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

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

Bone mineral content (BMC) was measured with the Norland Cameron apparatus in 120 renal stone formers (RSF) with idiopathic stone disease and in 41 patients with primary hyperparathyroidism. RSF were classified, according to an oral calcium load test, into three groups: no hypercalciuria (HC; 41 cases); absorptive HC (53 cases), and resorptive or renal HC (25 cases). BMC values in RSF as a group were significantly lower than normal (p less than 0.001, Mann-Whitney test) though higher than in hyperparathyroid patients. There was a trend for BMC to decrease from male RSF without HC to patients with renal or resorptive HC. No statistical difference was found between the groups, however, BMC values in absorptive HC were different from normal (p less than 0.001). Why patients with HC are demineralized is unclear since no correlation was found between BMC and basal values of serum phosphate, TRP, calculated TmP/GFR, urinary calcium or hydroxyproline. Nevertheless our results indicate that urolithiasis, and possibly its treatment, is not a benign condition for the skeleton.
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PMID:Bone mineral content in idiopathic renal stone disease and in primary hyperparathyroidism. 682 40

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

The intestinal absorption of magnesium (Mg) was estimated from the increment in urinary Mg following oral administration of 25 mmol of Mg. Fasting urinary Mg did not differ between the control group and patient groups (absorptive hypercalciuria, primary hyperparathyroidism, and hypoparathyroidism). As compared to the value in the control group, the increment in urinary Mg above the fasting value was not significantly different in absorptive hypercalciuria. However, it was significantly increased in primary hyperparathyroidism and significantly reduced in hypoparathyroidism. In control subjects, the increment in urinary Mg was much higher during a low than during a high calcium diet. The results suggest that 1,25-(OH)2-vitamin D stimulates Mg absorption, since Mg absorption was elevated in situations associated with stimulated 1,25-(OH)2-vitamin D synthesis (primary hyperparathyroidism and low calcium diet) and reduced in a condition characterized by low 1,25-(OH)2-vitamin D production (hypoparathyroidism). Moreover, the data indicate that 1,25-(OH)2-vitamin D may not be pathogenetically important in absorptive hypercalciuria, since Mg absorption was normal.
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PMID:Oral magnesium load test for the assessment of intestinal magnesium absorption. Application in control subjects, absorptive hypercalciuria, primary hyperparathyroidism, and hypoparathyroidism. 689 41

Diagnostic evaluation was conducted on 34 patients with a single episode of renal stone formation. Absorptive hypercalciuria as disclosed in 55.9 per cent (23.5 percent type I and 32.4 per cent type II), renal hypercalciuria in 11.8 per cent, primary hyperparathyroidism in 2.9 per cent, hyperuricosuric calcium oxalate nephrolithiasis in 8.8 per cent and no metabolic abnormality in 20.6 per cent. Compared to the group with recurrent stone formation the group with a single stone episode had just as severe biochemical abnormalities or laboratory results, such as hypercalciuria and exaggerated calciuric response to oral calcium load in absorptive hypercalciuria, high fasting urinary calcium and cyclic adenosine monophosphate in renal hypercalciuria, hyperuricosuria in hyperuricosuria calcium oxalate nephrolithiasis and low urine volume in no metabolic abnormality. The results suggest that the same physiological and environmental disturbances characterize stone formation in patients with a single stone episode as in those with recurrent stone formation and indicate the need for diagnostic evaluation.
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PMID:Should patients with single renal stone occurrence undergo diagnostic evaluation? 708 82

Outpatient renal stone formers belonging to the established urolithiasis subgroups and controls were examined with respect to urinary and serum citrate (Cit) and several associated variables. Only in the normocalciuric majority of calcium and in uric acid stone formers was Cit in 24-hour urine decreased, but was normal in 2-hour fasting morning, and in 3-hour postprandial urine following a Cit-free test meal. Serum Cit was elevated in normocalciuria, renal and resorptive hypercalciuria. This Cit constellation was associated with either normal (absorptive, renal hypercalciuria) or low (normocalciuria, uric acid stone formers) parathyroid gland function as assessed by serum parathyroid hormone and nephrogenous urinary cyclic AMP, except in patients with primary hyperparathyroidism. In 2-hour morning urine the magnesium/creatinine ratio (normocalciuria) and ammonia excretion (uric acid stone formers) were decreased, while ammonia in 24-hour urine was low in all stone formers. It is suggested that Cit metabolism is altered in renal stone disease in general, and that in normocalciuria, stone inhibitors (Cit; magnesium) may be deficient.
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PMID:Citrate in urine and serum and associated variables in subgroups of urolithiasis. Results from an outpatient stone clinic. 712 65

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

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

Seventeen patients with documented medullary sponge kidney and nephrolithiasis underwent metabolic evaluation. These patients constituted 3.6% of our stone-forming population. Fifteen (88%) of 17 were hypercalciuric. The most common abnormality was absorptive hypercalciuria, occurring in 59%. Only three patients (18%) had renal hypercalciuria. None of the patients had primary hyperparathyroidism. Hyperuricosuria occurred together with hypercalciuria in five patients. In two patients, the precise cause of hypercalciuria could not be determined, and in another two patients, no metabolic abnormality could be detected. Thus, the patients with medullary sponge kidney and renal stones had the same spectrum of metabolic abnormalities as the overall population of stone formers. While these patients may theoretically have a greater anatomic propensity to form stones because of their anatomic abnormality, they should be evaluated and treated appropriately for any metabolic defect.
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PMID:Metabolic evaluation of nephrolithiasis in patients with medullary sponge kidney. 720 12


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