an elevated "set point". Finally, while complicated primary hyperthyroidism requires surgery, our limited knowledge of the natural history of asymptomatic forms makes it impossible to decide which of these patients will ultimately need to be operated upon.
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PMID:[Present status of primary hyperparathyroidism]. 623 8

24-h urinary cyclic adenosine 3', 5'-monophosphate/creatinine (cAMP/Cr) ratio was assessed in 10 patients with hypoparathyroidism, 6 with primary hyperparathyroidism, 7 with normocalcemic hypercalciuria and recurrent nephrolithiasis, 14 with osteomalacia, 25 with Paget's disease and 53 with symptomatic postmenopausal osteoporosis. In hypoparathyroid subjects the mean values of 24 h cAMP/Cr ratio were significantly lower than the control values, whereas in patients with parathyroid adenoma the mean values were higher and fell after parathyroid surgery. Patients with nephrolithiasis due to absorptive hypercalciuria showed low or normal cAMP/Cr ratio, whereas in those with osteomalacia and mean values of cAMP/Cr ratio were significantly higher than the control values and decreased after vitamin D treatment. The mean value of the 24 h urine cAMP/Cr ratio was normal in patients with Paget's disease or postmenopausal osteoporosis and increased significantly after long term treatment with calcitonin or diphosphonate. This increase paralleled a significant decrease of calcium plasma level. A significant improvement of fractional calcium absorption was observed in women with postmenopausal osteoporosis at the end of treatment with calcitonin or diphosphonate.
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PMID:The 24-h urinary cyclic adenosine 3', 5' monophosphate/creatinine ratio: an useful approach to the diagnosis of parathyroid disorders and function. 627 46

Four patients with milk-alkali syndrome (MAS) presented with many of the characteristics of primary hyperparathyroidism including hypercalcemia, low or normal serum phosphorus levels, normal or increased urinary calcium levels, and inappropriately high or elevated serum parathyroid hormone levels. These laboratory findings differ from those classically described in MAS, i.e., hypercalcemia without hypercalciuria and a normal or high plasma phosphate level. Because the serum calcium level failed to return to normal after two weeks of hydration and a low calcium diet, and because of the inability to distinguish this syndrome from primary hyperparathyroidism, two of the four patients underwent neck exploration. Four normal parathyroid glands were histologically proven in each, and at autopsy in a third patient, there was no evidence of parathyroid hyperplasia or adenoma. Hypercalcemia eventually resolved in all patients with a low-calcium diet for as long as six months. Of the several features of MAS, hypercalcemia, alkalosis in the presence of azotemia, a history of increased calcium and alkali intake, and a response to dietary calcium restriction are helpful in differentiating this syndrome from primary hyperparathyroidism. Laboratory tests in patients with MAS may be confusing and the return to normocalcemia in response to a calcium deficient diet may be delayed.
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PMID:Milk alkali syndrome. Does it exist and can it be differentiated from primary hyperparathyroidism? 683 Mar 49

Plasma levels of 1,25 dihydrovitamin D (1,25 (OH)2D) were measured in normal subjects and in patients with various diseases, using a radiocompetition method. Mean values of 89 +/- 58 pmol/l (1 s.d.) were found in normal adults, irrespective of sex. Plasma 1,25 (OH)2D values were high in 12/31 patients with lithiasis and hypercalciuria, in 1/7 patients with lithiasis and normal calciuria and in 2/4 patients with idiopathic parathyroid adenoma; they were normal in 2 patients with essential hypoparathyroidism. 1,25(OH)2D was undetectable in 5 patients with chronic renal failure, low in 7 and normal in 4. Following successful kidney transplantation (serum creatinine less than 120 mumol/l) one-half of the patients had normal values and the other half high values.
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PMID:[Measurement of plasma 1,25 dihydrovitamin D. Normal and pathological values in adults (author's transl)]. 701 71

The diagnosis of primary hyperparathyroidism was made in a 55-year-old female with marked hypercalcemia (15 mg/100 ml) and hypercalciuria and skeletal x-rays showing typical lesions of subperiosteal resorption and numerous cystic areas. At surgery a left lower parathyroid adenoma presumably was totally excised. Serum calcium returned to normal levels immediately postoperatively, but 4 months after surgery hypercalcemia (11.5 mg/100 ml) was again found. During the following 18 months the patient was free of symptoms, and radiologic studies revealed complete healing of the subperiosteal resorption and repair of the bone cysts. Cortical bone mineral content also increased. However, elevated levels of serum parathyroid hormone (PTH) and calcium clearly indicated the persistence of primary hyperparathyroidism. Thus, a decrease in the degree of PTH hypersecretion permitted the repair of the skeletal lesions caused by a more severe level of parathyroid hyperfunction.
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PMID:Healing of osteitis fibrosa cystica after partial parathyroidectomy despite persistent parathyroid hyperfunction: a case report. 715 36

28 adult patients with radiological evidence of medullary sponge kidney (MSK) were studied. Hypercalcemia and increased serum parathyroid hormone (PTH) values were found in 10 patients (36%). In 7 of them, parathyroid surgery was performed: a single adenoma was found in 6 cases and multiple-gland hyperplasia in 1 case. After surgery, 3 patients had normalization of calcium metabolism; 4 patients had persistence of hypercalciuria with progressive increase in serum PTH values (and recurrence of the adenoma in 1 case). Of the remaining patients, 10 (36%) had definite or marginal hypercalciuria, resulting from renal calcium leak in 8 and from intestinal calcium hyperabsorption in 2 of them. In 8 patients (28%), no evidence of disordered calcium metabolism was found. The association of MSK and hyperparathyroidism is not a chance occurrence. MSK might be a renal anatomical complication of primary hyperparathyroidism, or it might be regarded as an anatomic substrate--or rather as a consequence--of prolonged hypercalciuria, regardless of its pathogenesis. The lack of disordered calcium metabolism in a considerable number of patients, however, shows that the enigma of MSK is still far from being solved.
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PMID:Medullary sponge kidney and hyperparathyroidism--a puzzling association. 718 Sep 4


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