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PubMed1989

Renal hypercalciuria and acidification defect in kidney stone patients.

Calcium metabolism and renal acidification ability were examined in renal stone patients. On a random diet 33 of 52 patients excreted more than 4 mg. per kg. body weight per day of urinary calcium and were entered into a second study on a 300 mg. calcium diet. Absorptive and renal hypercalciuria was differentiated by fasting urinary calcium (mg. per 100 ml. glomerular filtration). Every absorptive hypercalciuria patient tested and 5 renal hypercalciuria patients had a normal renal acidification ability, and the serum parathyroid hormone and urinary cyclic adenosine monophosphate levels were normal. By calcium restriction urinary calcium decreased more in absorptive hypercalciuria than in renal hypercalciuria (2.48 +/- 0.14 versus 3.34 +/- 0.27 mg. per kg. body weight per day, p less than 0.05). However, urinary calcium remained high in 76 per cent of the patients with absorptive hypercalciuria. Nine patients had a defect in renal tubular acidification and the calcium metabolism was similar to those with renal hypercalciuria. Present studies show that renal hypercalciuria and renal tubular acidification defect cannot be differentiated without an ammonium chloride test.

Acidosis, Renal Tubular↗
PubMed1990

Idiopathic hypercalciuria: association with isolated hematuria and risk for urolithiasis in children. The Southwest Pediatric Nephrology Study Group.

A prospective multicenter study was designed to determine the frequency and prognostic importance of hypercalciuria in children with hematuria. Urinary calcium excretion was examined in 215 patients with unexplained isolated hematuria (no proteinuria, urolithiasis, infection or systemic disorder). Hypercalciuria (urinary calcium excretion greater than 4 mg/kg/day) was identified in 76 patients (35%). Compared to patients with normal urinary calcium excretion, children with hematuria and hypercalciuria were characterized by male preponderance, white race, family history of urolithiasis, gross hematuria and calcium oxalate crystals. Renal biopsies were performed in 10 patients with urinary calcium excretion 0.4 to 2.5 mg/kg/day; three had IgA glomerulonephritis, three had glomerular basement membrane thinning, one had proliferative glomerulonephritis and three were normal. Renal biopsies in three patients with hypercalciuria showed focal segmental glomerulosclerosis, hereditary nephritis or no abnormalities. Oral calcium loading tests showed renal hypercalciuria in 26 patients, absorptive hypercalciuria in 15 patients and were not diagnostic in 35 patients. Serum parathyroid hormone, bicarbonate and phosphorus and urinary cyclic adenosine monophosphate concentrations were similar in the three groups of hypercalciuric patients. Urinary calcium excretion after one week of dietary calcium restriction was higher (5.8 mg/kg/day) in renal hypercalciuria than in other hypercalciuric patients (3.4 mg/kg/day), P less than 0.01. One to four years follow-up was available for 184 patients. Eight of 60 hypercalciuric patients developed urolithiasis or renal colic compared to 2 of 124 patients with normal urinary calcium excretion (P less than 0.001). Hypercalciuria is commonly associated with isolated hematuria and represents a risk factor for future urolithiasis in children with hematuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Hypercalciuria in children with hematuria.

Urinary calcium excretion was assessed in 83 consecutive children with gross or microscopic hematuria in whom the presence of proteinuria or urinary-tract infection had been excluded. Twenty-three children had hypercalciuria. Clinical features that were more commonly associated with hypercalciuria included gross hematuria and a family history of urolithiasis. No clinical or pathological basis for the hematuria was determined in 22 of the 23 children with hypercalciuria or in 38 of the 60 children with normal calcium excretion. Urolithiasis developed in two children with hypercalciuria during the period of study. Oral calcium-loading tests were performed in all 23 children with hypercalciuria. Absorptive hypercalciuria was demonstrated in 10 children, whereas 13 had renal (fasting) hypercalciuria. Hematuria resolved during anticalciuric therapy in 20 of the 23 patients with hypercalciuria. We conclude that determination of urinary calcium excretion is warranted in the routine evaluation of children with hematuria.

Adolescent↗
PubMed1987

"Idiopathic" hypercalciuria and hereditary hypophosphatemic rickets. Two phenotypical expressions of a common genetic defect.

