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PubMed1978

An exaggerated augmentation of renal calcium excretion after oral glucose ingestion in patients with renal hypercalciuria.

The calciuric response to an oral glucose load (100 g) was determined in 16 patients with calcium oxalate urolithiasis (seven with renal hypercalciuria and nine with absorptive hypercalciuria) and seven normal subjects. The rates of renal calcium excretion increased significantly after glucose ingestion in all three groups. The calciuric response in patients with absorptive hypercalciuria and intestinal hyperabsorption of calcium was indistinguishable from that of normal subjects. However, the calcium excretions were significantly higher during 1 hr preceding and 3 hr after glucose ingestion in patients with renal hypercalciuria (with presumed "renal leak" of calcium) than in normal subjects. The increment in the calcium excretion rate was also higher in patients with renal hyperacalciuria, particularly during the 2nd hour of glucose ingestion. The results provide a further support for the concept of different etiologies of renal and absorptive hypercalciurias.

Adult↗
PubMed1983

Absence of secondary hyperparathyroidism in most patients with renal hypercalciuria.

We examined parathyroid gland function in 47 patients with idiopathic hypercalciuria in an effort to determine whether serum levels of parathyroid hormone (PTH) and/or urinary excretion of cyclic adenosine monophosphate (cyclic AMP) can discriminate between the various forms of hypercalciuria. Although we could separate our 47 patients into two groups, 21 patients with renal hypercalciuria (RH) and 15 patients with absorptive hypercalciuria (AH), there remained a group of 11 patients who did not exactly correspond to either group. Basal serum PTH was normal in the two groups: for RH, 10.32 +/- 0.93; for AH, 11.43 +/- 1.10 microliter Eq/ml. Similarly, urinary cyclic AMP did not differ between the two groups: for RH, 4.88 +/- 0.5; for AH, 4.87 +/- 0.55 nmoles/dl/min GFR. Moreover, the response of the parathyroid glands to acute hypocalcemia produced by intravenous infusion of EDTA was not different among patients with AH, RH, and control subjects. Only one patient showed a marked increase of serum PTH in response to acute hypocalcemia, and the bone biopsy revealed increased osteoclastic resorption. In conclusion, our data show that serum levels of PTH and urinary cyclic AMP do not differentiate between the various forms of idiopathic hypercalciuria. The EDTA test demonstrated that secondary hyperparathyroidism is very uncommon in these patients.

Adult↗
PubMed1993

Evidence of absorptive hypercalciuria in tuberculosis patients.

In patients with granulomatous diseases, disturbances in calcium metabolism have been described. The aim of the study was to evaluate alterations in calcium metabolism in patients with tuberculosis. Forty patients with tuberculosis (TB) were studied in a baseline state (calcium intake 1000 mg/day). Fourteen of these patients were also studied after restrictive calcium diet (400 mg/calcium/day) and after a load of oral calcium of 1000 mg. In all the studies, calcium and phosphorus were measured in serum and urine, and parathyroid hormone (PTH) in plasma. In addition, serum 25OHD and 1,25(OH)2D (calcitriol) levels were measured in the baseline state and after the restrictive diet. In the baseline state, 25OHD levels were lower and urinary calcium higher in TB patients than in the control group. No patients had hypercalcemia, but hypercalciuria was present in 10 patients (25%). The patients with tuberculosis were divided according to the presence or absence of hypercalciuria. In both groups, the 25OHD levels were lower than in controls. Hypercalciuric patients had lower plasma parathyroid hormone levels and higher serum calcitriol levels than the control group and the TB patients without hypercalciuria. Urinary calcium excretion after a calcium load was higher in TB patients with hypercalciuria than in controls. A positive correlation was found between the calcitriol levels and postcalcium load urinary calcium excretion in patients with calcium hyperabsorption. These data indicate that absorptive hypercalciuria is frequently observed in patients with TB and is possible due to inappropriately high serum calcitriol levels.

