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)

Studies were performed on 12 patients with idiopathic hypercalciuria to evaluate the hypothesis that the acid load accompanying potassium acid phosphate would adversely affect renal calcium reabsorption and citrate excretion compared to the neutral form of the phosphate salt. During acute clearance studies, neutral phosphate (NP) led to a fall in FECa (2.2 +/- 0.6% to 0.8 +/- 0.1%, P less than 0.02) and no change in titratable acidity (TA) or net acid excretion (NAE). Acid phosphate (AP) did not reduce FECa acutely, and led to a rise in TA (22 +/- 4 to 62 +/- 6 muEq/min, P less than 0.02) and NAE (46 +/- 6 to 6 89 +/- 7 muEq/min, P less than 0.02). During chronic administration, AP resulted in higher urinary calcium excretion in both absorptive (187 +/- 29 vs. 141 +/- 18 mg/day, P less than 0.02) and renal hypercalciuric patients (233 +/- 24 vs. 173 +/- 190.02 mg/day, P less than 0.02). Also, TA and NAE were higher following AP, whereas citrate excretion was lower (375.4 +/- 64.6 vs. 633.4 +/- 28.8 mg/day, P less than 0.01). These data suggest that the reported ineffectiveness of AP in the therapy of nephrolithiasis may be related to the deleterious effects of the acid load on calcium and citrate metabolism.
Kidney Int 1979 Dec
PMID:Differing effects of acid versus neutral phosphate therapy of hypercalciuria. 4 88

This investigation confirms that 1alpha-hydroxyvitamin D3 (1alpha-OHD3) is a potent drug for the treatment of patients with pseudo-deficiency rickets (Balsan et al., 1975a; Reade et al., 1975; Prader et al., 1976). 1alpha-OHD3 corrects their intestinal malabsorption of calcium and phosphorus, normalizes their serum calcium and phosphate concentrations and promotes healing of skeletal lesions. This study also shows differences in the needs for 1alpha-OHD3 of children with PDR. Three factors appear to be of importance: familial sensitivity, severity of chronic secondary hyperparathyroidism, and periods of increased growth velocity. Tolerance to long-term 1alpha-OHD3 therapy, at doses varying from 0.5 to 2 microgram/d is excellent. Surveillance of patients should include regular measurements of 24 h urinary excretion of calcium, since hypercalciuria is the first signal of overdosage.
Clin Endocrinol (Oxf) 1977 Dec
PMID:Long-term therapy with 1alpha-hydroxyvitamin D3 in children with 'pseudo-deficiency' rickets. 20 17

Idiopathic hypercalciuria constitutes two major variants-absorptive hypercalciuria, characterized by a primary intestinal hyperabsorption of calcium, and renal hypercalciuria, in which renal tubular reabsorption of calcium is primarily impaired. The two forms of hypercalciuria may be distinguished from each other, since a) parathyroid function is stimualted in renal hypercalciuria, but normal or suppressed in absorptive hypercalciuria, b) the renal leak of calcium is present in renal hypercalciuria, but not in absorptive hypercalciuria, c) intestinal calcium absorption is probably increased primarily in absorptive hypercalciuria, and secondarily in renal hypercalciuria (from parathyroid hormone excess), d) the increased calcium absorption in renal hypercalciuria probably results from the parathyroid hormone-dependent stimulation of 1,25-dihydroxyvitamin D synthesis, whereas that in absorptive hypercalciuria may be vitamin D-independent, e) the response of the two conditions to certain treatments is unique, and f) the sequelae of parathyroid hormone excess, such as low bone density and negative calcium balance, may be present in renal hypercalciuria, but not in absorptive hypercalciuria. These findings provide a physiological basis for the consideration of absorptive and renal hypercalciurias as distinct and separate entities.
Am J Physiol 1979 Dec
PMID:Physiological basis for absorptive and renal hypercalciurias. 22 36