Among 59 closely related members of one Bedouin tribe, we identified 9 who had the characteristic features of hereditary hypophosphatemic rickets with hypercalciuria (HHRH). We found "idiopathic" hypercalciuria in 21 of the 50 asymptomatic members. The biochemical abnormalities observed in these 21 subjects were qualitatively similar to those in the 9 with HHRH, but were quantitatively milder. The urinary calcium concentration was 0.43 +/- 0.14 mg per milligram of creatinine (mean +/- SD) in the patients with HHRH, 0.34 +/- 0.07 in the subjects with idiopathic hypercalciuria, and 0.14 +/- 0.05 in normal subjects from the same tribe. Tubular reabsorption of phosphorus and serum phosphorus concentrations were 3.0 and 4.3 SD units below the age-related mean, respectively, in HHRH, and 1.1 SD units below the normal mean for both variables in idiopathic hypercalciuria. Mean serum levels of 1,25-dihydroxyvitamin D (1,25-(OH)2D) were 303 pg per milliliter in HHRH and 145 pg per milliliter in idiopathic hypercalciuria (upper normal limit, 110). We conclude that the subjects with hypercalciuria and the patients with HHRH shared a hereditary renal phosphate leak that led to hypophosphatemia, elevated serum concentrations of 1,25-(OH)2D, increased intestinal calcium absorption, and hypercalciuria. The magnitude of the hypophosphatemia, which regulates 1,25-(OH)2D levels, appears to determine which subjects will have hypercalciuria alone and which will also have bone disease.

Adolescent↗
PubMed1988

The diagnosis of hypercalciuria in children.

Calcium loading tests were performed in 21 children with hypercalciuria, haematuria and/or nephrolithiasis and 10 control subjects. Comparisons of 24-h calcium excretion before and after loading were evaluated rather than fasting urinary calcium to urinary creatinine ratio. The differences in calcium excretion before and after loading clearly distinguished absorptive from renal hypercalciuria. A difference higher than 0.035 mmol/kg indicated absorptive hypercalciuria in 6 of 21 patients, whereas in the remaining 15 much lower differences indicated renal hypercalciuria. Resorptive hypercalciuria caused by low serum values of 25-hydroxyvitamin D was considered in 6 of the 15 patients with renal hypercalciuria. These patients had low values of phosphate reabsorption (TmP/GFR) and could be clearly separated by high values of calcium reabsorption (TmCa/GFR), in contrast to patients with renal hypercalciuria who had normal values of TmP/GFR and low values of TmCa/GFR. The correct treatment and prevention of nephrolithiasis caused by hypercalciuria in children should be based on accurate diagnosis; this can be achieved by using the calcium loading test described in this report.

Calcifediol↗
PubMed1988

Osteocalcin, parathormone and hypercalciuria.

Osteocalcin synthesis is dependent on the influence of the renal vitamin D metabolite, 1,25(OH)2D3. This metabolite is an etiological factor in some hypercalciurias, and osteocalcin may thus be a parameter for discovering them. In turn, parathormone, which stimulates 1,25(OH)2D3 synthesis, is also implicated in the hypercalciurias. Mean molecular parathormone, osteocalcin, 24-hour calciuria and the calcium/creatinine and hydroxyproline/creatinine ratios were determined in urine samples obtained after a 12-hour fast from 18 patients with absorptive hypercalciuria and 11 patients with renal hypercalciuria out of a total of 62 patients with renal lithiasis. No changes were observed in osteocalcin or parathormone, indicating that neither is valid for the diagnosis of hypercalciuria. Significant differences were only found in the Ca/Cr ratio (p less than 0.001), which was higher (0.31 +/- 0.07 vs. 0.13 +/- 0.04 mg/mg) in renal hypercalciuria than in absorptive hypercalciuria. No changes in osteocalcin have been reported in the hypercalciurias, but variations in parathormone have been reported, therefore requiring further study and thought to understand the processes involved.

Adult↗
PubMedDate not supplied

Hypercalciuria and nephrocalcinosis in cystic fibrosis patients.