Absorption↗
PubMed1997

Salt intake, urinary sodium, and hypercalciuria.

Several studies have reported that high sodium (Na) intake increases not only urinary Na but also urinary calcium (Ca), suggesting that high Na intake could be involved in the pathogenesis of hypercalciuria. No research data are available on the relationship of Na intake to the prevalence of hypercalciuria within the general population. Moreover, it is not clear if Na intake relates only to urinary Ca or also to other indices of Ca homeostasis, including intestinal Ca absorption. In the present paper, two distinct studies addressed these points using 24-hour urinary Na as an index of salt intake in individuals on their habitual unrestricted free diet. Study 1 analyzed the relationship between 24-hour urinary Na and hypercalciuria (24-hour urinary Ca > or = 7.5 mmol in men, > or = 6.25 mmol in women) in a population sample of 203 men and women, aged 20-59 years. Study 2 analyzed the relationship between 24-hour urinary Na and intestinal strontium (Sr) absorption, used as an index of intestinal Ca absorption, urinary (24-hour and fasting) and plasma Ca, and plasma parathyroid hormone in 36 healthy men and women, aged 18-65 years. Within the population sample (study 1), 24-hour urinary Na was directly and significantly correlated with prevalence of hypercalciuria when controlling for gender, age, weight, and urinary creatinine: the relationship was continuous and linear for urinary Na ranging between 40 and 200 mmol/24 h. In the 36 volunteers (study 2), 24-hour urinary Na was related to 24-hour and fasting urinary Ca (p < 0.001) but not to intestinal Sr absorption: the relationship between 24-hour urinary Na and urinary Ca (both 24 h and fasting) was also significant, controlling for other variables. The results indicate that in adults on their habitual diet, urinary Na, which reflects dietary salt intake, correlates with the prevalence of hypercalciuria independently of intestinal Ca absorption and mainly via renal mechanisms.

Adolescent↗
PubMed1995

(Ca+Mg)ATPase and calcium influx in erythrocytes of patients with idiopathic hypercalciuria.

Increased erythrocyte (Ca+Mg)ATPase activity was previously observed in idiopathic hypercalciuria. In order to verify if this alteration is a primary or a secondary event, we studied Sr influx in erythrocytes from subjects with idiopathic hypercalciuria. (Ca+Mg)ATPase activity was significantly higher in hypercalciuric than in hypercalciuric than in normocalciuric subjects whereas no difference in Sr influx was found between the two groups. (Ca+Mg)ATPase activity positively correlated with the erythrocyte Sr content found after 5 min of incubation and with urine Ca excretion. The normal Sr permeability suggests that (Ca+Mg)ATPase is primarily altered in idiopathic hypercalciuria. The primary increase of (Ca+Mg)ATPase activity may enhance passive Ca influx by reduction of cellular Ca concentration. It may induce a defect in cellular Ca metabolism that may cause idiopathic hypercalciuria by stimulating bone Ca turn-over and enteral Ca absorption.

Biological Transport↗
PubMed1979

Hypercalciuria in idiopathic Fanconi syndrome.

A 9 year old girl with idiopathic Fanconi syndrome and hypercalciuria is described. In order to determine whether the increased calcium excretion was directly or indirectly due to the disturbed phosphate metabolism, the behavior of the calcium excretion during therapy, the serum levels of 1,25-dihydroxyvitamin D and parathyroid hormone, and the effect of parathyroid hormone on the renal tubules were investigated. Normal serum 1,25-dihydroxyvitamin D and parathyroid hormone levels, lack of a correlation between the serum phosphate concentration and the degree of hypercalciuria, as well as unsuccessful therapy of the hypercalciuria with oral phosphate indicate that the increased calcium excretion cannot be explained by impaired renal phosphate reabsorption. The hypercalciuria in the patient was therefore regarded as being due to a primary decrease of tubular calcium reabsorption.

Calcium↗
PubMed1994

Hematuria associated with hypercalciuria and hyperuricosuria: a practical approach.

