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)

Chronic mineralocorticoid excess results in the predicted retention of salt and water followed by a period of escape from sodium retention and hypercalciuria. We studied a rat model during mineralocorticoid escape (ME) with clearance and micropuncture studies to ascertain the nephron site and possible role of parathyroid hormone. Rats during ME were hypercalciuric compared with a matched saline group. Clearance studies revealed a marked difference in the calcium-to-sodium fractional excretion ratio (FECa/FENa) between saline-expanded and mineralocorticoid (desoxycorticosterone acetate, DOCA)-escaped animals (saline-expanded, 0.40 +/- 0.09 vs. DOCA, 1.02 +/- 0.14; P less than 0.01). The addition of either hydrochlorothiazide (HCTZ) or amiloride (AMIL) to the ME animals significantly lowered this ratio from that seen in the intact ME group (DOCA-HCTZ, 0.47 +/- 0.07; DOCA-AMIL, 0.83 +/- 0.14). Neither parathyroidectomy (PTX) nor parathyroid hormone infusions (PTH) in ME animals altered the FECa/FENa from that seen in the intact ME group (DOCA-PTX, 1.15 +/- 0.20; DOCA-PTH, 1.25 +/- 0.18). Segmental micropuncture along the length of superficial nephrons demonstrated no differences in calcium delivery to late proximal, early distal, and late distal sites. However, FECa was markedly increased in ME animals compared with saline controls (saline, 0.48 +/- 0.13% vs. DOCA, 1.62 +/- 0.24%; P less than 0.05). We conclude that the hypercalciuria of ME is independent of PTH and can be significantly reduced by HCTZ or AMIL. Micropuncture and clearance data suggest that the hypercalciuria of ME is mediated in the terminal nephron. The differences in the results when superimposing various factors that influence distal nephron calcium reabsorption on ME may be related to differences in their site(s) of activity on calcium transport.
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PMID:Hypercalciuria of mineralocorticoid escape: clearance and micropuncture studies in the rat. 377 84

With oral furosemide administration and salt loading, urinary calcium was significantly increased in 8 normal subjects, accompanied by parallel natriuresis. In spite of the excessive calcium loss in the urine, total and ionized serum calcium remained unchanged. All subjects had significant increases in nephrogenous cyclic AMP, suggesting that parathyroid activity is elevated in subjects with furosemide-induced hypercalciuria. With furosemide, fecal calcium was significantly decreased, and resultantly, there was no significant change in the cumulative calcium balance. It is suggested that urinary calcium loss with furosemide is compensated for by secondary hyperparathyroidism via increased intestinal calcium absorption in order to maintain serum calcium at a normal level. The experimental model thus mimics the condition of the renal type of idiopathic hypercalciuria.
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PMID:Effects of oral furosemide and salt loading on parathyroid function in normal subjects. Physiological basis for renal hypercalciuria. 608 14

The case of a two month-old child admitted because of dystrophy is presented. At physical examination she presented a growth retardation (-2DS) as well as cutaneous and mucosal pallor. Metabolic acidosis, hyponatremia, hyperkaliemia and salt loss were demonstrated. Aldosterone, both plasmatic and urinary, was increased. Plasma renin activity, was also increased. In respect to renal function, hypercalciuria was found but not other abnormalities neither in the renal nor suprarrenal function were noticed. The electrolytic levels in sweat, saliva and feces were also normal. The clinical and laboratory findings were not modified with the DOCA test. Spirolactone caused an increase in salt loss. Treatment with indometacine improved both the clinical and analytical findings. On the other hand, treatment with chloride sodium (4 gr p.o. per day) also improved dramatically the disturbances. In the last 12 months she has growth up normally. At the same time, the renal loss of sodium has decreased and aldosterone, both plasmatic and urinary, is not so increased as it was at diagnosis. Finally, electrolytic parameters are fully normal.
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PMID:[Review of pseudohypoaldosteronism. Apropos of a clinical case in a 2-month-old girl]. 639 46

In hypoparathyroidism the absence of parathyroid hormone leads to a reduction in the absorption of calcium by renal tubular cells. In spite of treatment with vitamin D, hypercalciuria persists and normocalcaemia can only be maintained by providing the kidney with a large load of calcium. Thiazide diuretics enhance tubular calcium reabsorption and it has been suggested that they can be used as an alternative to vitamin D. Bendrofluazide in a dose of 10 mg daily was given to 9 patients with severe hypoparathyroidism in addition to their usual treatment with calcium and vitamin D. Following the introduction of Bendrofluazide the calculated renal threshold for calcium reabsorption (TmCa/GFR) increased by a mean value of 0.14 mmol/l, and the mean rise in serum calcium was 0.13 mmol/l. This increase was due to a direct effect of the drug and was not caused by salt restriction or changes in glomerular filtration rate. The rise in serum calcium is modest compared to the rise following the introduction of vitamin D and except for patients with mild hypoparathyroidism, thiazides are not an alternative to vitamin D. They may however reduce the oral calcium load required to maintain normocalcaemia.
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PMID:Effect of bendrofluazide on calcium reabsorption in hypoparathyroidism. 648 26

