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

Hypercalcemia, hypercalciuria, and hyperphosphatemia are common findings in acromegaly, yet there are only a few reports on the occurrence of urinary stones in these patients. We reviewed the files of 64 patients with acromegaly. A total of 8 patients had evidence of renal calculi: 4 patients underwent nephrolithotomy, 3 had stones which were seen on intravenous pyelography, and 1 patient voided a stone. Moreover, 2 other patients suffered from recurrent typical episodes of renal colic. In view of the high incidence of urolithiasis in our series we believe that more attention should be paid to detection of urinary stones in acromegalics to avoid further complications and suffering.
Urology 1985 Sep
PMID:Urolithiasis in acromegaly. 403 39

Urinary excretion of N-acetyl-beta-glucosaminidase (NAG), a lysosomal enzyme, was examined in 33 children with hypercalciuria. Urinary NAG excretion in 13 healthy children was 5.84 +/- 9.35 nmole/hr/mg of creatinine (NAG/Cr) (mean +/- SD) compared with 35.61 +/- 42.04 nmole/hr/mg of creatinine in 23 children with renal hypercalciuria, and 28.99 +/- 13.69 nmole/hr/mg of creatinine in ten children with absorptive hypercalciuria. In children with renal hypercalciuria, NAG/Cr excretion was not statistically different between children with either urolithiasis or hematuria without calculi. In six children with renal hypercalciuria, no significant change in NAG/Cr excretion occurred after a mean duration of 25 weeks of hydrochlorothiazide therapy although urinary calcium to creatinine ratios (UCa/Cr) decreased from 0.24 +/- 0.11 to 0.16 +/- 0.11. We conclude that increased urinary calcium excretion produces renal tubular injury and that the renal injury may not be reversed by short-term alterations in urinary calcium excretion.
Am J Dis Child 1985 Sep
PMID:Increased urinary excretion of renal N-acetyl-beta-glucosaminidase in hypercalciuria. 403 32

We have investigated and treated 176 patients who were suffering from renal calculi. The stones contained calcium in 87% of patients, predominantly urate in 11%, and rarely contained magnesium ammonium phosphate or cystine. Of the patients with calcium stones, hypercalciuria was present in 75% and was identified in 57% by the measurement of the 24-hour urinary calcium excretion, and in a further 18% by a standardization calcium "fast-and-load" test. Nine patients were found to have primary hyperparathyroidism and were treated surgically. A further 21% were suspected to have normocalcaemic hyperparathyroidism, and metabolic studies are being developed to clarify this. The treatment of hypercalciuria included a low-calcium diet, and various combinations of a thiazide diuretic, phosphate supplements and sodium cellulose phosphate. Hypercalciuria was controlled in all compliant patients, and only two developed further stones. Hyperuricosuria was rarely the sole metabolic abnormality in patients with calcium stones, though this might reflect the referral pattern of the Unit. Uric acid stones were frequently, but not invariably, associated with hyperuricosuria and acid urine, and even large uric acid calculi dissolved with a combined therapy of high fluid intake, allopurinol and an alkalinizing agent. Surgical treatment was rarely required in these patients. A stone in the renal pelvis of one patient was removed percutaneously and did not require ultrasonic fragmentation. Modern methods of investigation and treatment have greatly improved the outlook for patients with recurrent renal calculi.
Med J Aust 1985 Sep 30
PMID:Investigation and treatment of renal calculi. 404 15

The effects of commonly used therapeutic doses of hydrochlorothiazide and probenecid, given singly and in combination, on the urinary excretion of monovalent and divalent ions and on acid-base equilibrium were studied in four patients with idiopathic hypercalciuria.Probenecid had no effect on the urinary excretion of monovalent ions but resulted in a sustained increase in the urinary excretion of calcium, magnesium and citrate and a temporary increase in the urinary excretion of ammonium, in addition to its well-known effects on uric acid metabolism. A temporary fall in serum phosphorus levels was also observed.Probenecid also modified the response to hydrochlorothiazide in that the urinary excretion of calcium, magnesium and citrate was greater during combined therapy than when hydrochlorothiazide was administered alone. Probenecid prevented or abolished the increase in serum uric acid levels associated with the use of thiazide but did not modify the effects of hydrochlorothiazide on the urinary excretion of sodium, chloride, potassiu, phosphorus, ammonium, titratable acid and bicarbonate.
Can Med Assoc J 1970 Sep 12
PMID:The effects of probenecid and thiazides and their combination on the urinary excretion of electrolytes and on acid-base equilibrium. 546 17

Hypercalcaemia and hypercalciuria are common complications of advanced mammary cancer. Of 127 patients with the disease 63 (49.5%) had some abnormality of calcium balance. Eighteen (14%) of these patients developed severe progressive hypercalcaemia and became acutely ill.Most patients had skeletal metastases, and the usual cause of hypercalcaemia was rapid destruction of bone by the cancer. One patient with severe uncontrollable hypercalcaemia and minimal skeletal involvement probably developed the complication due to inappropriate secretion of a parathyroid-hormone-like substance by massive hepatic deposits.Severe hypercalcaemia was controlled successfully in 13 of the 18 patients, the serum calcium levels returning to normal and the acute symptoms disappearing. Unfortunately, successful correction of the hypercalcaemia rarely was followed by prolonged survival from the underlying malignant disease. The incidence of subsequent objective response to pituitary ablation was less than usual, and only three patients survived for more than one year after the episode of hypercalcaemia.
Br Med J 1971 Sep 04
PMID:Hypercalcaemia in patients with advanced mammary cancer. 557 56