Hematuria is one of the most common urinary abnormalities found in children. When hypercalciuria was identified as a potential etiology of painless hematuria, many questions arose concerning the general importance of this observation. Subsequently, increased uric acid excretion also has been purported to cause hematuria in children. This review traces the history of these observations and describes the clinical characteristics of the clinical syndrome of hematuria associated with hypercalciuria and hyperuricosuria. Diagnostic criteria of excessive urinary excretion of calcium and uric acid are reviewed; differences in urinary calcium and uric acid excretion between infants and older children are emphasized. Aside from urolithiasis, few long-term consequences from hypercalciuria or hyperuricosuria have been identified, although some debate exists concerning the effect of chronic hypercalciuria upon bone mineralization.

Calcium↗
PubMed2005

Hypomagnesemia with hypercalciuria and nephrocalcinosis: case report and a family study.

A 7-month-old male infant was referred for investigation after a documented febrile urinary tract infection. His past medical history was characterized by episodes of unexplained fever and mild dehydration. The ultrasound examination of his kidneys demonstrated bilateral diffuse medullary nephrocalcinosis. His serum and urine biochemistry revealed hypomagnesemia (0.4 mmol/l), hyperuricaemia (506 micromol/l), mildly increased iPTH (71 pg/ml) and hypercalciuria (16.0 mg/kg/day). The diagnosis of familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) was confirmed by mutational analysis of the CLDN16 gene, encoding paracellin-1. Sequencing displayed a homozygous Leu151Phe exchange affecting the first extracellular loop of paracellin-1. There were eight family relatives who underwent biochemical analysis, renal ultrasound and genetic investigation for CLDN16 mutations. Five of them were found to be heterozygous for the Leu151Phe mutation. Two heterozygotes (the mother and the maternal grandfather) presented with hypercalciuria. The grandfather had a history of recurrent passage of calculi. These findings point to the role of heterozygous CLDN16 gene mutations in renal pathophysiology. In conclusion, patients suspected of having FHHNC should be screened for CLDN16 mutations, especially with respect to genetic counseling. In addition, heterozygotes at risk should be clinically assessed in order to prevent renal complications of hypercalciuria.

Adult↗
PubMed2000

Idiopathic hypercalciuria of childhood: 4- to 11-year outcome.

Apart from a minority with urolithiasis, the majority of children diagnosed with idiopathic hypercalciuria present with macro- or microhematuria, abdominal or back pain, or voiding symptoms. With dietary and pharmacological interventions, most such children become asymptomatic and are lost to follow-up, hence their long-term outcome is unclear. In the present study, we evaluated the status of 14 males and 19 females aged 8-17 years (mean 11.9 years, median 11.2 years) 4-11 years (mean 6.9 years, median 6.5 years) after the initial diagnosis of idiopathic hypercalciuria not associated with urolithiasis. A questionnaire was answered and two random urine samples provided 3-4 weeks apart were analyzed for calcium (Ca), sodium (Na), potassium (K), and creatinine (Cr). Urine Ca/Cr ratio > or =20.21 (mg/mg) was defined as hypercalciuria. At the time of the study none were under follow-up, although 7 children were still exhibiting voiding symptoms. No child developed clinical urolithiasis. Based on the first urine specimen, 16 of the 33 (48.4%) were hypercalciuric. Their 2nd urinalysis showed persistent hypercalciuria in 8 and normocalciuria in 8. Urine Na/K ratio (mEq/mEq) decreased in the latter 8 from 5.08+/-2.67 to 3.03+/-2.23 (P<0.05). Of the 17 initially normocalciuric children, 5 did not submit a 2nd specimen, 11 remained normocalciuric, and 1 became hypercalciuric with an increase in urine Na/K ratio. Twenty-three children (all 8 persistently and 9 intermittently hypercalciuric plus 6 normocalciuric) were studied by ultrasonography. Only in 1 asymptomatic persistently hypercalciuric child was a single small renal calcification noted. Introduction of a low-Na/high-K diet in 7 persistently hypercalciuric children resulted in a decrease in UNa/K ratio from 7.34+/-2.15 to 4.14+/-3.09 (P<0.01) and UCa/Cr ratio from 0.25+/-0.04 to 0.13+/-0.03 (P<0.01). We conclude that even though over time most hypercalciuric children become asymptomatic, many remain hypercalciuric. Further follow-up is required to ascertain whether these children are at risk of developing kidney stones. If they are at risk then long-term compliance with a low-Na/high-K diet might be beneficial, as it can normalize calciuria in the majority of these children.

