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Query: UMLS:C0020438 (
hypercalciuria
)
2,502
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
12 adult patients with medullary sponge kidney (MSK), followed up for 1 to 14 years (mean 7 years) are presented. MSK was initially diagnosed in 4 cases. In 8 cases the initial diagnosis included pyelonephritis, nephrocalcinosis, and nephrolithiasis. Renal calculi (4 patients), urinary tract infection (8) and hematuria (5) were the most frequent symptoms. Renal tubular acidosis was documented in 2 patients and
hypercalciuria
without
hyperparathyroidism
in 2. Over the years renal calculi increased in size in 4 patients. Renal function was stable in 11. In one patient with associated, well controlled hypertension, serum creatinin rose from 141 to 298 mumol/l over 14 years.
...
PMID:[Medullary sponge kidney. Diagnosis and course in 12 cases]. 397 81
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.
...
PMID:Postmenopausal osteoporosis as a manifestation of renal hypercalciuria with secondary hyperparathyroidism. 400 11
Due to a hypercalcaemia and changeably appearing
hypercalciuria
13 patients with relapsing urolithiasis were under suspicion of a primary hyperparathyroidism. After selective sounding and withdrawal of blood from the cervical veins in all cases the determination of parathormones was performed and always an increased activity of parathormones was found. The exploration of the cervical region carried out could in 11 performed operations in 8 cases prove an adenoma and in 3 cases a hyperplasia as cause of
hyperparathyroidism
. A localization of the suspected adenoma was in 5 cases possible in combination with the angiography of the thyroid gland. By equally high activity in 3 cases no clear evidence was possible. An improvement of the diagnostics of localization might be achieved by supraselective sounding of the veins. On principle the authors recommend to perform a selective determination of parathormones before operation, which in case of need is to be supplemented by a selective angiography of the thyroid gland.
...
PMID:[Diagnosis of primary hyperparathyroidism by selective determination of parathyroid hormones]. 403 77
Patients with
hypercalciuria
have been reported to have an exaggerated response to hydrochlorothiazide (HCTZ), implying a renal tubular defect in solute reabsorption. To determine whether this disturbance is generalized or unique to a particular pathogenetic type of
hypercalciuria
, we measured the increments in urinary sodium (delta Na), calcium (delta Ca), and magnesium after a 100-mg dose of oral HCTZ in 10 normal subjects and 31 patients with different types of hypercalciuric nephrolithiasis. Eleven patients with renal
hypercalciuria
had significantly greater delta Na (P less than 0.005) and delta Ca (P less than 0.005) than the normal subjects. Ten patients with absorptive
hypercalciuria
and 10 patients with fasting
hypercalciuria
without parathyroid stimulation had delta Na and delta Ca indistinguishable from those of normal subjects. In all groups, urinary HCTZ and basal 24-h urinary Na did not differ. The results suggest that the unique natriuretic and calciuric responses to HCTZ occur only in renal hypercalciuric patients with secondary
hyperparathyroidism
. The data support a renal tubular defect in renal hypercalciuric in contrast to other diagnostic categories of hypercalciuric nephrolithiasis.
...
PMID:Exaggerated natriuretic and calciuric responses to hydrochlorothiazide in renal hypercalciuria but not in absorptive hypercalciuria. 404 75
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.
...
PMID:Investigation and treatment of renal calculi. 404 15
The highest degree of urinary supersaturation with respect to calcium oxalate monohydrate (COM) and brushite at which secondary nucleation and growth of small amounts of COM and hydroxyapatite (HAP) are inhibited was determined by new and simple methods. There were 39 subjects who produced 24 h-urine collections (11 idiopathic stone formers (ISF), 12 patients suffering from primary hyperparathyroidism (
HPT
) and 16 healthy controls (HC). These subjects had a moderate calcium and low oxalate intake. The results obtained were compared with the state of urinary saturation and with urine chemistry. The measurements of crystallization conditions with respect to COM were repeated in 26 subjects (11 ISF, 5
HPT
, 10 HC) after a dietary oxalate load. In 24 h-urines of HC diluted to 2.4 1/24 h the degree of supersaturation necessary to induce crystallization of COM and HAP was 2-5 times higher than the state of urinary saturation measured under the same test conditions. ISF showed a decreased pyrophosphate concentration and a decreased inhibitory activity to HAP crystallization in their 24 h-urine. The urinary inhibitory activity towards crystallization of HAP showed a positive correlation to urinary pyrophosphate concentration. In the 24 h-urine of
HPT
hypercalciuria
and increased saturation with respect to brushite which reached values to induce HAP crystallization were found. After a dietary oxalate load urinary supersaturation with respect to COM reached values to induce COM crystallization in ISF and
HPT
but not in HC.
...