The renal handling of Ca in response to Na intake was evaluated in 12 patients with hypercalciuria and active kidney stone disease. There was no depression of urinary Ca excretion in response to the hypocalciuric effect of metolazone. Patients were hospitalized and their Ca and Na excretions measured while on a 190-mEq Na, 800-mg Ca, 1200-mg PO4- diet. These measurements were then repeated after Na intake decreased to 35 mEq/day while other variables, including diuretic dose and Ca intake, were unchanged. Two distinct responses were elicited by patients after Na restriction. In group I or the "responders" (n = 4), Ca excretion was reduced from 255 +/- 31 to 62 +/- 6 mg/24 hr. In the control group (n = 4), Ca excretion decreased from 95 +/- 8 to 57 +/- 11 mg/24 hr at similar levels of Na excretion. In group II or the "nonresponders" (n = 8), Ca excretion fell from 317 +/- 31 to 154 +/- 17 mg/24 hr when Na excretion was less than 50 mEq/24 hr. Metolazone with Na restriction normalized urine Ca excretion to the same order as in control subjects in group I. This is indicative of a mild Ca leak or a salt-sensitive leak. Despite diuretic and Na restriction most of the patients with hypercalciuria (group II) did not reabsorb Ca in a normal manner. This is indicative of a severe reabsorptive defect for Ca despite normal Na handling.
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PMID:Renal handling of sodium and calcium in hypercalciuria. 669 41

The author reports certain data from the literature and based upon his own experience. The urinary excretion of calcium is dependent upon diet and in particular sodium intake. Urinary calcium decreases when sodium intake is reduced. The administration of rapidly absorbed sugars and protein rich diets cause an increase in urinary calcium. It is thus of fundamental importance to be aware of the nature of the diet in patients in whom 24 hour urinary calcium is measured. In particular, such measurements are of no value during the immediate postoperative period. Is the existence of hypercalciuria (defined by a urinary calcium greater than 0.1 mmol/kg/day) truly responsible for an increase in the frequency of recurrences of lithiasis? In two groups of patients, one with progressive lithiasis and the other with non-progressive lithiasis, the mean urinary calcium for each of the two groups was the same. In addition, patients with a high daily calcium excretion were not necessarily those with progressive lithiasis. Three groups of patients were also compared, according to whether they had a high fluid intake, a fluid intake associated with a hydrochlorothiazide or a fluid intake associated with a neutral phosphorus salt. Phosphate therapy was a failure. In comparison with their previous state, patients receiving merely a high fluid intake or in combination with thiazides had less recurrences than before such treatment. The group treated with thiazides had significantly less recurrences than the group treated by simple high fluid intake. However urinary calcium was not lowered by thiazides. Thus the role of thiazides probably does not lie in hypocalciuria but merely in an increase in urine output.
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PMID:[Value of the measurement of urinary calcium in calcium lithiasis]. 672 72

Earlier studies have shown that an oral sodium (Na) load may induce hypercalciuria in previously normocalciuric subjects and may also increase intestinal calcium (Ca) absorption. To probe the cause of the increased intestinal Ca absorption, we simultaneously measured parathyroid function, serum 1,25-dihydroxyvitamin D [1,25-(OH)2D], and fractional intestinal 47Ca absorption before and after a salt load. Eleven normal subjects and two patients with postsurgical hypoparathyroidism were placed on a 10 meq Na, 400 mg Ca per day diet for 10 days, followed by another 10-day period in which the same diet was supplemented by 240 meq Na daily. Measurements were performed on the final 3 days of each phase. In the normal subjects, urinary Na excretion increased from 7 +/- 2 to 226 +/- 8 meq/day (mean +/- SEM), urinary Ca rose from 110 +/- 14 to 167 +/- 16 mg/day, serum parathyroid hormone (PTH) increased from 20 +/- 1 to 22 +/- 1 muleq/ml, serum 1,25-(OH)2D rose from 38 +/- 4 to 51 +/- 7 pg/ml, and fractional intestinal 47Ca absorption increased from 0.39 +/- 0.03 to 0.49 +/- 0.03 (P less than 0.05 for all changes). Serum Ca corrected for total protein did not change (9.9 +/- 0.1 to 9.8 +/- 0.1 mg/dl). The patients with hypoparathyroidism who were maintained on vitamin D therapy also showed increases in urinary Na (20 +/- 12 to 245 +/- 11 meq/day) and urinary Ca (271 +/- 48 to 305 +/- 43; P less than 0.05). However, there were no increases in serum PTH (13 +/- 1 to 11 +/- 1 muleq/ml), serum 1,25-(OH)2D (44 +/- 1 to 40 +/- 6 pg/ml), or intestinal Ca absorption (0.41 +/- 0.03 to 0.42 +/- 0.05). Corrected serum Ca decreased from 9.4 +/- 0.2 to 8.6 +/- 0.2 mg/dl. We conclude that in normal subjects, Na-induced renal hypercalciuria is accompanied by increased 1,25-(OH)2D synthesis and enhanced intestinal Ca absorption. Since this adaptive mechanism did not occur in two patients with hypoparathyroidism, mediation by PTH is suggested.
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PMID:The role of dietary sodium on renal excretion and intestinal absorption of calcium and on vitamin D metabolism. 689 38

