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PubMedDate not supplied

[Inheritance and prevalence of hypercalciuria in the children from the island of La Gomera].

The urinary elimination of calcium has been studies in 549 school children from the island of La Gomera (Canary Islands) and in 100 children of a control group from the capital of the Canaries, Santa Cruz de Tenerife. The diet was not manipulated and it was proven that the water that they consumed was of characteristic equal. The 95th centile for the distribution of the calcium/creatinine index was 0.2 in the control group, we calculated the prevalence of hypercalciuria of this group (3.8%) and of the study group (16%). The prevalence was analyzed by areas of the island and it this showed that it was higher (28.4%) in those from isolated communities and therefore, with history of more inbreeding that in those with good communications (10.6%). It was observed that the risk of suffering hypercalciuria among the children that have four grand-parents who are natives of the island of La Gomera is 2.85 times higher than in those that don't have any grand-father/mother coming from the island. Hypercalciuria siblings of children with hypercalciuria found in 50%.

Adolescent↗
PubMedDate not supplied

Idiopathic external root resorption associated to hypercalciuria.

Although external root resorption (ERR) is a physiological process in deciduous dentition, it is very infrequent in permanent dentition - where the phenomenon is related to the existence of inadequate occlusal forces, periodontal pathology and microtraumatisms, etc. However, in many cases root resorption cannot be attributed to any concrete cause; such cases are defined as idiopathic external root resorption (IERR). Epidemiological studies have found that the underlying cause can only be established in 5% of all ERR. The present study describes three cases of IERR with different degrees of involvement and associated to mild calciuria and a history of nephrolithiasis. Hypercalciuria with normal blood calcium levels is usually idiopathic and exhibits a familial trait, with a prevalence of 20-40 cases per 1,000 individuals in adults. A form of hypercalciuria associated to nephrolithiasis with a mutation of the CLCN5 gene has been identified, involving low molecular weight proteinuria - though this mutation has not been uniformly demonstrated in most cases of idiopathic hypercalciuria. The peculiarity of the cases described in the present study is attributable to the coexistence of IERR with normocalcemic hypercalciuria and nephrolithiasis - thus pointing to the need for in-depth evaluation of the possible association of these three clinical situations.

Adolescent↗
PubMedDate not supplied

Bone mass loss in calcium stone disease: focus on hypercalciuria and metabolic factors.

BACKGROUND: Several authors have observed that idiopathic calcium stone formers show a bone mass reduction, which is more evident in those with idiopathic hypercalciuria. The aim of this work was the evaluation of osteopenia and osteoporosis rate in a group of idiopathic calcium stone formers. The influence of hypercalciuria, nutritional factors and anthropometric parameters on bone mass was evaluated in these patients as well. METHODS: We enrolled 196 idiopathic calcium stone formers; 102 males, and 94 females. All subjects underwent a metabolic study. BMC and BMD were evaluated as well as QUS. RESULTS: Males showed greater weight, height, BMI, densitometric values and plasma creatinine, uric acid, urea, sodium, magnesium, GFR and urinary osmolarity than females. Moreover males excreted more uric acid, urea, creatinine, sulphate, phosphate, oxalate and citrate than females. The prevalence of osteopenia and osteoporosis, according to T-score, was 54% and 14% respectively. Hypercalciuria was demonstrated in 21.7% of the patients. Hypercalciuric men showed a higher excretion of urea, phosphate, sulphate and magnesium. CONCLUSIONS: Our results confirm the importance of QUS in the evaluation of stone formers' bone mass. Anthropometric characteristics and dietary habits seem to play a role in bone loss. We did not demonstrate any influence of hypercalciuria on bone mass. Although the pathogenesis of bone loss in stone formers still remains unclear, it can be hypothesized that a slight degree of metabolic acidosis, probably of alimentary origin, may be involved in the reduction of bone mass.

Absorptiometry, Photon↗
PubMed2001

Familial hypomagnesemia--hypercalciuria and pseudotumor cerebri.