PMID:Crystallization conditions in urine of patients with idiopathic recurrent calcium nephrolithiasis and with hyperparathyroidism. 404 2
Calcium phosphate metabolism was thoroughly investigated in twenty-four patients with calcium nephrolithiasis and
hypercalciuria
. Increased absorption was demonstrated in twelve cases. In two patients findings suggested normocalcemic
hyperparathyroidism
. Results were normal in the remaining ten cases. Metabolic investigations failed to noticeably improve the specificity of therapeutic indications over the conventional prevention by adequate fluid intake and an appropriate diet. Nevertheless continuing metabolic investigations are needed as they allow more accurate designing of studies on renal lithiasis.
...
PMID:[Calcium stones: are current metabolic studies warranted in everyday practice?]. 408 38
Extensive experimental evidence has established a significant role of calciferol in the maintenance of normal calcium homeostasis. Present knowledge indicates that vitamin D(3) must first be converted to 25-OH-D(3) and then to 1,25(OH)(2)D(3), the most active known form of the steroid. Many of the factors regulating the rate of production of this last steroid from its precurser have been evaluated, and the concept that vitamin D functions as a steroid hormone seems to be well established. Deranged action of calciferol, caused by impaired metabolism of the steroid or through altered sensitivity of target tissues, may be involved in the pathophysiology of several disease states with abnormal calcium metabolism. It is noted that liver disease, osteomalacia due to anticonvulsant therapy, chronic renal failure, hypophosphatemic rickets, hypoparathyroidism,
hyperparathyroidism
, sarcoidosis and idiopathic
hypercalciuria
have possible relation to alterations in metabolism or action of vitamin D. The future clinical availability of 1,25(OH)(2)D(3) and other analogs of this steroid may offer potential therapeutic benefit in the treatment of certain of the disease entities discussed.
...
PMID:Metabolism and action of the hormone vitamin D. Its relation to diseases of calcium homeostasis. 436 34
Circulating levels of immunoreactive parathyroid hormone (PTH) were measured in 40 patients with idiopathic
hypercalciuria
(IH) before and during reversal of
hypercalciuria
with thiazide, and in four normal subjects before and during induction of
hypercalciuria
with furosemide. 26 patients with IH had elevated serum PTH levels. The remaining patients had normal levels. Although the correlation was not complete, high PTH levels were generally found in patients who had more severe average urinary calcium losses. When initially elevated. PTH levels fell to normal or nearly normal values during periods of thiazide administration lasting up to 22 months. When initially normal, PTH levels were not altered by thiazide. Reversal of
hyperparathyroidism
by thiazide could not be ascribed to the induction of hypercalcemia, since serum calcium concentration failed to rise in a majority of patients. Renal
hypercalciuria
produced by furosemide administration elevated serum PTH to levels equivalent to those observed in patients with IH. The findings in this study help to distinguish between several current alternative views of IH and its relationship to
hyperparathyroidism
. Alimentary calcium hyperabsorption cannot be the major cause of IH with high PTH levels, because this mechanism could not elevate PTH. Idiopathic hypercalciuria cannot be a variety of primary hyperparathyroidism, as this disease is usually defined, because PTH levels are not elevated in all patients and, when high, are lowered by reversal of
hypercalciuria
. Primary renal loss of calcium could explain the variable occurrence of reversible
hyperparathyroidism
in IH, since renal
hypercalciuria
from furosemide elevates serum PTH in normal subjects. Consequently, a reasonable working hypothesis is that IH is often due to a primary renal defect of calcium handling that leads, by unknown pathways, to secondary
hyperparathyroidism
.
...
PMID:Evidence for secondary hyperparathyroidism in idiopathic hypercalciuria. 468 79
The pathogenesis of renal calculi is reviewed in general terms followed by the results of investigation of 439 patients with renal calculi studied by the author at Toronto General Hospital over a 13-year period. Abnormalities of probable pathogenetic significance were encountered in 76% of patients. Idiopathic hypercalciuria was encountered in 42% of patients, primary hyperparathyroidism in 11%, urinary infection in 8% and miscellaneous disorders in 8%. The incidence of uric acid stones and cystinuria was 5% and 2% respectively. In the remaining 24% of patients in whom no definite abnormalities were encountered the mean urinary magnesium excretion was less than normal. Of 180 patients with idiopathic
hypercalciuria
, only 24 were females. In the diagnosis of
hyperparathyroidism
, the importance of detecting minimal degrees of hypercalcemia is stressed; attention is also drawn to the new observation that the upper limit of normal for serum calcium is slightly lower in females than in males. The efficacy of various measures advocated for the prevention of renal calculi is also reviewed. In the author's experience the administration of thiazides has been particularly effective in the prevention of calcium stones. Thiazides cause a sustained reduction in urinary calcium excretion and increase in urinary magnesium excretion. These agents also appear to affect the skeleton by diminishing bone resorption and slowing down bone turnover.
...
PMID:Renal calculi. 543 66
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