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

An unusual case of rickets associated with hypercalciuria is described. In addition to proteinuria, the patient had phosphaturia, aminoaciduria, renal glucosuria and impaired renal concentration but no renal tubular acidosis. Studies did not support the diagnosis of primary hyperparathyroidism. The findings in the patient were very similar to those in 4 previously reported cases and are suggestive of a new combination of multiple renal tubular defects.
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PMID:Hypercalciuric rickets: a rare cause of nephrolithiasis. 624 64

Using the ambulatory protocol previously described, 241 patients with nephrolithiasis were evaluated. They could be categorized into 10 groups from the results obtained. Absorptive hypercalciuria type I (87 per cent male) comprised 24.5 per cent and was characterized by normocalcemia, normal fasting urinary calcium (less than 0.11 mg/100 ml glomerular filtration), an exaggerated urinary calcium following an oral calcium load (greater than 0.20 mg/mg creatinine), normal urinary cyclic adenosine monophosphate (AMP) (less than 5.4 nmol/100 ml glomerular filtration) and serum parathyroid hormone (PTH), and hypercalciuria (greater than 200 mg/day during a calcium- and sodium-restricted diet). Absorptive hypercalciuria type II (50 per cent male) accounted for 29.8 per cent; its biochemical features were the same as those for absorptive hypercalciuria type I, except for normocalciuria during a restricted diet and low urine volume (1.42 +/- 0.55 SD liter/day). Renal hypercalciuria (56 per cent male), disclosed in 8.3 per cent, was represented by normocalcemia and high values for fasting urinary calcium (0.160 +/- 0.054 mg/100 ml glomerular filtration), urinary cyclic AMP (6.80 +/- 2.10 nmol/100 ml glomerular filtration) and serum PTH. Primary hyperparathyroidism (57 per cent female), accounted for 5.8 per cent, typically included hypercalcemia, hypophosphatemia, hypercalciuria and high urinary cyclic AMP. Hyperuricosuric calcium urolithiasis (100 per cent male) comprised 8.7 per cent, and was characterized by hyperuricosuria (776 +/- 164 mg/day) and urinary pH exceeding pK for uric acid (5.91 +/- 0.33). In enteric hyperoxaluria (60 per cent female), encountered in 2.1 per cent of cases, urinary oxalate was increased (6.29 +/- 13.2 mg/day). Noncalcium-containing stones were found in 2.1 per cent of the patients with uric acid lithiasis (100 per cent male) and in another 2.1 per cent of the patients with infection lithiasis (60 per cent female). These conditions were typified by low urinary pH (5.29 +/- 0.12) and high urinary pH (6.69 +/- 1.16), respectively. Renal tubular acidosis was found in one patient (male, 0.4 per cent). In 10.8 per cent of the patients (81 per cent male), no metabolic abnormality could be found, although urine volume was low (1.41 +/- 0.51 liter/day). Hypercalciuria could not be differentiated between absorptive hypercalciuria and renal hypercalciuria in 5.4 per cent of the patients. Thus, this ambulatory protocol disclosed a physiologic disturbance in nearly 90 per cent of the cases and provided a definitive diagnosis in 95 per cent of the patients.
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PMID:Ambulatory evaluation of nephrolithiasis. Classification, clinical presentation and diagnostic criteria. 624 14

Ten patients with subtle primary hyperparathyroidism and intermittent hypercalcaemia were followed serially for periods of 2--18 months (mean 10 months). Fasting serum calcium was elevated (greater than 10.6 mg/dl) in only 20% of determinations and fluctuated widely (9.1--11.2 mg/dl), yet the patients displayed a continuous, rather than episodic, basic disease process as defined by increases in nephrogenous cyclic AMP and serum iPTH. Identical findings were noted in short-term (2--3 successive days) studies in twelve patients. In response to a 1000 mg oral calcium tolerance test, twelve patients with primary hyperparathyroidism and intermittent hypercalcaemia (basal serum calcium 10.2 +/- 0.2 mg/dl, mean +/- SD) displayed: (1) hyperabsorption of calcium (mean calciuric response twice normal); (2) induced-hypercalcaemia (mean serum calcium 11.4 mg/dl, with a mean increase of 1.2 mg/dl versus 0.2 mg/cl in normal subjects); and (3) abnormal parathyroid suppressibility (nephrogenous cyclic AMP 2.66 +/- 0.57 nmol/100 ml GF versus 0.95 +/- 0.40 nmol/100 ml GF in normal subjects, mean +/- SD). The patients demonstrated striking hypercalciuria (452 +/- 123 mg/24 h) on a 1000 mg metabolic calcium diet. Serum levels of 1,25(OH)2D3, measured in ten patients, were markedly elevated at 90 +/- 20 pg/ml (mean +/- SD), and there was a strong positive correlation between the values for 1,25(OH)2D3 and the calciuric response to the calcium tolerance test (r = 0.75, P less than 0.001). These results (1) indicate that the calcium tolerance test is a simple and reliable technique for diagnosis of patients with primary hyperparathyroidism and intermittent hypercalcaemia, and (2) emphasize the important pathophysiologic features of this subtle clinical variant of primary hyperparathyroidism.
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PMID:Primary hyperparathyroidism with intermittent hypercalcaemia: serial observations and simple diagnosis by means of an oral calcium tolerance test. 624 72