Approximately 30 patients with familial hypomagnesemia-hypercalciuria have been reported. We describe an 8-year-old girl with cardinal findings of familial hypomagnesemia-hypercalciuria (hypomagnesemia, hypermagnesiuria, hypercalciuria, renal insufficiency, hyperuricemia, elevated serum parathormone, hyposthenuria and nephrocalcinosis), who received combination therapy consisting of magnesium salts, thiazide diuretic and potassium supplementation. At the 4-year follow-up investigation under this treatment, the patient was found to have cerebral pseudotumor (increased intracranial pressure with normal or small ventricles on neuroimaging, no evidence of an intracranial mass and normal cerebrospinal fluid composition) with papilledema and visual field defects. Thiazide therapy was terminated and the cerebral pseudotumor disappeared. The authors hypothesize that cerebral pseudotumor in this patient was related to severe hypocalcemia, as a consequence of profound hypomagnesemia induced by protracted thiazide treatment. To our knowledge, this is the first report of a child with familial hypomagnesemia-hypercalciuria who developed pseudotumor cerebri after thiazide therapy.

Calcium↗
PubMed1991

[Urinary excretion of sodium and magnesium in idiopathic hypercalciuria].

We have studied urinary sodium and magnesium excretion in 30 normal subjects (15 women and 15 men, mean age 43 +/- 14 years, mean weight 74 +/- 18 Kg) and in 60 hypercalciuric stone-forming patients, 30 with renal hypercalciuria (HR) (15 women and 15 men, mean age 39 +/- 10 years, mean weight 71 +/- 16 Kg) and 30 with absorptive hypercalciuria (HA), (15 women and 15 men, mean age 41 +/- 13 years, mean weight 69 +/- 12 Kg). The diagnosis of hypercalciuria and the classification in HA and HR was made with our ambulatory study protocol. Hypercalciuria was defined by a daily calcium excretion above 300 mg (men) or 220 mg (women), and patients with fasting calcium to creatinine ratio, and calcium per 100 ml of glomerular filtrate average value above 0.11 were considered to have HR. Control subjects and hypercalciuric patients were maintained on a diet containing 1200 mg Ca, 800 mg P, 200 mg Mg and 100 mmol Na per day for a 7-day period. Two 24-hour urine samples were collected on days 6 and 7 of this diet. On the morning of day 8, following a 12-hour fast, 300 ml of distilled water was drunk and a 2-hour urine sample was collected. A blood sample was taken halfway this time. In all blood and urine samples, calcium, magnesium, sodium, phosphorus and creatinine were quantified. Creatinine clearance and calcium, sodium and magnesium per 100 ml of glomerular filtrate were calculated from these determinations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1975

Pathophysiology and therapy of hypercalciuria in patients who form recurrent stones.

There are two alternative mechanisms that might be responsible for idiopathic hypercalciuria in recurrent stone formers: increased intestinal absorption of calcium with parathyroid suppression and overflow hypercalciuria (primary intestinal hyperabsorption) or renal calcium leak with compensatory hyperparathyroidism and intestinal hyperabsorption (primary renal-tubular hypercalciuria). In this study, urinary excretion of cAMP, the intracellular effector substance synthetised under parathyroid hormone stimulation, was found to be in the normal range. This finding would argue against intestinal hyperabsorption of calcium as the primary cause of hypercalciuria.

Benzothiadiazines↗
PubMedDate not supplied

[Idiopathic hypercalciuria. Differential diagnosis].

In 50 children with hematuria or urolithiasis and idiopathic hypercalciuria, and in 15 control children, urinary calcium/creatinine concentration rates were measured after fasting and after calcium loading. Patients were classified into two groups depending on the results of an orally administered calcium loading test. Children were considered to have absorptive hypercalciuria (42%) when they had low fasting urinary calcium/creatinine concentration ratio (less than 0.21), and a large increase of this index after calcium administration (greater than 0.28). Patients were labeled as renal hypercalciuria (32%) if they had high fasting urinary calcium/creatinine concentration ratio (greater than 0.21), and variable increases of it after calcium overload. A third group of children (26%), were not classifiable by means of this test. Our data support the contention that this simple ambulatory test is very useful in the diagnostic workup of idiopathic hypercalciuria.

