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

The authors report 17 personal cases of lithiasis of the upper urinary tract discovered in the course of pregnancy. They discuss the diagnostic and therapeutic problems, taking into account the double risk of mother and foetus. The essential diagnostic sign is renal colic, with or without fever. Spontaneous excretion of these calculi is possible, but in 8 of the 17 cases, a ureteric catheter had to be passed or an operation was required. Neither the delivery nor the health of the infants delivered seemed to be harmed by this renal calculi disease. The authors recall that the most common cause of non-obstetrical abdominal pain in the course of pregnancy is in fact urinary calculi. The incidence is about 1 cases of lithiasis per 1,000 pregnancies. It appear that a physiological hyperparathyroidism of pregnancy is responsible for a hypercalciuria which could be a factor favouring the development of lithiasis during pregnancy. The important point is to know how to distinguish those forms of pyelonephritis of pregnancy which are due to a stone obstructing the upper urinary tract, as any purulent retention in the upper tract can lead to a pyonephrosis, a bacteraemia or even a septicaemia. The presence of the foetus makes interpretation of a plain abdominal film difficult. In any case, its indication is questionable, whenever the urine is septic, particularly with Proteus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lithiasis of the upper urinary tract and pregnancy]. 663 Oct 37

Four preterm infants receiving long-term furosemide therapy were examined for hypercalciuria, hyperparathyroidism, renal calcification, and bone demineralization. All four infants had increased urinary calcium excretion. Three infants had high serum concentrations of parathyroid hormone, and in these three infants, bone mineral content was below the mean of "osteopenic" preterm infants of comparable gestational and postnatal age. In two of these infants, there was ultrasound evidence of renal calcification. In one infant, autopsy disclosed bone changes of hyperparathyroidism, gallstones, and calcification in the heart and kidney.
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PMID:Secondary hyperparathyroidism and bone disease in infants receiving long-term furosemide therapy. 663 31

A 22-year-old man with renal stones had persistent hypercalcemia with massive idiopathic hypercalciuria due to a primary renal tubular phosphorus leak. He did not have hyperparathyroidism or sarcoidosis but did have an elevated dihydroxycholecalciferol level, which contributed to his hypercalcemia.
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PMID:Hypercalcemia with elevated dihydroxycholecalciferol levels and hypercalciuria. A parathyroid concentration-independent mechanism. 669 52

Renal and systemic magnesium metabolism has not been adequately characterized in states of prolonged PTH excess in humans. Whereas acute experimental PTH administration uniformly results in enhanced renal magnesium reabsorption in many species, including humans, numerous clinical reports have documented renal magnesium wasting in human primary hyperparathyroidism. The possibility has been raised, therefore, that secondary consequences of sustained hyperparathyroidism (eg, hypercalcemia, nephrocalcinosis) might override the direct renal effects of PTH. Accordingly, the present studies assessed the effects of chronic (12 days) continuous intravenous (IV) b-(1-34)-PTH infusion in four normal human subjects on plasma, urinary, and intestinal magnesium and calcium homeostasis under metabolic balance conditions. Chronic PTH infusion resulted in a steady-state of hypercalcemia, hypercalciuria, and persistent negative calcium balance, which returned to baseline values in a recovery period. In contrast to plasma calcium concentration, plasma magnesium concentration was not altered by PTH infusion. Significant hypermagnesuria was observed during the period of PTH administration (control, 8.21 +/- 0.43 mEq/24 hours; PTH days 7-12, 10.75 +/- 0.74 mEq/24 hours, P less than 0.05) resulting in an initial, but transient, negative magnesium balance. During days 7-12 of PTH administration, net intestinal magnesium absorption increased sufficiently to result in a return to control magnesium balance. These findings suggest that hypermagnesuria associated with clinical primary hyperparathyroidism results from either direct or indirect effects of PTH excess, per se, and does not require the long-term consequences or complications of the clinical disorder (eg, nephrocalcinosis, renal insufficiency, acidosis).
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PMID:Renal and systemic magnesium metabolism during chronic continuous PTH infusion in normal subjects. 673 67