Three indices of circulating parathyroid hormone (PTH) activity were compared between two groups: the first a group of 23 patients from three large kindreds with autosomal dominant hypercalcemia without hypercalciuria [familial hypocalciuric hypercalcemia (FHH)] and the second a group of 64 patients with typical primary hyperparathyroidism (1HPT) manifesting comparable hypercalcemia. The group with 1HPT differed from normal with respect to plasma PTH 1HPT concentration (normal, less 0.2 ng/ml), urinary cAMP excretion per 100 ml glomerular filtrate (U cAMP/GF) (normal, 2.3 x/divided by 0.6 nmol/100 ml glomerular filtrate; mean, x/divided 1 SD), and renal tubular maximum of phosphate transport corrected for glomerular filtration rate (TMP/GFR; normal, 3.4 +/- 0.4 mg/dl; mean, +/- 1 SD). The group with 1HPT also diverged significantly from the group with FHH for all three indices: for PTH, 0.37 x/divided by .48 vs. 0.25 x/divided .46 (P less than 0.05); for UcAMP/GF, 4.3 x/divided by .53 vs. 2.6 x/divided .60 (P less than 0.0005); and for TMP/GFR, 2.0 +/- 0.6 vs. 2.6 +/- 0.7 (P less than 0.01). The between-group differences for all three indices were also significant after adjustment for their variation with serum calcium. However, only the difference in TMP/GFR remained significant after adjustment for covariance attributable to serum calcium concentration, age, and creatinine clearance. The group with FHH differed from normal for TMP/GFR but not for UcAMP/GF. However, analysis of changes in UcAMP/GF and serum calcium concentration around the time of parathyroidectomy in three patients with FHH suggested that the parathyroid glands contributed to the abnormalities of mineral homeostasis in at least one. It was concluded that higher serum concentrations of PTH do not account for the lower renal clearance of calcium and magnesium in FHH calcium concentration, the group with FHH showed indices suggesting lower circulating PTH activity than the group with 1HPT.
J Clin Endocrinol Metab 1978 Dec
PMID:Circulating parathyroid hormone activity: familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism. 23 92

The handling of an acute oral calcium load in 22 men with recurrent calcium stone disease was studied before and after diuretic therapy. As a group, the patients had marginal hypercalciuria (150 mg calcium per gram of creatinine in a 24-hr urine collection). Metolazone, a diuretic with an action in the cortical thick ascending limb of Henle's loop, was given in oral daily doses of 5.0 mg for periods of 9 to 34 mo. An oral calcium load induced a rapid rise in urine calcium exeretion, which was blunted markedly by metolazone. Further analysis of the subjects revealed that one group (11 subjects) had higher baseline 24-hr calcium excretion levels and higher parathyroid hormone (PTH) than the others. The effect of metolazone in reducing the calciuric response was significant only in this group. Thus, while long-term treatment with metolazone inhibited the rise in urinary calcium excretion elicited by an oral calcium load, the effect was significant only in patients who had high baseline urinary calcium and PTH values. The reduction in calcium excretion in response to an acute calcium challenge may explain in part the beneficial effects of cortical diluting segment diuretics in recurrent stone formers.
Clin Pharmacol Ther 1979 Dec
PMID:Changes in calcium excretion after prolonged metolazone therapy in recurrent stone formers. 49 17