Calcium↗
PubMed1990

The usefulness of an oral calcium tolerance test in the choice of management of patients with idiopathic hypercalciuria.

We studied 40 patients with calcium urolithiasis and idiopathic hypercalciuria in an attempt to identify patients with an absorptive or renal type of hypercalciuria. An oral calcium tolerance test was performed in all patients, resulting in a rise in serum calcium in all cases (2.35 +/- 0.09 mmol/l vs 2.49 +/- 0.09 mmol/l; P less than 0.001). This was also true for serum phosphate (0.96 +/- 0.17 mmol/l vs 1.09 +/- 0.18 mmol/l; P less than 0.001), TmPO4/GFR (0.95 +/- 0.19 mmol/l vs 1.20 +/- 0.25 mmol/l; P less than 0.001) and fasting calcium excretion (3.14 +/- 1.16 mmol/100 l GF vs 6.17 +/- 2.02 mmol/100 l GF; P less than 0.001). All patients showed a drop in nephrogenous cAMP excretion (1.33 +/- 0.95 nmol/dl GF vs 0.74 +/- 0.72 nmol/dl GF; P less than 0.001). iPTH levels declined significantly (2.70 +/- 1.50 pmol/l vs 2.11 +/- 1.19 pmol/l; P less than 0.001). However, discordant individual changes in suppression of nephrogenous cAMP excretion, and rises in fasting calcium excretion prohibited a distinction between the absorptive or renal type of hypercalciuria. It is concluded that an oral calcium tolerance test is not helpful in the choice of management of patients with idiopathic hypercalciuria.

Administration, Oral↗
PubMedDate not supplied

[Hypercalciuria and hyperuricosuria causing hematuria in the absence of nephrolithiasis].

A prospective study was made of 38 adult patients (15 male and 23 female, age 30.5 +/- 10.8 years) with isolated hematuria of unknown etiology in which presence of hypercalciuria and/or hyperuricosuria without lithiasis was observed. Eighteen patients also referred episodes of macroscopic hematuria. Twenty-six patients had hypercalciuria (5.1 +/- 1.4 mg/kg/day), 29 hyperuricosuria (1053 +/- 198 mg/day) and 17 presented both alterations. A four months treatment was instituted with thiazides in patients with hypercalciuria and allopurinol in those with hyperuricosuria. From the first months and throughout the whole therapy, urinary excretion of calcium an uric acid became normalized in all cases. In 22 patients (57.8%) (Group I: Respondents) hematuria disappeared coinciding with normalization of calcium and uric acid values in urine and was maintained during the follow-up months. In the remaining 16 patients (Group II: Non-Respondents) the hematuria condition persisted in spite of such normalization, in most cases other causes for hematuria becoming clear later. No differences with regard to age, relationship male/female nor basal calciuria and uricosuria values were seen between both Groups. Group I had a greater incidence of macroscopic hematuria episodes (64% vs 12% in Group II, p less than 0.01) and of family nephrolithiasis (64 vs 25% in Group II, p less than 0.05). We conclude that hypercalciuria and hyperuticosuria are potentially reversible causes of hematuria in adults. Therefore, urinary determination of calcium and uric acid should be included in urinary evaluation of patients with hematuria even though they do not present renal lithiasis.

Allopurinol↗
PubMed1986

Hypercalciuria, hyperphosphaturia, and growth retardation in children with diabetes mellitus.