The objective of this study was to determine the frequency of nephrocalcinosis and hypercalciuria in cystic fibrosis (CF) patients, and to search possible causes of this phenomenon. Forty-three CF children (24 boys, 19 girls; mean age 64.9 months, range 5 months-18 years) were included in this study. Plasma sodium, potassium, chloride, BUN, creatinine, calcium, phosphorus, magnesium, alkaline phosphatase; spot urine sodium, potassium, chloride, creatinine, calcium, magnesium; and serum 25-hydroxyvitamin-D levels were measured in all patients. Urine samples were examined for microscopic hematuria. Fractional sodium, potassium, chloride excretion and estimated glomerular filtration rate (GFR) were calculated. All patients underwent renal ultrasonography. Hypercalciuria, nephrocalcinosis and microscopic hematuria were detected in 15 patients (34.2%), 10 patients (23.2%) and two patients (5%), respectively. There was no significant but borderline correlation between 25-hydroxyvitamin-D levels and hypercalciuria (r: 0.308, p:0.05). There were no correlations between Shwachman clinical scoring system results and hypercalciuria (r: 0.221, p: 0.148) and age and hypercalciuria (r: -0.229, p: 0.135). Patients with chronic Pseudomonas colonization showed no hypercalciuria or nephrocalcinosis. There was no difference for plasma biochemical results, renal function tests, hypercalciuria and nephrocalcinosis between CF patients who had or had not experienced pseudo Bartter's syndrome (PBS) before. There was no relation between detected CF mutations of the patients and hypercalciuria and nephrocalcinosis. These results suggested that it is a primary abnormality of calcium metabolism in the kidney.

Adolescent↗
PubMedDate not supplied

Renal function in children with hypercalciuria.

Hypercalciuria is a common problem causing symptoms such as abdominal pain, hematuria and enuresis, and leading to stone formation. It results from a renal tubular calcium "leak" or intestinal hyper-reabsorption of calcium. This study was performed to determine whether renal functional impairment was present in children with hypercalciuria. The study group comprised 298 children who were screened for hypercalciuria by means of urinary calcium/creatinine (UCa/UCr) ratio. The renal functions of 18 children (6.4%) detected as having hypercalciuria with Ca/Cr ratios of greater than 0.18 in their spot urines were evaluated. Results were compared with those of the healthy control group. The rate of hypercalciuria did not very significantly between the boys and girls (p > 0.05). The mean value of daily calcium excretion was 6.42 + 3.93 mg/kg/day in the children with hypercalciuria, which was significantly different from that of the control group (p < 0.01). When the values of creatinine, osmolar and free water clearances, fractional excretion of sodium and tubular reabsorption of phosphorus were compared between the patient and control groups, the difference was not significant (p > 0.05). Urinary N-acetyl-beta-D-glucosaminidase (NAG) excretion, which was described as the creatinine ratio, was significantly higher in the children with hypercalciuria. These findings suggest that in the presence of normal renal functional studies in children with hypercalciuria, tubular injury can be detected by NAG, which is a more sensitive marker of renal tubular injury.

Acetylglucosaminidase↗
PubMed1984

Idiopathic hypercalciuria. Renal and absorptive subtypes in children.

Twelve children with urolithiasis or unexplained episodes of gross hematuria, hypercalciuria, and normal serum calcium levels were examined with an oral calcium loading test. Eight patients displayed elevated fasting urinary calcium excretion, consistent with renal hypercalciuria; four exhibited normal fasting calcium excretion, which increased excessively with calcium loading, suggesting hyperabsorption of intestinal calcium. Evidence of secondary hyperparathyroidism was detected in three children with renal hypercalciuria on the basis of urinary cyclic adenosine monophosphate (cAMP) excretion. Serum calcium concentrations obtained four hours after loading increased significantly in children with renal hypercalciuria and were directly correlated with fasting urinary calcium excretion. Among patients with renal hypercalciuria, serum calcium level was higher in patients with normal fasting cAMP excretion. These results suggest that hyperabsorption of intestinal calcium occurs in renal hypercalciuria and may account for the lower-than-predicted incidence of secondary hyperparathyroidism in these patients. Idiopathic hypercalciuria may arise from one fundamental metabolic disturbance with varying degrees of expression, rather than from two separate pathogenic mechanisms.