Increased calcium (Ca) excretion is characteristic of chronic phosphate (PO(4)) depletion (PD). To study the changes in tubular transport and the site of the hypocalciuric effect of PO(4) administration, clearance and micropuncture experiments were performed in intact rats pair fed either a control diet (0.5% PO(4)) or a PO(4)-depleted (PD) diet (0.01% PO(4)) plus Al(OH(3)) and in parathyroidectomized (PTX) PD rats, infused either with saline or with neutral sodium PO(4). Intact PD rats, compared with intact rats on a control diet, exhibited a lower plasma ultrafiltrable (UF) PO(4) (5.8+/-0.5 vs. 7.8+/-0.3 mg/dl), higher fractional excretion (FE) of Ca (4.1+/-1.2 vs. 0.6+/-0.1%), and reduced FE PO(4) (0.1+/-0.01 vs. 10.2+/-1.8%). Tubular fluid/plasma inulin was lower in the late proximal tubule of PD rats, associated with increases in fractional delivery (FD) from the proximal tubule of Na and Ca.The%FD of Ca to the early distal tubule of PD rats was increased (20+/-3 vs. 11+/-2%), but this difference was abolished by the late distal tubule (5.1+/-1.2 vs. 3.3+/-0.9%). In PTX-PD rats, PO(4) infusion increased plasma UF PO(4) (13.8+/-0.7 vs. 7.8+/-0.7 mg/dl). FE of Ca was reduced (1.08+/-0.35 vs. 4.59+/-1.57%) without correcting the increased Ca delivery to the late distal tubule. These data indicate that PD impairs Ca reabsorption in tubular segments before but not within the distal convoluted tubule, so that hypercalciuria is ultimately a result of decreased Ca transport either in the terminal nephron or in deeper nephrons where PO(4) infusion stimulates Ca transport independent of parathyroid hormone or changes in the filtered load of Ca.
J Clin Invest 1979 Dec
PMID:Renal tubular sites of altered calcium transport in phosphate-depleted rats. 50 Aug 33

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
Nouv Presse Med 1977 Dec 03
PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

Absorptive hypercalciuria was treated in 27 patients with cellulose phosphate. In all patients urinary calcium decreased and stone formation virtually ceased. The most striking side effect was an excessive hyperoxaluria, necessitating withdrawal of the drug in 8 patients. Succinate decreased the hyperoxaluria in 14 of 19 patients. All patients had mild hypercalciuria and hypermagnesiuria. This study was done to determine the therapeutic value and the side effects in the treatment of absorptive hypercalciuria with sodium cellulose phosphate and of hyperoxaluria with succinate.
J Urol 1978 Dec
PMID:Calcium oxalate stone disease: effects and side effects of cellulose phosphate and succinate in long-term treatment of absorptive hypercalciuria or hyperoxaluria. 73 12

A young man, investigated because of tetanic convulsions and arthritic pains, was shown to have hypomagnesemia, hypermagnesuria, hypokalemia, hypercalciuria, progressive nephrocalcinosis and chondrocalcinosis. In this syndrome, renal function was normal except for the abnormal excretion of electrolytes. Renal sodium conservation was normal. Light and electron microscopic studies of renal biopsy specimens showed the presence of several abnormal tubules. Immunofluorescent staining showed deposits of immunoglobulins in the glomeruli and tubules. Magnesium therapy was started under balance study conditions and resulted in decreased calciuria and complete remission of subjective symptoms. The progression of nephrocalcinosis was halted, and there was some decrease in the intra-articular calcium deposits after two years of continuous oral magnesium therapy. The administration of spironolactone decreased urinary magnesium but did not normalize it, whereas triamterene administration was without effect in this respect. The results of the morphologic and electrolyte balance studies are discussed. The patient was found to exhibit several features which have not been described before in connection with hypomagnesemia of unknown origin.
Am J Med 1975 Dec
PMID:Hypomagnesemia due to renal disease of unknown etiology. 119 Feb 59

Three patients with nonpulmonary sarcoidosis had chronic erythema nodosum within the first 2 years of life. Each subsequently had renal sarcoidosis and nephrocalcinosis; hypercalcemia was documented in each patient and hypercalciuria in two patients. Treatment with prednisone was not uniformly successful in normalizing creatinine clearance. Nephrocalcinosis may be more common than previously reported in patients with sarcoidosis.
J Pediatr 1992 Dec
PMID:Sarcoidosis associated with nephrocalcinosis in young children. 144 62


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