The role of hypercalciuria and hyperphosphaturia in the growth retardation of children with diabetes mellitus was investigated in 157 children with diabetes whose mean height was less than that of 37 nondiabetic siblings of similar age (P less than .025). Hyperglycemia, hypercalciuria, and hyperphosphaturia were assessed coincident with the height measurement of each child in a cross-sectional survey. The distribution of height percentiles of the children with diabetes was skewed to the left with 61% at or below the 50th percentile. Eleven percent of the insulin-dependent children with diabetes mellitus were shorter than would be anticipated by a normal distribution of the 157 children. The duration of diabetes (hyperglycemia) had the greatest influence upon the children's height. Children with diabetes were shorter than the nondiabetic subjects by the fourth year of hyperglycemia, and this difference in height became statistically significant after 7 years or more of diabetes. The degree of hypercalciuria and hyperphosphaturia was more closely associated with reduced height in children with diabetes than was the degree of hyperglycemia, although the renal wastage of calcium and phosphorus seemed to be the result of glucosuria. Because hypercalciuria and hyperphosphaturia impair growth in nondiabetic children, they may also play an important role in the poor growth of children with diabetes mellitus.

Adolescent↗
PubMed1986

Pathogenesis of hypercalciuria in spontaneously hypertensive rats.

The etiology of hypercalciuria remains unknown in spontaneously hypertensive rats (SHR). In order to differentiate absorptive versus renal hypercalciuria, serial measurements of urinary calcium (UCaV) excretion were made weekly under fasting (3-hour urine collection) and after oral administration of CaCl2 (50 mg/100 g; 4-hour urine collection) from age 8 to 14 weeks in SHR (n = 14) and normotensive Wistar Kyoto rats (WKY; n = 14). Fasting UCaV was significantly greater in WKY than in SHR throughout the periods of observation. In contrast, after oral Ca loading UCaV was greater in SHR after 13 weeks of age (13 weeks: SHR UCaV = 954 micrograms/mg creatinine, WKY UCaV = 541 p less than 0.01; 14 weeks: SHR UCaV = 988 micrograms/mg creatinine, WKY UCaV = 534, p less than 0.01). Fasting urinary cyclic adenosine monophosphate (AMP) excretion was not different between WKY and SHR. However, cyclic AMP excretion of SHR, but not WKY, was decreased after calcium loading when compared to the fasting values. The cyclic AMP was also significantly lower in SHR than in WKY rats after calcium loading. Calcium handling by the kidney was not different between SHR and WKY with or without parathyroidectomy. Calcium disposition kinetic studies were performed on these animals at age 15 and 16 weeks. No significant difference of intravenous 45Ca was observed between WKY (n = 6) and SHR (n = 6) in total plasma clearance, nonrenal clearance, biologic half-life, and elimination rate constant from the central compartment. However, the WKY had a significantly greater renal clearance of 45Ca than the SHR (0.48 +/- 0.04 vs. 0.24 +/- 0.02 ml/n, p less than 0.001). Since tissue disposition of intravenous 45Ca was not different between WKY and SHR, the increased renal excretion of calcium after oral administration in SHR, therefore, reflects increased intestinal absorption of calcium. Correction of established hypertension did not abolish the hypercalciuria. We believe that increased gastrointestinal absorption of calcium is responsible for the hypercalciuria in SHR.

Administration, Oral↗
PubMed1984

Relationship of hypercalciuria to diet and bladder stone formation in spinal cord injury patients.

We have investigated the effectiveness of a low calcium diet, low sodium diet, and hydrochlorthiazide to reduce urinary calcium excretion in ten spinal cord injured patients during the early phase of their rehabilitation. Five patients were given the regular hospital diet and low calcium diet (300 mg calcium/day diet) on a randomized cross-over design. The other five patients were given four treatment modalities: a. regular diet, b. low calcium diet, c. low sodium diet (2 gm sodium/day diet), d. low calcium diet plus hydrochlorthiazide 25 mg twice a day according to a cross-over randomized block design. Each treatment regimen lasted two weeks and 24-hour urinary calcium concentrations were determined weekly. The result indicated that low calcium diet, low sodium diet or low calcium diet plus hydrochlorthiazide reduced hypercalciuria significantly (P less than 0.01). Low calcium diet combined with hydrochlorthiazide was the most effective treatment for hypercalciuria. In retrospective studies, we found that recently injured patients developed hypercalciuria, however, there was no significant difference in the incidence of bladder stone formation in patients with hypercalciuria compared with those with normal urinary calcium excretion.

