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

A test was developed to diagnose various forms of hypercalciuria. A two-hour urine sample after an overnight fast and a four-hour urine sample after 1 g of calcium by mouth were tested for calcium, cyclic AMP and creatinine. The 24 patients with absorptive hypercalciuria had normocalcemia and normal fasting urinary calcium (less than 0.11 mg per milligram of urinary creatnine). Urinary calcium was high (greater than or equal to 0.2 mg per milligram of creatinine) after a calcium load. Of the 28 patients with primary hyperparathyroidism (resorptive hypercalciuria), 25 had hypercalcemia and 21 had high fasting urinary calcium. Urinary cyclic AMP, elevated in 30 per cent of fasting patients, was high (greater than 4.60 mu moles per gram of creatinine) in 82 per cent of cases after calcium load. Six patients with renal hypercalciuria had normocalcemia, high fasting urinary calcium, and high (greater than 6.86 mu moles per gram of creatinine) or high-normal fasting urinary cyclic AMP was normal. This simple test should facilitate the differentiation of various causes of hypercalciuria.
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PMID:A simple test for the diagnosis of absorptive, resorptive and renal hypercalciurias. 16 60

Effects of parathyroidectomy on parathyroid function and calcium (Ca) metabolism were carefully evaluated in 6 patients with primary hyperparathyroidism without symptoms normally attributed to the disease and in 7 with bone disease or nephrolithiasis. Before parathyroidectomy, both groups of patients demonstrated evidence of the sequelae of parathyroid hormone (PTH) excess, since they presented one or more of the following features: low bone density by 125I-photon absorption, hypercalciuria (urinary Ca greater than 200 mg/day on an intake of 400 mg/day), negative Ca balance (absorbed Ca less than urinary Ca), elevated fasting urinary Ca greater than 0.2 mg/mg creatinine for a night-time sample after a 6-hour fast), and decreased renal function (creatinine clearance of less than 65 ml/min). Following parathyroidectomy, most of these deleterious effects were reversed commensurate with the return of immunoreactive serum PTH, serum Ca, and urinary cyclic AMP toward normal. These quantitative non-invasive techniques may be useful for the initial evaluation and follow-up of patients with asymptomatic primary hyperparathyroidism.
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PMID:Metabolic effects of parathyroidectomy in asymptomatic primary hyperparathyroidism. 17 69

Urine excretion of magnesium (Mg), calcium (Ca) and sodium(Na) was studied in patients with renal Ca stones having normal kidney function (n= 60), and in matched controls (n= 60), on a free diet following an overnight fasting period. In some formers, Mg was lower than in normals, whereas Ca was unusually high resulting in a significantly higher molar Ca/Mg ratio (p less than 0.001). 2. In 3 out of 4 stone groups Na excretion was significantly elevated because of reduced tubular reabsorption. In normals, fractional Na excretion varied between 0.44 and 0.54% of endogenous creatinine clearance, whereas it exceeded 1% in the stone patients. Conversely, the molar ratio Na/Ca was equal in all groups. 3. Fasting urinary cyclic AMP was comparable in both populations supporting the assumption that in the majority of patients Ca- or Mg- wasting via urine may not be responsible for secondary hyperparathyroidism. In small selected groups, losses of divalent cations may act in concert, leading to stimulation of the parathyroid glands. 4. Correlations between minerals and Na reveal a close relationship between Na, Ca and Mg in terms of clearance and excretion rate in patients and controls. Fractional Na and Ca excretion are correlated in patients but not in normals. This suggests that in the absence of phosphaturia, factors other than extracellular volume expansion and/or hyperparathyroidism are operative in stone disease. 5. The origin of fasting natriuresis and relative hypercalciuria may be ascribed to a change, as yet not causally identified, in distal tubular Na reabsorption.
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PMID:Fasting urine excretion of magnesium, calcium, and sodium in patients with renal calcium stones. 18 86

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.
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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.
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PMID:Changes in calcium excretion after prolonged metolazone therapy in recurrent stone formers. 49 17

A study of normal subjects and patients with hypercalciuria and recurrent renal stones has identified three main types of hypercalciuria: complex, absorptive and renal. Complex hypercalciuria is a combination of absorption, renal leak and resorption factors. Absorption and renal leak were examined by means of a 45Ca test. Resorption is defined as an increase of the urinary calcium:creatinine ratio while the subjects are being maintained on an intake of 400 mg of calcium per 24 h.
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PMID:Different types of hypercalciuria in patients with renal lithiasis and evidence of the calcium renal waste. 50 71

Eleven patients with kidney stone disease and idiopathic hypercalciuria (urinary calcium above 4 mg/kg/j), without phosphorus renal leak and 6 control subjects have been put for 3 days on a diet containing 1 g calcium and 1 phosphorus daily (period A), and then for 4 days on a diet containing 1 g calcium, 450 mg phosphorus and 3 g aluminium hydroxyde daily (period B). During period A, no significant difference in blood calcium, phosphorus and magnesium, not in phosphaturia, rate of phosphorus reabsorption (RPR) and ratio maximum RPR/creatinine clearance was found between the two groups. After 2 days on a low phosphate diet (period B) the blood phosphorus decreased significantly in the hypercalciuric patients but not in the control subjects, thus revealing among the forme a latent abnormality in the retention of phosphates. This abnormality could play an important role in the pathogenesis of hypercalciuria.
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PMID:[Idiopathic hypercalciuria: effects of acute phosphorus deficiency (author's transl)]. 53 14

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.
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PMID:Mechanism of lithium-induced hypercalciuria in rats. 62 44

The urinary calcium/creatinine ratio was estimated in two groups of schoolboys--village Arabs and urban Jewish (Ashkenazic) schoolboys, aged 10 to 11 years. Both the mean calcium/creatinine ratio and the frequency of hypercalciuria were higher among the Arab boys, and may be related to the higher incidence of chilidhood urolithiasis in Arab children in Israel.
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PMID:Urinary calcium excretion in schoolboys. Ethnic group differences. 66 19

We have studied a family in which nine members present hyperchloremic acidosis with normal plasma creatinine and good ability to acidify urine. Renal functions, other than bicarbonate wasting, are normal, which identifies the condition as a pure form of proximal renal tubular acidosis. The acidosis persists into adult life and appears to be inherited as an autosomal dominant trait. All affected members are asymptomatic and the only peculiar finding is a decrease in stature. No hypercalciuria was detected, and no evidence of rickets or osteomalacia was found by x-ray studies. We consider these findings characteristic of a familial trait different from that in previously reported cases of renal tubular acidosis.
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PMID:Familial proximal renal tubular acidosis. A distinct clinical entity. 88 46


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