The prevalence of kidney stones has steadily risen during this century; passage of a calculus and a positive family history increase the probability of recurrence. Findings from recent studies on the cause of renal calculi have stressed crystallization and crystal aggregation of stone minerals from supersaturated urine, rather than excessive organic matrix. Absence of normal urine inhibitors of calcium salts is also stressed. Formation of calcium oxalate stones is the major problem. Therapy with decreased calcium and oxalate intake, thiazides, phosphate salts and allopurinol in various combinations has substantially decreased the prevalence of recurrent stones. The rationale for the use of allopurinol is that uric acid salts enhance the tendency for calcium oxalate to crystallize from supersaturated urine. The hypercalciuria seen in 30 percent to 40 percent of patients with oxalate stones is usually caused by intestinal hyperabsorption of calcium. Although patients with uric acid calculi constitute only a small fraction of those in whom stones form, they represent a group in whom good medical therapy, based on sound physiologic principles, has proved extremely successful. Renal tubular syndromes lead to nephrocalcinosis and lithiasis through hypercalciuria, alkaline urine and hypocitraturia, the latter an inhibitor of calcium salt precipitation. Recent advances in surgical techniques are discussed, including the rationale for removing staghorn calculi. The ileal ureter and coagulum pyelolithotomy deserve special emphasis.
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PMID:Kidney stones. 738 35

Both salt-loading studies and reports of free-living populations find that urinary calcium excretion increases approximately 1 mmol (40 mg) for each 100 mmol (2300 mg) increase in dietary sodium in normal adults. Renal calcium stone-formers with hypercalciuria appear to have greater proportional increases in urinary calcium (approximately 2 mmol) per 100 mmol increase in salt intake. Thus, reduction of dietary NaCl may be a useful strategy to decrease the risk of forming calcium-containing kidney stones.
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PMID:Dietary salt, urinary calcium, and kidney stone risk. 766 85

A new slow-release, neutral potassium phosphate salt (UroPhos-K) has been formulated in order to minimize gastrointestinal side effects and avoid sodium-induced calciuria. It was tested in a prospective randomized, double-blind trial in a group of 21 kidney stone patients with absorptive hypercalciuria type I (AH). Twelve patients allocated to the UroPhos-K group received four tablets twice daily with breakfast and an evening snack providing 1240 mg of phosphorus and 63.5 mEq of potassium daily. Nine patients assigned to the placebo group received placebo tablets of the same appearance containing excipient only. Subjects were studied during a 3-day period in the hospital while consuming a constant metabolic diet containing 400 mg Ca, 100 mEq Na, and 800 mg P per day before and after 3 months of treatment. Treatment with UroPhos-K did not cause any significant gastrointestinal side effects; nor did it raise fasting serum K or phosphorus, or reduce hemoglobin or creatinine clearance. It was associated with a rise in urinary K from 46 +/- 7 to 98 +/- 9 mEq per day and phosphorus from 744 +/- 185 to 1535 +/- 112 mg per day (p < 0.001 each). UroPhos-K treatment reduced urinary Ca from 288 +/- 63 to 171 +/- 49 mg/day (p < 0.001), without altering oxalate excretion. It reduced the urinary saturation of calcium oxalate without altering that of brushite. Moreover, by increasing urinary excretion of inhibitors (citrate and pyrophosphate), it reduced the propensity for spontaneous nucleation of brushite (increased formation product of brushite) and inhibited crystal agglomeration of calcium oxalate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Physicochemical effects of a new slow-release potassium phosphate preparation (UroPhos-K) in absorptive hypercalciuria. 778 60


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