Adolescent↗
PubMed1991

Hypercalciuria in children severely affected with osteogenesis imperfecta.

To investigate our impression that hypercalciuria is relatively common in children with osteogenesis imperfecta, we performed a retrospective study of data accumulated from our pediatric population with this skeletal disorder. Children with osteogenesis imperfecta (17 girls, 30 boys; mean (+/- SD) age 7.8 +/- 4.6 years; range 0.7 to 16.8 years) had undergone detailed inpatient evaluation of mineral homeostasis during periods of clinical stability and controlled dietary calcium intake. Hypercalciuria was found in 36% of the patients and averaged (+/- SEM) 6.1 +/- 0.3 mg/kg per 24 hours (0.15 +/- 0.01 mmol/kg per 24 hours) or 392 +/- 28 mg/gm of creatinine (1.10 +/- 0.07 mmol calcium/mmol creatinine) in the group with hypercalciuria. There were no statistically significant differences in age, gender, or dietary calcium intake (per kilogram of body weight) between the normocalciuric and hypercalciuric children. However, the group with hypercalciuria was shorter than the normocalciuric group and had a greater lifelong fracture rate. When patient height z scores were regressed against urinary calcium levels, a significant negative correlation was found in the group with hypercalciuria (r = -0.76; p less than 0.001). Although serum alkaline phosphatase activity was lower in the group with hypercalciuria, no difference was found between groups with regard to serum levels of calcium, phosphate, magnesium, creatinine, immunoreactive parathyroid hormone, or osteocalcin. The groups were also similar with respect to both their total body mineral density, as determined by dual-photon absorptiometry (n = 17), and their static indexes of bone formation and resorption, as assessed histomorphometrically with iliac crest specimens (n = 19). We conclude that hypercalciuria occurs frequently in children with osteogenesis imperfecta, and that its magnitude appears to reflect the severity of the skeletal disease.

Adolescent↗
PubMed1987

Idiopathic hypercalciuria in children: pathophysiologic considerations of renal and absorptive subtypes.

Sixteen children with idiopathic hypercalciuria and seven control children were observed. Patients were classified into two groups by means of an orally administered calcium loading test. Individuals with renal hypercalciuria (five children) had a high fasting urinary calcium/creatinine concentration ratio (0.27 +/- 0.05), a mild increase of this value after calcium administration (0.29 +/- 0.07, P less than 0.05), and elevated mean serum parathyroid hormone (PTH) concentrations (0.95 +/- 1.14 ng/ml). Patients with absorptive hypercalciuria (11 children) had fasting urinary calcium/creatinine concentration ratio of 0.11 +/- 0.04, a large increase of this index after calcium loading (0.25 +/- 0.06, P less than 0.0005), and normal levels of serum PTH (0.29 +/- 0.10 ng/ml). Next, we examined the effects of two different calcium intakes on urinary calcium excretion, serum calcium, PTH, and 1,25-dihydroxyvitamin D3 concentrations. In patients with absorptive hypercalciuria, the increased calcium intake resulted in significant increments of calciuria (P less than 0.0005), mild elevation of serum calcium concentration (P less than 0.05), and reduction of serum 1,25-dihydroxyvitamin D3 concentrations (P less than 0.005). By contrast, these values were not modified in children with renal hypercalciuria. Serum PTH did not change within each group. After dietary calcium supplementation, serum ratios of 1,25-dihydroxyvitamin D3 to calcium, phosphate, and PTH concentrations decreased significantly only in the group of children with absorptive hypercalciuria. Our data support the contention that 1,25-dihydroxyvitamin D3 metabolism is different in the two groups of patients with hypercalciuria.

Absorption↗
PubMed2003

Enuresis subtypes based on nocturnal hypercalciuria: a multicenter study.