Idiopathic hypercalciuria (IH) was diagnosed in 11 children aged 5 3/12 to 10 6/12. Eight patients investigated 1-12 years later still had hypercalciuria. When compared to a control group of 10 healthy children, 5 patients demonstrated an excessive rise in urinary Ca excretion following an oral Ca load. These patients also demonstrated low urinary cAMP, normal serum iPTH and high normal iTCT levels. The remaining 3 patients responded normally to Ca loading, but otherwise showed similar metabolic findings as the above group. These findings suggest a hyperabsorptive mechanism for all our patients. The finding of relatively low values for TmP/GFR in most IH patients further suggests that here, as in many adult patients, this may be the primary pathogenic mechanism, causing low serum P, increased synthesis of 1,25 dihydroxyvitamin D and, thus, absorption of Ca. We believe this represents a physiologic variant state and not a disease state.
Int J Pediatr Nephrol 1983 Sep
PMID:Pathophysiologic studies in idiopathic hypercalciuria presenting in childhood. 631 14

A 36-year-old woman presented with hypercalcemia, hypercalciuria, elevated serum parathyroid hormone levels and prolonged fever. Surgical removal of the hyperplastic and adenomatous parathyroid glands led to reversal of the biochemical abnormalities as well as return of her temperature to normal.
Can Med Assoc J 1984 Sep 01
PMID:Prolonged fever associated with primary hyperparathyroidism. 646 19

Secondary hyperparathyroidism (HP) has been reported to be characteristic of idiopathic hypercalciuria (IHC) of the renal type. Out of the 155 patients with urinary stone disease and a normal plasma calcium level, only 1 had a distinctively increased plasma parathyroid hormone (PTH) level; however, he was found to be hypercalcemic in a second control study. In 33 patients with renal IHC, none had an elevated PTH level measured under normal, low, and high calcium intake. The mean basal PTH level of these patients was identical to that of 86 normal controls; it was significantly lower than that of the patients with primary or secondary HP who had normal PTH levels. During EDTA infusion, seven of eight patients with primary HP and a normal basal PTH level showed PTH responses greater than those observed in six patients with renal IHC, all of the latter responses being in the normal range. Chlorthalidone, given to seven patients with renal IHC during 4 weeks (100 mg/day), did not decrease the PTH levels. Measurement of nephrogenous cAMP performed in only a few patients revealed a slightly increased value in one of them who had an exceptionally severe hypercalciuria. Beside this latter result, no evidence for secondary HP could be found. Although secondary HP is tempting pathophysiological explanation for many characteristics of renal IHC, it seems to be quite rare.
J Clin Endocrinol Metab 1981 Sep
PMID:Secondary hyperparathyroidism in idiopathic renal hypercalciuria: fact or theory? 679 May 59

Enzyme replacement therapy for a severely affected 6-month-old girl with hypophosphatasia was attempted by repeated intravenous infusions of alkaline phosphatase-rich plasma, obtained by plasmapheresis, from two men with Paget bone disease. Circulating Paget AP activity was found to have a half-life (two days) similar to that reported in adults, which did not change during a five-week period of six AP infusions. Normalization of the patient's serum AP activity was followed by better control of her hypercalcemia and hypercalciuria. Sequential radiographic studies revealed arrest of worsening rickets with slight remineralization of metaphyses, although urinary excretion of the AP substrates phosphoethanolamine and inorganic pyrophosphate was unaltered by therapy. Our findings suggest that the infantile form of hypophosphatasia results from defective production of AP rather than from accelerated destruction of circulating enzyme, and that hydrolysis of AP substrates like PEA and PPi occurs primarily in tissue rather than blood. Study of additional cases of hypophosphatasia will be necessary to assess the clinical efficacy of this form of enzyme replacement therapy.
J Pediatr 1982 Sep
PMID:Infantile hypophosphatasia: enzyme replacement therapy by intravenous infusion of alkaline phosphatase-rich plasma from patients with Paget bone disease. 710 57

During the last four years ten premature infants developed renal calcifications while receiving long-term furosemide therapy. The drug was used in infants with present ductus arteriosus and later in the same infants with chronic lung disease. They had received furosemide in a dose of at least 2 mg/kg/day for at least 12 days before calcifications were noted on abdominal roentgenograms. Calcifications included small flecks, isolated stones, staghorn calculi, and nephrocalcinosis. Analysis of stones received from our infants showed calcium oxalate and calcium phosphate. Infants who were not receiving furosemide had no calcifications. The infants with renal calcifications had rates of calcium excretion ten to 20 times that of normal, age-matched premature infants in our nursery. When chlorothiazide was given to the infants, in addition to furosemide, a four- to 15-fold decrease in calcium excretion and a radiologic dissolution of the renal calcifications were documented. It is concluded that furosemide, in doses of at least 2 mg/kg/day for at least 12 days can be associated with renal calcifications. The probable mechanism of the stone formation is hypercalciuria, primarily caused by furosemide.
Pediatrics 1982 Sep
PMID:Renal calcifications: a complication of long-term furosemide therapy in preterm infants. 711 Aug 8


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