Previous studies have shown that thiazide diuretic agents reverse secondary hyperparathyroidism and reduce circulating 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and intestinal calcium absorption rates in patients with idiopathic hypercalciuria of the renal-leak variety. We have investigated whether thiazides can reverse the secondary increase in serum parathyroid hormone (PTH) and 1,25(OH)2D3 levels or intestinal calcium absorption induced by feeding rats a diet low in calcium (LCD, 0.02% calcium) but adequate in phosphorus and vitamin D. We found that LCD increased circulating immunoreactive PTH [chow vs. LCD, 0.52 +/- 0.06 vs. 1.06 +2- 0.1 (SE) ng/ml, P less than 0.001], 1,25(OH)2D3 (chow vs. LCD, 101 +/- 15 vs. 325 +/- 38 pg/ml, P less than 0.001), calcium uptake by everted gut sacs from duodenum, ileum, and descending colon, and net calcium absorption by descending colon studied in Ussing chambers in vitro. Chlorothiazide (CTZ) prevented the increase in PTH during LCD (chow + CTZ vs. LCD + CTZ, 0.69 +/- 0.07 vs. 0.73 +/- 0.06, NS) but not the increase in 1,25(OH)2D3 (chow + CTZ vs. LCD + CTZ, 88 +/- 10 vs. 277 +/- 31, P less than 0.002) or intestinal calcium transport. The drug caused no change in serum 1,25(OH)2D3 or intestinal calcium absorption in rats fed normal chow. In rats given exogenous 1,25(OH)2D3 to stimulate intestinal calcium absorption, CTZ reduced urine calcium excretion greatly but did not alter intestinal calcium absorption.
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PMID:Effects of chlorothiazide on 1,25-dihydroxyvitamin D3, parathyroid hormone, and intestinal calcium absorption in the rat. 689 3

Urolithiasis is a rare complication following kidney transplantation. Experience with this complication in 6 of 426 transplantations performed from 1968 to 1979 is reviewed. The clinical symptoms are different from the disease in non-transplant patients. Three major predisposing causes for the development of calculi after kidney transplantation were found in our patients--urodynamic disorders following complications of the ureterovesical anastomosis, persistent bacteriuria and renal tubular acidosis and, less importantly, the presence of hypercalcemia and hypercalciuria as a result of secondary hyperparathyroidism. Crystal-optical and x-ray-diffraction studies contributed to the interpretation of the constituents and texture of the calculi and of the aetiological factors concerned.
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PMID:Urolithiasis after kidney transplantation--clinical and mineralogical aspects. 701 27

In a group of patients with idiopathic hypercalciuria and an increased fasting urinary calcium excretion we re-examined the question: does secondary hyperparathy-roididsm exist? Eight out of 51 patients with calcium renal stones had a high calcium excretion in both fasting and in 24 h urines. The carboxyl-terminal immunoreactive PTH (iPTH) values in these patients were 16 +/- 5 ngeq/ml (M +/- SD), no higher than the iPTH values in the other groups, e.g. normocalciuric patients had an iPTH of 23 +/- 8 ngeq/ml. The existence of secondary hyperparathyroidism in a subgroup of stone patients with increased fasting urinary calcium excretion is questionable.
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PMID:Parathyroid hormone is normal in renal stone patients with idiopathic hypercalciuria and high fasting urinary calcium. 717 13

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

Urinary lithiasis, hypercalciuria and hyperparathyroidism are strictly related diseases, and the urologist diagnoses primary hyperparathyroidism (PHP) in the majority of cases. Herein we retrospectively analyze our experience of 20 cases of surgically proved PHP, operated on in the last 4 years. Hypercalcemia was the keystone for the diagnosis of all our cases PTH radioimmunoassay on selectivity sampled blood revealed a fundamental tool in the management of patients with suspicious or certain hyperparathyroidism. It confirmed the diagnosis in all the cases and gave the preoperative localization of parathyroid adenomas in 70% of the cases. Besides, it made it possible to discriminate between parathyroid adenomas and diffuse hyperplasia preoperatively, so offering a considerable aid to the surgeon in deciding between the conservative and liberal approach to parathyroid surgery. At follow-up, 3 out of 14 cases revealed renal hypercalciuria, which could have been the cause of hyperparathyroidism, as proposed by Reiss and associates previously. The relationship between hypercalciuria and hyperparathyroidism and the problem of a new classification of parathyroid hyperfunction are discussed.
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PMID:Surgical hyperparathyroidism in calcium stone formers. A retrospective study of 20 cases. 720 51

10 patients with normocalcemic secondary hyperparathyroidism due to renal hypercalciuria and 1 patient with normocalcemic primary hyperparathyroidism are presented. The diagnostic criteria of both manifestations of disturbed calcium metabolism are outlined. Successful therapeutic approach depends on the exact discrimination between each form of normocalcemic hyperparathyroidism.
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PMID:Normocalcemic hyperparathyroidism. 728


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