PURPOSE: Desmopressin may not be effective for nocturnal enuresis associated with polyuria and hypercalciuria. Nighttime hypercalciuria in an enuretic population from 5 centers and its correlation with nighttime polyuria were verified. MATERIALS AND METHODS: A total of 450 enuretic patients (278 males, 172 females, mean age 9.7 years) were evaluated with 72-hour micturition charts, urinalysis, serum creatinine and osmolarity, diurnal and nocturnal electrolytes with fractional Na+ and K+ urinary excretion, and nocturnal (4 a.m.) plasma vasopressin. Creatinine electrolytes and osmolarity were measured in daytime (8 a.m. to 8 p.m.) and nighttime (8 p.m. to 8 a.m.) urine volumes. Patients were divided into group 1 with nocturnal polyuria and group 2 without nocturnal polyuria. Hypercalciuria was defined as urinary calcium-to-urinary creatinine ratio greater than 0.21. Statistic evaluation was performed using chi-square, Pearson correlation and ANOVA tests. RESULTS: Nighttime polyuria was demonstrated in 292 bedwetters (65% group 1). Nocturnal hypercalciuria was present in 179 of the 450 children (39.7%), including 125 in group 1 (42.8%) and 54 in group 2 (34.2%), which was statistically significant (chi-square p = 0.008, Pearson correlation test r = 0.157). Daytime calciuria was not statistically modified in either group (group 1 p = 0.054, group 2 p = 0.56). Adrenocorticotropic hormone (ADH) was normal in 18.5% and low in 81.5% of enuretics with nocturnal hypercalciuria. ADH levels and nocturnal hypercalciuria significantly correlated (p = 0.003, r = 0.148). Conversely, the group 2 patients had normal ADH levels. CONCLUSIONS: Nocturnal hypercalciuria has a pivotal role in nocturnal enuresis, as it is significantly associated with low ADH levels and nocturnal polyuria. A new classification of nocturnal enuresis subtypes based on nighttime calciuria levels is mandatory to address treatment properly.

Adolescent↗
PubMed2002

Low prevalence of hypercalciuria in Japanese children.

BACKGROUND/AIM: There are several factors, such as race, age, sex, and geographical variations, associated with renal stone formation. Although it is known that the prevalence of urolithiasis in Japanese children is low, the reason remains obscure. We hypothesize that the low prevalence of urolithiasis is associated with the urinary calcium excretion. The aim of our study was to investigate the prevalence of hypercalciuria in Japanese children. METHODS: This investigation is a population-based school survey. A group of 529 healthy Japanese children was screened for hypercalciuria by measurement of the urinary Ca/Cr ratio using the morning fasting urine. In addition, the urinary Na/Cr ratio was also calculated for each subject. RESULTS: Hypercalciuria regarded as an urinary Ca/Cr value of more than 0.17 was noted only in 3 out of 529 children (0.6 %), while most cases (494/529, 93.4%) demonstrated hypocalciuria (urinary Ca/Cr <0.05). The mean urinary Ca/Cr value was 0.024 in all subjects combined. Linear regression analysis revealed a positive direct correlation between urinary Ca/Cr and Na/Cr values (rs = 0.14, p < 0.01). The urinary Ca/Cr ratio was not related to age in either sex. CONCLUSIONS: The present study demonstrates that the prevalence of hypercalciuria in Japanese children is low as compared with other countries, even though absorptive hypercalciuria and dietary hypercalciuria might be missed in this setting. This low prevalence of hypercalciuria may be associated with the lower prevalence of urolithiasis in Japanese children. As it is suggested that a low dietary intake of calcium and sodium may play some role in the low urinary calcium excretion, a randomized, controlled study comparing the efficacy of different modes of therapy, such as a low-calcium diet and/or a low-salt diet, might provide valuable information for the prevention of urolithiasis.

Calcium↗
PubMed1973

Evidence for secondary hyperparathyroidism in idiopathic hypercalciuria.

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.

Calcium↗
PubMed1978

The use of a test for the differential diagnosis of hypercalciuria.

28 renal stone formers (18 men and 10 women) with idiopathic hypercalciuria (IH) and 27 controls have been subjected to a test proposed for the diagnosis of absorptive, resorptive and renal hypercalciurias. Fasting serum calcium concentration, urinary calcium and cyclic AMP excretion were measured after overnight fasting and an oral load of calcium. Absorptive hypercalciuria was demonstrated in 14 patients. High fasting urinary calcium first suggested resorptive or renal hypercalciurias in 5 other patients, but since fasting urinary calcium was normalized following cellulose phosphate therapy, absorptive hypercalciuria was more likely. Renal hypercalciuria was a possibility in 1 single case. Both fasting and post-load urinary calcium were normal in 7 men and 1 woman. The test did not appear as useful as expected since it was of no diagnostic value in about 30% of the cases and erroneously suggested resorptive or renal hypercalciuria in about 15% of the cases. On the other hand it indicated that absorptive IH is common and renal IH exceptional.

