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

The results are presented of an oral calcium tolerance test with 1,000 mg calcium in 20 patients with recurrent renal calcium calculosis, a woman with primary hyperparathyroidism and incipient renal failure (serum creatinine 1.8 mg%), creatinine clearance 55 ml/min) and 9 healthy persons as controls. The serum osteocalcin level was determined before and after the oral test. The results show that the serum osteocalcin level alone is of no differential diagnostic value for differentiation of the various types of hypercalciuria in patients with recurrent renal calcium calculosis. As a marker of osteoblasts functional state however the determination of serum osteocalcin level is of great importance for the early diagnosis of osteoporosis. In 3 patients with renal hypercalciuria, often leading to general osteoporosis, an acute rise of serum osteocalcin level was found after the oral calcium tolerance test. High osteocalcin level was also found in the patient with primary hyperparathyroidism and incipient renal failure.
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PMID:[Serum osteocalcin level as a marker of the functional state of osteoblasts after oral calcium tolerance test]. 326 44

Primary hyperparathyroidism and idiopathic hypercalciuria are important causes of calcium stone disease. Hypercalcemia is usually the clue to the presence of primary hyperparathyroidism, but a minority of patients are intermittently or persistently normocalcemic. In these patients there appears to be a resistance to the effect of parathyroid hormone on renal calcium transport, to which calcitriol may contribute. Such patients mimic those with idiopathic hypercalciuria, the commonest metabolic cause of stone formation. The pathophysiology of idiopathic hypercalciuria remains controversial, but abnormalities of renal tubule function and disordered vitamin D metabolism are commonly present. The separation into so-called renal and absorptive types does not appear to be of practical importance, since thiazide diuretics provide effective prophylaxis regardless of type.
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PMID:Primary hyperparathyroidism and idiopathic hypercalciuria. 330 15

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

A neonate with severe primary hyperparathyroidism was successfully managed by parathyroidectomy and heterotopic autotransplantation (one third of one gland of the infant was implanted in the forearm). In vitro studies of parathyroid tissue from the infant revealed a severe defect in parathyroid suppressibility. Postoperatively, the infant had modest hypercalcemia, normal serum immunoreactive parathyroid hormone levels, hypermagnesemia, and relative hypocalciuria. The parents were related and both had asymptomatic hypercalcemia with mean serum immunoreactive parathyroid hormone levels that were within the normal range. Similar to the findings in the infant postoperatively, relative hypocalciuria in the presence of hypercalcemia was found in the mother; in contrast, the father had hypercalciuria. The presumed dominantly transmitted hypercalcemia in this kindred is consistent with familial hypocalciuric hypercalcemia with a confounding factor of ethanol possibly accounting for the hypercalciuria in the father.
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PMID:Severe primary hyperparathyroidism in a neonate with two hypercalcemic parents: management with parathyroidectomy and heterotopic autotransplantation. 373 2

The high incidence of renal lithiasis in hyperparathyroidism (55 p. 100) suggests that PTH plays a causal role in stone production. It also motivates a systematic search for primary hyperparathyroidism in all patients with renal stones although it is only found in about 7 p. 100 of cases. PTH acts through the stimulation of 1.25(OH)2 vitamin D production and therefore, the absorption of calcium from the intestine, which in turn increases the filtrable calcium, hence the calciuria. In renal stones, in general, hypercalciuria represents one of the major metabolic disturbances, besides the hyperoxaluria, hyperuricosuria and the reduction of the inhibitors of crystallization. However, hypercalciuria is rarely the indirect result of excess PTH. It is usually caused by increased dietary ingestion of NaCl, meat, calcium and possibly carbohydrates.
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PMID:[Renal lithiasis in idiopathic hypercalciuria and primary hyperparathyroidism]. 376 88

Three cases of mild metabolic hyperoxaluria (with glycollaturia) are described. They showed different types of response to pyridoxine. One responded to low dose, one responded at first to low dose but became resistant, and the third showed temporary response to high dose. One case also had primary hyperparathyroidism and one had medullary sponge kidneys and hypercalciuria. It is important to measure urinary oxalate (and glycollate) in all cases of calcium oxalate urolithiasis.
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PMID:Mild metabolic hyperoxaluria and its response to pyridoxine. 381 Oct 39

Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.
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PMID:Hypercalcaemia. What does it signify? 394 Aug 49

The stimulation of cyclic AMP production by human renal cortical membranes in the presence of the GTP analogue 5'-guanylimidodiphosphate and a calcium chelator represents a homologous assay system for the evaluation of biologically active parathyroid hormone (bioPTH) in human serum. Bioactive PTH was raised above normal (normal range: undetectable to 4.6 pmol human PTH(1-34) per 1) in 13/17 (76%) patients with primary hyperparathyroidism, in 5/6 (83%) patients with surgically proven hyperparathyroidism secondary to chronic renal failure, in 4/5 (80%) patients with hyperparathyroidism secondary to hypocalcaemia, in all three patients with pseudohypoparathyroidism, in 5/17 (29%) patients with osteoporosis and in 1/9 (11%) patients with renal stones and/or hypercalciuria. Bioactive PTH correlated positively with immunoreactive PTH (iPTH) measured with a radioimmunoassay predominantly recognizing the middle- and carboxyl-terminal region of the PTH molecule (r = 0.503, P less than 0.001). A positive correlation (r = 0.572, P less than 0.05) was found between values of serum calcium and bioPTH in the group with primary hyperparathyroidism. Immunoreactive PTH did not correlate significantly with calcium in this group. In the other patients except those who had chronic renal failure, a negative correlation between serum calcium and both bioPTH and iPTH was observed (P less than 0.01). When alkaline phosphatase was compared with bioPTH in all patients, the correlation was positive (r = 0.390, P less than 0.01); no significant correlation existed between iPTH and alkaline phosphatase in the patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal adenylate cyclase assay for biologically active parathyroid hormone: clinical utility and physiological significance. 394 39

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


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