An increased calcium excretion in 24-hour urine was found in 32 of 42 out-patients with recurrent calcium nephrolithiasis (calcium excretion > 300 mg in males, > 250 mg in females). Subsequent hospitalization of the 32 patients revealed the following diagnosis after a calcium tolerance test: absorptive hypercalciuria in 18, renal hypercalciuria in 4, primary hyperparathyroidism in 2 and dietary hypercalciuria in 7. Normocalciuria in 10 out-patients was confirmed in 6; in one instance there was, however, primary hyperparathyroidism, in 3 there was absorptive hypercalciuria. In one patient it was not possible to classify the hypercalciuria. Total as well as nephrogenic cAMP showed wide scatter and was unsuitable, therefore, in differential diagnosis. In 2 of 3 cases of hyperparathyroidism the serum level of parathormone was distinctly elevated.
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PMID:[Diagnosis of hypercalciuria in calcium nephrolithiasis (author's transl)]. 625 Jul 84

Twenty-five normal subjects, 45 patients with idiopathic hypercalciuria, and 50 patients with primary hyperparathyroidism were studied with an oral calcium tolerance test and with measurements of 24-h calcium and total cAMP excretion on defined 400-mg and 1000-mg calcium diets. There was a strong positive correlation (r = 0.62; P less than 0.001) between the calciuric response to the tolerance test and the increase in calcium excretion on the 100-mg relative to the 400-mg calcium diet. The increase in daily calcium intake was associated with a significant (P less than 0.001) suppression in total cAMP excretion in each patient group. The suppression in cAMP excretion was sufficient to completely segregate patients with absorptive hypercalciuria from those with renal hypercalciuria on the 1000-mg calcium diet (ranges, 1.24-3.50 and 3.97-4.87 nmol/100 ml glomerular filtrate, respectively). In patients with primary hyperparathyroidism, results for total cAMP excretion were elevated in 48 (96%) patients on the restricted calcium diet but were within the normal range in 14 (28%) patients on the high-normal calcium diet. Net intestinal calcium absorption has a prominent influence on results for 24-h total cAMP excretion, which may be used to diagnostic advantage or seriously impair diagnostic accuracy, depending upon the patient population and the conditions of study.
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PMID:The influence of calcium intake and the status of intestinal calcium absorption on the diagnostic utility of measurements of 24-hour cyclic adenosine 3',5'-monophosphate excretion. 626 62

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

Recent studies have emphasized the pathophysiological importance of circulating 1,25-dihydroxyvitamin D ((1,25-(OH)2D] in the pathogenesis of hypercalciuria and renal stone formation in primary hyperparathyroidism. Reasoning that phosphate administration might be capable of reducing the plasma concentration of 1,25-(OH)2D in patients with a prominent 1,25-(OH)2D-mediated absorptive component to their disease, 10 carefully selected patients were treated with oral phosphate (1500 mg elemental phosphorus daily) for 1 yr. Phosphate treatment significantly reduced circulating 1,25-(OH)2D levels (84 to 56 pg/ml), the calciuric response to an oral calcium tolerance test (0.30 to 0.21 delta mg calcium/dl GF), and calcium excretion on an unrestricted calcium diet (438-269 mg/day), in essence reversing the absorptive pattern of abnormalities observed before treatment. This response, however, was accompanied by an increase in biochemical hyperparathyroidism, as assessed by circulating immunoreactive PTH and nephrogenous cAMP excretion. In patients with biochemical evidence of an increase in bone resorption before therapy, histomorphometric, radiographic, and biochemical data revealed a trend toward a reduction in bone turnover during phosphorus therapy, with an apparent maintenance of coupled bone resorption and bone formation. This trend, however, was of marginal statistical significance in the patient group as a whole. It is concluded 1) that phosphate therapy represents a viable medical alternative in selected patients with primary hyperparathyroidism, 2) that the net response in treated patients is multifaceted and complex, and 3) that the efficacy of phosphate therapy will ultimately depend upon its long term effects on skeletal homeostasis.
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PMID:A detailed evaluation of oral phosphate therapy in selected patients with primary hyperparathyroidism. 630 Jan 78