Adolescent↗
PubMed1999

Hypercalciuria and recurrent urinary tract infection in Venezuelan children.

Recurrent urinary tract infection (UTI) has not been widely recognized as a clinical manifestation of hypercalciuria in children. We studied 59 children with two or more episodes of UTI, a normal urinary tract, and with hypercalciuria. Clinical manifestations were fever, dysuria, straining with micturition, hematuria, polyuria, abdominal pain, and failure to thrive. Urinary calcium/creatinine ratio was 0.36+/-0.15 mg/mg. Renal function studies included serum bicarbonate (21+/-3 mmol/l), urinary/blood PCO2 difference (11+/-11 mmHg), urinary net acid excretion (63+/-3 micromol/min per 1.73 m2), uric acid fractional excretion (13%+/-12%), and maximal urinary osmolality (920+/-236 mosmol/kg). Treatment included promotion of fluid intake, avoiding excessive salt and protein, and keeping dietary calcium between 900 and 1,200 mg/day. Potassium citrate or hydrochlorothiazide were indicated if hypercalciuria persisted. With this treatment, in 95% of the children, no further episodes of UTI occurred once normocalciuria was achieved. It is possible that hypercalciuria may play a predisposing role for recurrent UTI in children by promoting the formation of microcrystals which damage the uroepithelium. We advocate the investigation of urinary calcium excretion in children with recurrent UTI and a normal urinary tract.

Acidosis, Renal Tubular↗
PubMed1979

Familial absorptive hypercalciuria and renal tubular acidosis.

Hypercalciuria was considered as a secondary condition when associated with familial renal tubular acidosis. Later studies suggested that hypercalciuria could lead to renal tubular acidosis and nephrocalcinosis. Selected members of a family spanning five generations were studied. Renal tubular acidosis was present in eight subjects in three consecutive generations. Increased 24-hour urinary calcium excretion was present in nine subjects in three consecutive generations, alone in the younger generation, and in combination with renal tubular acidosis and nephrocalcinosis in the older generation. Calcium loading tests showed the absorptive nature of hypercalciuria in nine of 18 subjects studied. This report suggests that in this family the absorptive hypercalciuria is an autosomal dominant genetic defect with complete penetrance and variable expressivity which leads to renal tubular acidosis and nephrocalcinosis.

Acidosis, Renal Tubular↗
PubMed1979

Selective jejunal hyperabsorption of calcium in absorptive hypercalciuria.

Calcium absorption in the jejunum and ileum of patients with absorptive hypercalciuria was studied by in vivo intestinal perfusion. Net calcium absorption in the jejunum was markedly increased at four luminal calcium concentrations (1 to 20 mM) in the patients with absorptive hypercalciuria when compared to that in normal subjects. In the ileum, net calcium absorption was only slightly increased in the patients with absorptive hypercalciuria. Experiments with radioactive calcium (47Ca) revealed increased unidirectional flux out of the jejunal lumen in the patients but no difference in the unidirectional flux into the lumen, when compared to that in normal control subjects. Net magnesium absorption was normal in the patients. These results suggest that hyperabsorption of calcium in patients with absorptive hypercalciuria is mainly due to enhanced calcium transport in the jejunum and that the defect is specific for calcium since magnesium is absorbed normally.

Adult↗
PubMed1982

Effects of low-calcium diet on urine calcium excretion, parathyroid function and serum 1,25(OH)2D3 levels in patients with idiopathic hypercalciuria and in normal subjects.

