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 52-year-old man with an acromegalic appearance of prolonged duration suffered abdominal colic attacks and hematuria during the middle of the course of the disease. The patient was diagnosed as having urolithiasis caused by increased urinary calcium. The calcium metabolic disorder was not considered to be due to hyperparathyroidism because serum calcium and PTH levels were within the normal range and no abnormality was observed in a parathyroidal scintigraph. The serum 1,25-dihydroxyvitamin D (1,25-(OH)2D) levels (55.0 and 73.0 pg/ml) were higher than the normal range (27.2-53.8 pg/ml). A selective adenomectomy by the transsphenoidal route (Hardy's method) was performed, resulting in an improvement in the hypercalciuria and urolithiasis, and a decrease in the levels of serum 1,25-(OH)2D (23.0 and 23.0 pg/ml). These findings suggest that GH may promote the activation of vitamin D in the kidney in acromegaly, resulting in an acceleration of calcium absorption in the intestine through the action of activated vitamin D and the induction of increased urinary calcium excretion by the urinary excretion of excessive blood calcium.
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PMID:An acromegalic patient with recurrent urolithiasis. 384 20

The physiopathology of metabolic bone disease described during long term total parenteral nutrition is poorly understood. We therefore prospectively assessed bone status of seven adult patients [mean age, 42 +/- 16 (SD) yr] treated with cyclic total parenteral nutrition for a period of 7 +/- 2 (SD) months. All patients had hypercalciuria (381 +/- 96 mg/day) associated with negative calcium balance in six of seven patients (-49 +/- 120 mg/day). A correlation was found (r = +0.74, P less than 0.01) between protein intake and calciuria. Two patients developed slight transient hypercalcemia. Serum magnesium and phosphate levels remained within the normal range. A high aluminum load due to the added phosphate solution (253 +/- 84 micrograms/day) was associated with increased serum aluminum levels (52 +/- 38 micrograms/liter). Normal serum levels of 25 hydroxyvitamin D (12 +/- 7 ng/ml) and low normal 1,25 dihydroxyvitamin D levels (21 +/- 8 pg/ml) were found. Serum PTH was normal in five and increased in two of the seven patients. However, in these two patients skeletal unresponsiveness to the action of PTH was found. A new histomorphometric picture of bone was observed; it consisted of a markedly reduced bone formation with subnormal osteoclastic activity leading to a low trabecular bone volume. No osteomalacia was found. The aluminum load may have played a role in these bone defects. The hypercalciuria with negative calcium balance was attributed to the cyclic amino-acid delivery during TPN.
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PMID:Multifactorial low remodeling bone disease during cyclic total parenteral nutrition. 391 65

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

An apparently unique presentation of osteoporosis was encountered in eight postmenopausal women (mean age, 56.8 yr). They had renal hypercalciuria, since they had fasting hypercalciuria [0.17 +/- 0.04 (+/- SD) mg/100 ml glomerular filtrate (GF)] in the setting of normocalcemia and parathyroid stimulation (high serum immunoreactive PTH and/or urinary cAMP). Serum 1,25-dihydroxyvitamin D was not significantly different (28 +/- 7 vs. 34 +/- 2 pg/ml) from that in a nonelderly control group, but fractional intestinal calcium (Ca) absorption was significantly lower (0.382 +/- 0.123 vs. 0.49 +/- 0.06; P less than 0.025). Thus, the patients did not have compensatory intestinal hyperabsorption of Ca despite PTH excess. Treatment with hydrochlorothiazide (50 mg/day) produced a decline in fasting urinary Ca (to 0.07 +/- 0.02 mg/100 ml GF; P less than 0.01), serum PTH (from 39 +/- 19 to 21 +/- 1 microliters eq/ml; P less than 0.05), and urinary cAMP excretion (from 5.30 +/- 0.57 to 3.57 +/- 0.59 nmol/100 ml GF; P less than 0.0025). The results suggested that hyperparathyroidism was secondary. Histomorphometric analysis of bone showed reduced trabecular bone volume without mineralization defect, compatible with osteoporosis. Four of eight patients had high or high normal fractional resorption surfaces, fractional formation surfaces, and fractional osteoid volumes. That these abnormalities may reflect PTH-dependent osteoclastic resorption and bone turnover was supported by the reduction of these indices after correction of secondary hyperparathyroidism with hydrochlorothiazide therapy. The remaining four patients, however, had normal histomorphometric results. In summary, postmenopausal osteoporosis may occur sometimes with renal hypercalciuria and secondary hyperparathyroidism. The lack of compensatory intestinal hyperabsorption of Ca predisposes to negative Ca balance, and the hyperparathyroid state may be manifested by stimulated osteoclastic and osteoblastic activities.
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PMID:Postmenopausal osteoporosis as a manifestation of renal hypercalciuria with secondary hyperparathyroidism. 400 11