Thirty-four patients presenting to a urology clinic over a five-year period with renal calculi and either hypercalciuria or hypercalcemia were investigated by measurements of serum parathyroid hormone and urinary calcium and cAMP. Ten patients were hypercalcemic and were found to have primary hyperparathyroidism. Of the remaining patients all but one had excessive urine calcium excretion after an oral calcium load. In addition, 9 patients were shown to have elevated fasting urinary calcium levels while on a low-calcium diet, raising the possibility of impaired renal calcium conservation as one factor causing their hypercalciuria. The measurement of urinary cAMP levels did not contribute to the accuracy of diagnosis and did not permit further subclassification into different types of hypercalciuria. There was a decrease in urinary calcium excretion and a marked reduction in stone-related events in 10 patients with severe renal stone disease during treatment with hypocalciuric agents.
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PMID:Investigation and treatment of renal calculi associated with hypercalciuria. 630 59

We studied the effect of calcium deprivation and loading in 17 healthy subjects and 76 patients with renal calculi. Five had primary hyperparathyroidism with an elevated plasma ionised calcium and detectable plasma parathyroid hormone. Forty-nine had idiopathic hypercalciuria, defined by a urine calcium greater than 7 mmol/day on a free diet. Twenty-two were normocalciuric. Fasting plasma calcium, corrected for albumin, was higher in the patients with idiopathic hypercalciuria (2.40 +/- 0.10 mmol/l) than in controls (2.28 +/- 0.05 mmol/l, p less than 0.005). Plasma calcium was intermediate in the normocalciuric stone formers (2.35 +/- 0.08 mmol/l) and elevated in the patients with primary hyperparathyroidism (2.62 +/- 0.07 mmol/l). Nephrogenous cyclic adenosine monophosphate (cAMP) and parathyroid hormone levels were highest in the primary hyperparathyroid group and did not differ significantly within the other groups. Nephrogenous cAMP correlated positively with plasma calcium in the patients with primary hyperparathyroidism and negatively in controls; there was no correlation in the idiopathic hypercalciuria group. Following an oral calcium load, plasma calcium rose and nephrogenous cAMP fell similarly in all groups. Fasting urinary calcium and its increase after load were greatest in the idiopathic hypercalciuria and primary hyperparathyroid groups, with intermediate results in the normocalciuric patients. Neither the initial metabolic patterns nor the response to thiazide fitted with the previously described patterns of absorptive and renal hypercalciuria. Increased parathyroid gland activity is the most probable cause of idiopathic hypercalciuria.
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PMID:The pathogenesis of idiopathic hypercalciuria: evidence for parathyroid hyperfunction. 632 69

From 1957 through 1981, 550 cervical explorations for presumed primary hyperparathyroidism were performed in 536 patients at the North Carolina Baptist Hospital. Fifty-one of those patients who did not have persistent hypercalcemia are the basis of this report. Twenty-six patients with hypercalciuria and normal renal function had recurrent passage of calcium-containing renal stones, but never had documented hypercalcemia. Only five patients (19%) had positive findings at exploration: small, hyperplastic glands (n = 3); small adenomas (n = 2). Seventeen of the 23 patients for whom follow-up data were available continued to form and pass renal stones postoperatively, including three of the five patients with "pathologic" glands (follow-up range: 4 months to 21.3 years; mean--7 years, 9 months). Twenty-five patients (also with normal renal function) had chronic calcium nephrolithiasis, hypercalciuria, and isolated or occasional elevations of serum calcium ranging from 10.6 to 10.9 mg/dl. Thirteen of these patients had abnormal parathyroid glands: adenomas (n = 12); hyperplasia (n = 1). All but two of the 13 were cured of their nephrolithiasis, but all ten of the patients with no abnormal glands for whom follow-up data were available continued to pass renal stones (follow-up range--8 months to 18 years; mean--5 years, 7 months). Thus, our experience with treating "normocalcemic" hyperparathyroidism has been disappointing. Although a substantial number of patients with occasional mild hypercalcemia may benefit from cervical exploration, those patients are not, by definition, truly normocalcemic. Metabolic evaluation can separate hypercalciuric recurrent stone formers with autonomous secondary hyperparathyroidism from patients with suppressible secondary hyperparathyroidism, and can thus more accurately identify patients who may benefit from parathyroid exploration.
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PMID:Normocalcemic hyperparathyroidism revisited. 654 87


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