Adult↗
PubMed1983

Hypercalciuria in a child with primary Fanconi syndrome and hearing loss.

A hitherto undescribed association of sensorineural hearing loss and Fanconi syndrome (FS) is reported in a 10 year old black male. The patient presented with growth failure developing at the age of 6 and rachitic changes were detected the following year. No known cause for FS was identified, and renal biopsy was within normal limits. Distal tubular acidification and the threshold for proximal tubular bicarbonate reabsorption were normal, as was urine concentrating capacity. He was found to have significant hypercalciuria (urine calcium excretion 10 mg/kg/day) despite dietary calcium restriction, and urine calcium excretion increased further following an oral calcium load. Dietary sodium restriction to 16 mEq/kg/day resulted in a fall in urine calcium loss, which remained elevated at 6 mg/kg/day. Serum parathyroid hormone and 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) concentrations were in the normal range. Treatment with neutral phosphate dietary supplementation resulted in partial healing of rickets and normal growth rate. Hypercalciuria resolved during phosphate administration (urine calcium excretion 3 mg/kg/day) without a fall in urine sodium excretion. It is concluded that in this patient with FS, hyperphosphaturia resulted in phosphate depletion and secondary hypercalciuria. A similar mechanism of hypercalciuria may be operative in a variety of renal tubular disorders affecting children and adults.

Calcium↗
PubMed1980

Effect of thiazides on the hypercalciuria of phosphate depletion.

The present investigation was carried out to examine the effect of thiazides on the hypercalciuria of phosphate depletion. Studies were done on 160 to 190 gm male rats, utilizing metabolic balance techniques. Animals were assigned to a phosphate-deficient diet and divided into a vehicle and thiazide-treated group. Both groups raised on a phosphate-deficient diet developed hypophosphatemia, hypercalciuria, and hypercalcemia; the latter was significantly greater in the thiazide-treated group. The magnitude of the hypercalciuria was significantly smaller in the thiazide-treated group. This occurred despite a significantly greater elevation in the concentration of serum calcium and its filtered load in the rats treated with the diuretic. Thiazides failed to produce natriuresis in the phosphate-deficient rats, suggesting a possible tubular resistance to the natriuretic action of the drug in phosphate depletion. Our data demonstrate that thiazide administration blunts the hypercalciuria of phosphate depletion. The results are consistent with the postulates that (1) phosphate depletion suppresses tubular calcium reabsorption at a site proximal to the segment where thiazides enhance calcium transport or (2) thiazide enhances calcium reabsorption at a terminal site in the nephron where a decrease in calcium transport may occur during phosphate depletion.

Animals↗
PubMed1993

The tale of parathyroid function in idiopathic hypercalciuria.

At the origin, idiopathic hypercalciuria has been described as a syndrome consisting of normocalcemia, low plasma phosphate levels and abnormally high urinary calcium excretion. The cause of this syndrome was subject to many investigations throughout the years. Two main pathophysiologic hypotheses have been proposed: a) primary intestinal hyperabsorption of calcium, leading to depression of parathyroid hormone (PTH) secretion ("absorptive" hypercalciuria); and b) primary renal tubular leak of calcium which stimulates PTH secretion (secondary hyperparathyroidism). Most of the published studies indicate that intestinal hyperabsorption of calcium with subsequent relative hypoparathyroidism is the primary event causing idiopathic hypercalciuria, and that this occurs as a consequence of increased production of 1,25(OH)2-vitamin D3 (calcitriol). Fasting hypercalciuria, originally taken as evidence for a "renal leak" of calcium, appears to be, at least in part, the consequence of relative hypoparathyroidism.

Calcitriol↗
PubMed1996

Renal and absorptive hypercalciuria: a metabolic disturbance with varying and interchanging modes of expression.