We evaluated the effects of chronic massive elevations of serum GH and PRL on calcium metabolism in rats bearing the MStT/W15 and 7315a transplantable pituitary tumors. MStT/W15 tumor rats manifest elevated serum GH and PRL levels, hypercalcemia, hypercalciuria, and elevated serum levels of PTH and 1,25-dihydroxyvitamin D. The hypercalcemia was not reversed by dexamethasone or propranolol treatment, but was ameliorated by starvation. Parathyroidectomy produced hypocalcemia in the MStT/W15 tumor rats, confirming the parathyroid dependence of the hypercalcemia. The 7315a tumor produced a milder degree of hypercalcemia, along with elevated serum levels of PRL, ACTH, and corticosterone; serum GH was normal. In high concentrations, PRL and/or GH may stimulate the secretion of PTH as well as enhance dietary calcium absorption, in part through the mediation of 1,25-dihydroxyvitamin D.
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PMID:Hypercalcemia in rats bearing growth hormone- and prolactin-secreting transplantable pituitary tumors. 402 91

The frequency of renal tubular acidosis was evaluated in 28 adult patients with recurrent calcium nephrolithiasis (19 with 'renal' hypercalciuria, 9 with normocalciuria and no metabolic abnormality) and no evidence of obstruction or infection of the urinary tract. Eight patients with hypercalciuria (42%) had a defective renal reabsorption of bicarbonate, based on a fractional excretion of bicarbonate higher than 7% and a TmHCO3/GFR lower than 2.2 mEq/dl; 2 of them had an associated distal defect of acidification, as judged by a U-B pCO2 lower than 18 mm Hg in maximally alkaline urine. One patient with hypercalciuria had distal tubular acidosis, based on a urine pH higher than 5.3 during acidosis. Only 1 patient with normocalciuria had associated proximal and distal acidification defects. The remaining 8 patients displayed a normal renal acidifying capacity. The bicarbonate wastage was independent of serum PTH levels, vitamin D status and hypercalciuria and was associated with a defective tubular reabsorption of phosphate, increased random urinary pH and more active nephrolithiasis, with a prevalence of mixed calcium oxalate and phosphate stones. Our study shows a high incidence of defective tubular reabsorption of bicarbonate in patients with calcium nephrolithiasis and 'renal' hypercalciuria and suggests that the proximal acidification defect plays a pathogenetic role in promoting calcium nephrolithiasis.
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PMID:Renal acidification defects in patients with recurrent calcium nephrolithiasis. 406 1

A family of idiopathic hypercalciuria (IH), 3 symptomatic and 2 asymptomatic, plus 3 normal subjects were given the 1 Gm oral calcium challenge. Biochemical parameters measured included: serum and urinary calcium and phosphate, urinary cyclic AMP, and serum intact and carboxyl-terminal parathyroid hormone. Major differences between the normal control and the family with IH include: (1) higher calcemic response in the family with IH (0.9 vs 0.4 mg/dl); (2) a fall in carboxyl-terminal PTH and urinary cyclic AMP in the IH family in contrast to control subjects in whom there were no changes; (3) a rise in serum phosphorus in the IH family (0.8 vs 0.2 mg/dl, p less than 0.05). Urinary excretion of calcium, phosphorus, and sodium after the calcium challenge was minimal. The oral calcium challenge is a simple and useful test in demonstrating increased calcium absorption even in asymptomatic relatives of patients with idiopathic hypercalciuria.
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PMID:Altered responses in serum calcium phosphorus and parathyroid hormone to oral calcium load in symptomatic and asymptomatic members of family with idiopathic hypercalcemia. 608 33