We have used a low-calcium diet providing only 2 mg/kg (body weight) per 24 hours of calcium to distinguish between "renal" and "absorptive" idiopathic hypercalciuria. Sixteen of 27 hypercalciuric subjects excreted calcium in excess of intake during days seven, eight and nine of he diet, suggesting some element of renal hypercalciuria; however, all patients had low or normal serum PTH and urine cAMP levels. In general, fasting urine calcium was elevated in these 16 subjects and normal in the remaining 11, who conserved calcium more normally. SErum 1,25(OH)2D3 levels were the same in patients and normal subjects, even though PTH levels of the patients were below those of he normal subjects. Urine magnesium excretion and phosphorus excretion were both increased in the patients who excreted calcium in excess of intake. Our findings suggest that renal and absorptive hypercalciuria may not be distinct entities but rather the two extremes of a continuum of behavior. A uniform elevation of intestinal calcium absorption and a variable defect of renal calcium reabsorption could explain our results far better than the hypothesis of distinct absorptive and renal forms of hypercalciuria.

Calcitriol↗
PubMed1992

The dose-dependency of alcohol-induced hypoparathyroidism, hypercalciuria, and hypermagnesuria.

Ingestion of alcohol evokes hypoparathyroidism, hypercalciuria, and hypermagnesuria. The dose-dependency of these changes has not been assessed before. We measured the serum concentrations of intact parathyroid hormone (PTH), and serum and urine calcium and magnesium in six normal men before and at intervals up to 6 h after the ingestion of fruit juice (control) and 0.5, 1.0 and 1.3 g of alcohol per kg of body weight. As compared with the control experiment the maximum reductions in the mean PTH concentration were 31% (P = 0.19), 31% (P = 0.20) and 45% (P = 0.01) with the three alcohol doses, respectively. After stopping drinking, the urinary excretion of calcium was 85%, 142% and 207% higher during the three alcohol experiments than during the control session (P < 0.05, < 0.01 and < 0.01, respectively), also urinary magnesium increased up to threefold. We conclude that in nonalcoholic subjects acute alcohol intake induces hypoparathyroidism, hypercalciuria, and hypermagnesuria, the latter two being dose-dependent. The direct renal effects of alcohol are the major mechanisms for hypercalciuria and hypermagnesuria, but hypoparathyroidism contributes to hypercalciuria at high levels of alcohol intoxication.

Adult↗
PubMed1998

Physiological effects of slow release potassium phosphate for absorptive hypercalciuria: a randomized double-blind trial.

PURPOSE: We examined the physiological effects and tolerance of UroPhos-K, a slow release neutral form of potassium phosphate (155 mg. phosphate and 8 mEq. potassium per tablet) in patients with absorptive hypercalciuria. MATERIALS AND METHODS: A total of 31 patients with absorptive hypercalciuria were studied at baseline and after 3 months of treatment with 4 tablets twice daily of UroPhos-K or placebo (identical in appearance) in a prospective randomized, placebo controlled, double-blind trial during a 4-day inpatient study with a daily constant metabolic diet containing 400 mg. calcium, 100 mEq. sodium and 800 mg. phosphate. RESULTS: Treatment with UroPhos-K did not cause significant gastrointestinal side effects, increase fasting serum potassium or phosphorus, or reduce hemoglobin or creatinine clearance. It reduced urinary calcium excretion from 277 +/- 72 to 166 +/- 43 mg. per day (p < 0.001), associated with a reduction in serum 1,25-dihydroxyvitamin D concentration from 50 +/- 11 to 42 +/- 9 pg./ml. (p < 0.001). Indexes of intestinal calcium absorption and markers of bone turnover also decreased modestly. None of these changes was seen in the placebo group. CONCLUSIONS: In patients with absorptive hypercalciuria UroPhos-K seems to correct hypercalciuria by a combination of reduced intestinal absorption, bone resorption and improved renal calcium reabsorption. The drug is well tolerated compared to placebo.