Adult↗
PubMedDate not supplied

Idiopathic hypercalciuria: effects of calcium load test on magnesiuria.

Twenty-three children with idiopathic hypercalciuria and 7 control children were studied. Patients were classified into three groups according to the response to an oral calcium load. Five children displayed absorptive hypercalciuria (UCa/Cr 0.14 +/- 0.04 mg/mg with poor calcium diet and 0.33 +/- 0.16 after loading, p less than 0.01); 10 were classified renal hypercalciuria (UCa/Cr during the fasting state of 0.28 +/- 0.09 and 0.31 +/- 0.11 after loading) and 8 were classified as alimentary hypercalciuria (UCa/Cr 0.14 +/- 0.07 during the fasting state and 0.15 +/- 0.04 after loading). The urinary cAMP showed no significant differences in any of the three groups compared to the control. Magnesiuria did not show significant differences between the two forms of hypercalciuria and the control; a significant increase was observed after the loading and a positive correlation between magnesiuria and calciuria in the absorptive form. Our study supports the validity of the test for the classification of the different forms of hypercalciuria in children. The urinary cAMP is not a valid approach for classification. The difference observed in the magnesiuria suggests a different pathogenic mechanism between the two types of idiopathic hypercalciuria.

Administration, Oral↗
PubMed1988

[So-called "renal" idiopathic hypercalciuria most often has a dietary origin].

Among renal stone formers with idiopathic hypercalciuria, patients who remain hypercalciuric despite low calcium intake have often been regarded as having a primary renal leak of calcium, i.e. renal hypercalciuria. However, at any given intake of calcium, dietary factors other than calcium can generate hypercalciuria, e.g. high intakes of sodium, of animal protein or of carbohydrates, or obesity itself. Thus, the incidence of renal hypercalciuria among stone formers has probably been overestimated. To address this issue, the aforementioned dietary and/or metabolic factors have been evaluated in 51 stone formers with idiopathic hypercalciuria refractory (i.e. U-Ca. V greater than 250 mg/24 h) to 5 days on low calcium intake (max. 400 mg/day). In 15 patients (all had U-Na. V greater than 200 mmol/24 h), U-Ca.V was within the 95% confidence limits of a nomogram U-Ca.V versus U-Na.V, suggesting that their idiopathic hypercalciuria was related, at least in part, to the high sodium intake. 7 patients had severe hyperuricosuria (greater than 1 g/24 h) suggesting high animal protein intake. 20 patients were obese (greater than 120% ideal weight) with (7 cases) or without (13 cases) concomitant fasting hyperinsulinemia (greater than 18 microU/ml). In addition, a careful retrospective analysis of intravenous pyelograms disclosed medullary sponge kidneys in 8 cases which had remained undiagnosed so far; in one of them histological confirmation was obtained after surgical removal of a renal pole and a radiologico-histological comparison. Thus, only 14 out of 51 patients had an otherwise unexplained idiopathic hypercalciuria on low calcium intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed1983

Assessment of the calcium loading test in differentiating between various forms of idiopathic hypercalciuria.

The oral calcium loading test for the differential diagnosis of the various forms of idiopathic hypercalciuria has raised much interest, since it might provide the basis for a selective, optimal treatment of the different hypercalciuric states. We have assessed the ability of this test to differentiate between the two major forms of idiopathic hypercalciuria: renal and absorptive hypercalciuria. The test was performed in 32 idiopathic hypercalciuria patients. Based on generally accepted criteria that have been established according to the results of calcium and cAMP measurements in plasma and urine, 31% of the patients could be classified as having renal hypercalciuria and 13% as having absorptive hypercalciuria, whereas the remaining 56% did not fit either of these categories. In view of the expense and logistics involved in performing the test, the finding of an approximately 50% efficacy rate in distinguishing between the forms of idiopathic hypercalciuria raises serious doubts regarding the value of its routine implementation.

Adult↗