The role of 1,25-dihydroxyvitamin D (1,25(OH)2D) in the pathogenesis of idiopathic hypercalciuria was studied in 37 renal stone formers who, during two 10-day periods, followed first a normal and then a low calcium diet. The following samples were taken during each diet; 24 h urine; fasting blood and urine; blood and urine following a 1 g oral calcium load. Patients were divided according to serum calcium level, 24 h urinary calcium excretion on the first diet and fasting calcium excretion on the second diet. Eight patients were found to be normocalciuric (NSF), 16 had absorptive hypercalciuria (AH), five renal hypercalciuria (RH) and eight primary hyperparathyroidism. In NSF and AH, a positive correlation was found between the fasting and the 24 hour urinary calcium (r = 0.787, P less than 0.001), while negative correlations were found between the fasting urinary calcium and the serum parathyroid hormone (r = -0.703, P less than 0.001) or the fasting urinary cyclic AMP (r = -0.434, P less than 0.01). Patients with RH had higher serum PTH and urinary cAMP levels for a given degree of fasting calciuria mainly on the low calcium diet. Mean serum 1,25(OH)2D was similar in NSF (43.6 +/- 4.5 pg/ml), AH (43.6 +/- 2.3 pg/ml) and RH (40.4 +/- 4.8 pg/ml) on the first diet; increases were similar in all groups after 10 d of calcium restriction. A positive correlation was found between the serum 1,25(OH)2D concentrations and the 24 h urinary calcium excretion on the first diet in NSF (r = 0.889, P less than 0.001) but not in AH or RH. There was no evidence of such correlation with the low calcium diet. No correlation between the calciuric response to calcium loading and the serum concentrations of 1,25(OH)2D was found. The results suggest that serum concentrations of 1,25(OH)2D may be related to urinary calcium excretion in NSF more than in AH or RH. The factors responsible for the hyperabsorption of calcium in the latter patients remain to be elucidated.
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PMID:Influence of dietary calcium on serum 1,25-dihydroxyvitamin D concentrations in renal stone formers. 609 46

Patients with idiopathic recurrent calcium nephrolithiasis (n = 57) and controls (n = 16) were investigated regarding the relationship between renal phosphate handling, other renal tubular functions and calcium metabolism. Incomplete renal tubular acidosis (RTA) was disclosed in 13 patients. RTA patients together with stone formers with normal renal acidification capacity (SF) exhibited low values for serum phosphate and renal threshold phosphate concentration (TmP/GFR) compared with controls. TmP/GFR was lower in RTA patients than in stone formers with normal renal acidification. Hypercalciuria of the absorptive type with normal serum PTH and urinary cAMP concentrations was a common finding in both stone patient groups, whereas no patient displayed unequivocal evidence of parathyroid hyperfunction. Fractional excretion of sodium was raised in both SF and RTA patients compared with controls. There was a positive relationship between the fractional excretion of phosphate and sodium in all subjects as a group. TmP/GFR was negatively correlated to fractional excretion of sodium. Twenty-three percent of RTA patients and 8% of SF displayed tubular proteinuria which often was associated with low TmP/GFR levels and enhanced natriuresis. It is concluded that a defective renal tubular phosphate handling is common in calcium stone formers and often associated with signs of other tubular dysfunctions. The altered phosphate handling seems to be unrelated to hypercalciuria.
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PMID:Phosphate metabolism in renal stone formers. (II): Relation to renal tubular functions and calcium metabolism. 627 2

We have used a low-calcium diet providing only 2 mg/kg (body weight) per 24 hours of calcium to distinguish between "renal" and "absorptive" idiopathic hypercalciuria. Sixteen of 27 hypercalciuric subjects excreted calcium in excess of intake during days seven, eight and nine of he diet, suggesting some element of renal hypercalciuria; however, all patients had low or normal serum PTH and urine cAMP levels. In general, fasting urine calcium was elevated in these 16 subjects and normal in the remaining 11, who conserved calcium more normally. SErum 1,25(OH)2D3 levels were the same in patients and normal subjects, even though PTH levels of the patients were below those of he normal subjects. Urine magnesium excretion and phosphorus excretion were both increased in the patients who excreted calcium in excess of intake. Our findings suggest that renal and absorptive hypercalciuria may not be distinct entities but rather the two extremes of a continuum of behavior. A uniform elevation of intestinal calcium absorption and a variable defect of renal calcium reabsorption could explain our results far better than the hypothesis of distinct absorptive and renal forms of hypercalciuria.
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PMID:Effects of low-calcium diet on urine calcium excretion, parathyroid function and serum 1,25(OH)2D3 levels in patients with idiopathic hypercalciuria and in normal subjects. 627 90


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