Adult↗
PubMed1991

Vertebral mineral content in diet-dependent and diet-independent hypercalciuria.

The vertebral mineral content was measured using dual photon absorptiometry in 41 calcium stone patients with idiopathic hypercalciuria. These patients had been previously divided into 2 groups (diet-dependent and diet-independent hypercalciuria) during a low sodium and low calcium diet. In some of the patients (11 with diet-dependent and 11 with diet-independent hypercalciuria) the vertebral mineral content was evaluated in relation to serum ionized calcium, intact parathyroid hormone, alkaline phosphatase and osteocalcin determined after a low sodium and low calcium diet. The vertebral mineral content, expressed as Z-VMD, was normal in diet-dependent and lower in diet-independent hypercalciuric stone patients (-0.30 +/- 1.19 versus -0.26 +/- 1.18, p less than 0.02). In 7 of 21 patients (33.3%) the vertebral mineral content was less than 2 standard deviations of the normal value, indicating a true involvement in bone metabolism. Serum intact parathyroid hormone and osteocalcin levels were not different from the controls in both groups, while alkaline phosphatase activity and ionized calcium were higher in diet-independent hypercalciuric patients. Serum ionized calcium was negatively correlated with bone vertebral density. The results suggest that an increased bone turnover may be a primary event in causing hypercalciuria in calcium stone patients unable to decrease urinary calcium to less than the calcium intake.

Absorptiometry, Photon↗
PubMed1989

Idiopathic hypercalciuria.

Idiopathic hypercalciuria, defined as the urinary excretion of more than 300 mg. calcium per day in men or more than 250 mg. calcium per day in women, or more than 4 mg. calcium per kg. per day, is observed in about 50 per cent of the patients with calcium oxalate/apatite nephrolithiasis and is one of the risk factors for stone formation. These patients do not exhibit hypercalcemia, elevated serum parathyroid hormone concentrations or urinary cyclic adenosine monophosphate excretion nor clinical evidence of sarcoidosis, other granulomas or a malignancy. Hypophosphatemia may be present. Augmented rates of intestinal absorption of dietary calcium account for most of the increments in urinary calcium. Serum 1,25-dihydroxyvitamin D concentrations are in the upper normal range or elevated among many patients and are normal but not suppressed in the others. Activation of 1,25-dihydroxyvitamin D formation may be secondary to hypophosphatemia or other, as yet undefined, factors. Since, 1,25-dihydroxyvitamin D apparently can up-regulate its own receptor, small increments in its synthesis and blood levels could amplify the effect of the hormone to stimulate intestinal calcium absorption. Calcium balances are slightly but significantly negative and urinary hydroxyproline excretion may be increased so that a generalized disorder of calcium homeostasis also involving bone may be present. Additional studies are required to determine the genetic basis for the occurrence of idiopathic hypercalciuria in families, the cause of greater expression of idiopathic hypercalciuria in men and whether environmental factors (high dietary sodium chloride, protein and purified carbohydrate intakes) contribute to the expression of idiopathic hypercalciuria. Although thiazide diuretics, inorganic phosphate, magnesium hydroxide and potassium citrate have provided effective therapy, prospective studies are needed to determine optimum therapy and the optimum duration of treatment.

Calcitriol↗
PubMed1981

Long-term persistence of metabolic abnormalities in absorptive or renal hypercalciuria.

Seven patients with absorptive hypercalciuria and seven with renal hypercalciuria were re-evaluated 1.67-7.33 years after the original diagnosis. When treatment was temporarily stopped, all showed the same metabolic abnormalities as before: those with absorptive hypercalciuria continued to show increased intestinal absorption of calcium and normal or suppressed parathyroid function, and those with renal hypercalciuria had persistent "renal leak" of calcium and parathyroid stimulation. In view of the persistence of metabolic abnormalities, medical therapy should be regarded as a long-term commitment.

Adult↗