BACKGROUND: In previous studies, the oral calcium loading and deprivation test has been used to distinguish between children with renal (fasting) hypercalciuria (RH) and absorptive hypercalciuria (AH). OBJECTIVE: We evaluated the long-term clinical course of 30 children with idiopathic hypercalciuria and investigated the influence of urinary sodium excretion, as a reflection of its intake, on urinary calcium excretion. METHODS: Thirty normocalcemic, normophosphatemic children (21 boys and 9 girls) with urinary calcium to creatinine ratios greater than 0.57 mmol/L/mmol/L ( > 0.21 mg/dL/mg/dL on the three consecutive examinations participated in this study. They were divided according to their responses to calcium deprivation and loading into AH (16 patients) and RH (14 patients). RESULTS: When restudied 3 to 7 years later, 6 of the 16 children with AH were normocalciuric and three demonstrated characteristics compatible with RH. The remaining seven patients maintained their initial AH pattern. Of the 14 children with RH, four were normocalciuric and four demonstrated AH. The remaining six children maintained their initial RH pattern. A significant positive correlation was observed between urine sodium and calcium excretion in children with AH or RH. Children who were normocalciuric at the second study had significantly lower values of urine sodium excretion when compared with those in whom hypercalciuria persisted. CONCLUSIONS: We suggest that AH and RH constitute a continuum. The change in characteristics observed during the second study suggests that any attempt to divide these patients into two physiologically distinct subtypes may be artificial. The main factor influencing urinary excretion of calcium in our patients seemed to be sodium intake.

Absorption↗
PubMed1995

[Pollakiuria and idiopathic hypercalciuria in childhood].

OBJECTIVE: To determine the incidence of pollakiuria in children with idiopathic hypercalciuria. METHODS: The clinical records of 56 children with idiopathic hypercalciuria were reviewed. In addition to pollakiuria, they were evaluated for other associated disorders, maximum urinary osmolality, urodynamic study and overall clinical course. RESULTS: Nine children (16%), 4 boys and 5 girls, presented with pollakiuria associated with urgency, nocturnal enuresis, hematuria and urinary incontinence. Two showed normal urodynamic studies and unstable bladder was observed in another case. All but one patient preserved normal renal concentration capacity. The course of the micturition symptoms was satisfactory and only three cases required pharmacological treatment. CONCLUSIONS: In the absence of urinary infection, pollakiuria might suggest the presence of hypercalciuria, a condition that can be managed successfully following correct diagnosis and treatment. Renal concentration capacity is not reduced by hypercalciuria.

Calcium↗
PubMed1998

Hypercalciuria and hematuria in juvenile rheumatoid arthritis.

OBJECTIVE: To investigate the frequency of hypercalciuria and the relationship between hypercalciuria and hematuria in patients with juvenile rheumatoid arthritis (JRA). METHODS: Twenty-eight children with JRA were studied, as well as 10 patients with acute arthritis unrelated to JRA and 14 healthy children as control groups. Cases with urinary calcium excretion (UCE) >4 mg/kg/day were considered hypercalciuric. Urinalysis was performed for detecting hematuria in all cases. RESULTS: UCE was 4.19 +/- 2.9 mg/kg/day in patients with JRA, 1.94 +/- 1.57 mg/kg/day in children with acute arthritis, and 2.0 +/- 1.45 mg/kg/day in healthy children. UCE was significantly higher in JRA compared with the other study groups. Of the 28 patients with JRA, 13 (46.4%) had hypercalciuria and 6 (21.4%) had hematuria. UCE was significantly higher in hematuric patients with JRA than in those with no hematuria (p<0.05). UCE in patients with JRA without hematuria was also higher than the UCE values detected in the disease and healthy control groups (p<0.05). CONCLUSION: Hypercalciuria is a frequent finding in patients with JRA [13/28 (46.4%)] and should be considered during the investigation of hematuria in patients with JRA.

Adolescent↗