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PubMed2002

Bone alterations in patients with idiopathic hypercalciuria and calcium nephrolithiasis.

OBJECTIVES: To verify whether alterations in bone density and turnover in patients with calcium nephrolithiasis and hypercalciuria are observable in various subgroups of patients divided according to the pathogenesis of the hypercalciuria. METHODS: Seventy patients with calcium nephrolithiasis and idiopathic hypercalciuria, 19 to 64 years old, were assessed for spine and femur mineral metabolism and bone density using a Dexa evaluation system. After a low calcium diet, the subjects were classified into two groups: fasting hypercalciuria (FH, 39 patients) and absorptive hypercalciuria (AH, 31 patients). RESULTS: Only in the patients with FH was the lumbar spine bone density lower than in the controls (P <0.001). Also, only the patients with FH had higher bone alkaline phosphatase and urinary hydroxyproline levels than the control group (P <0.005 and <0.015, respectively). The blood pH levels were lower, even though within the normal range, in the hypercalciuric patients than in the controls (P <0.01). There was a negative correlation between the urinary hydroxyproline level and lumbar spine and femoral neck density in patients with FH (P <0.001 and <0.005, respectively), and the blood pH correlated positively with the lumbar spine bone density. CONCLUSIONS: Altered bone metabolism and overall bone loss were found only in the patients with FH. Overloading of acid valences, perhaps of dietary origin, could be the pathogenic factor responsible.

Adult↗
PubMed1984

Transient hypercalciuria after commencing total intravenous nutrition.

A study of 28 patients receiving a standard regimen of total intravenous nutrition (I.V.N.) for periods of > 14 days has shown the transient development of hypercalciuria in 14 patients (50%). The peak incidence of hypercalciuria occurred in 11 patients (39%) after 1 week of I.V.N. and hypercalciuria persisted for 1-4 weeks. In only one patient was hypercalciuria present at the end of the treatment period. Urine calcium (Ca) and nitrogen (N) excretion rates correlated significantly (r = 0.48 p < 0.001) and urine N excretion varied from week to week in parallel with urine Ca excretion in the hypercalciuric group of patients. There was no significant difference in urine Ca excretion between 12 patients who received 3.75 mmol Ca/day and 16 patients who received 8.75 mmol Ca/day. It is concluded that transient hypercalciuria may be related to increased protein catabolism and N excretion and that it probably does not indicate a major problem in mineral metabolism.

Journal Article↗
PubMed1989

Hematuria due to hypercalciuria and hyperuricosuria in adult patients.

We have prospectively studied 37 adult patients (15 males, 22 females; age 31 +/- 10.6 years) with previously undiagnosed isolated hematuria in which hypercalciuria or hyperuricosuria was found. Eighteen of them had had episodes of gross hematuria. Isolated hypercalciuria (4.4 to 10.4, X 5.6 +/- 1.9 mg/kg/24 hr) was found in nine patients (Group I), isolated hyperuricosuria (784 to 1500, X 1088 +/- 228 mg/24 hr) in 11 (Group II), and both hypercalciuria (4 to 8, X 4.9 +/- 1 mg/kg/24 hr) and hyperuricosuria (752 to 1476, X 1042 +/- 181 mg/24 hr) in 17 patients (Group III). Thiazide treatment for patients with hypercalciuria and allopurinol for those with hyperuricosuria were administered; calciuria and uricosuria became normal by the first month of therapy in every case. In 22 (59.4%) cases (Responder patients) hematuria resolved completely as soon as calciuria and uricosuria became normal. In the remaining 15 cases (Nonresponder patients) hematuria persisted despite the normal calcium and uric acid excretions. Several disorders that explained hematuria were diagnosed later in most of Nonresponder patients. Responder patients persisted without hematuria on the follow-up; only in three patients a transient relapse of hematuria was seen associated with a sudden increase of calciuria and uricosuria because of treatment withdrawal. There were no differences in age, male/female ratio nor in the basal values of calciuria and uricosuria between Responder and Nonresponder patients. A familial history of urolithiasis was found more frequently in Responder patients (64%) than in Nonresponders (20%) (P less than 0.05). We conclude that hypercalciuria and hyperuricosuria are definable and potentially reversible causes of hematuria in adult patients.

Adolescent↗
PubMed2000

Localization of the nephron site of gentamicin-induced hypercalciuria in the rat: a micropuncture study.

In vivo renal micropuncture techniques were used to locate the nephron site of hypercalciuria induced by acute gentamicin infusion in anaesthetized Sprague Dawley rats. Three series of experiments were conducted. The effect of gentamicin on calcium reabsorption in the proximal tubule (Series I) and loop of Henle (Series II) was investigated using in vivo microperfusion whereas the effect on distal calcium handling (Series III) was studied using in vivo microinfusion. In all three experimental series, acute systemic gentamicin infusion at 0.28 mg kg(-1) min(-1) caused significant hypercalciuria within 30 min of commencing drug infusion. Gentamicin had no effect on the rates of urine flow or sodium excretion. Acute gentamicin infusion had no effect on unidirectional calcium reabsorption in the proximal tubule or loop of Henle despite a simultaneous and highly significant hypercalciuria at the whole kidney level. Net fluid reabsorption was also unaffected by the drug in these nephron segments. Acute gentamicin infusion significantly increased the urinary recovery of calcium following microinfusion into early distal tubules, whereas urinary calcium recovery was decreased after microinfusion into late distal tubules. We conclude that acute gentamicin-induced hypercalciuria is mediated by a decrease in calcium reabsorption in the early distal tubule. Thus, the acute hypercalciuric effect of gentamicin occurs at a different nephron site to the nephrotoxic effects associated with longer-term administration of the drug. It is, therefore, unlikely that gentamicin-induced hypercalciuria is involved in the pathogenesis of subsequent proximal tubular cell injury.

Animals↗
PubMed1980

[Diagnosis of hypercalciuria in calcium nephrolithiasis (author's transl)].

An increased calcium excretion in 24-hour urine was found in 32 of 42 out-patients with recurrent calcium nephrolithiasis (calcium excretion > 300 mg in males, > 250 mg in females). Subsequent hospitalization of the 32 patients revealed the following diagnosis after a calcium tolerance test: absorptive hypercalciuria in 18, renal hypercalciuria in 4, primary hyperparathyroidism in 2 and dietary hypercalciuria in 7. Normocalciuria in 10 out-patients was confirmed in 6; in one instance there was, however, primary hyperparathyroidism, in 3 there was absorptive hypercalciuria. In one patient it was not possible to classify the hypercalciuria. Total as well as nephrogenic cAMP showed wide scatter and was unsuitable, therefore, in differential diagnosis. In 2 of 3 cases of hyperparathyroidism the serum level of parathormone was distinctly elevated.

Calcium↗
PubMed1975

A simple test for the diagnosis of absorptive, resorptive and renal hypercalciurias.

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.

Bone Resorption↗
PubMed1988

Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria.

Idiopathic hypercalciuria is a common disorder whose inheritance suggests an enzyme abnormality in calcium transport. We measured calcium-magnesium-ATPase activity in erythrocytes from 38 patients (mean age [+/- SEM], 40 +/- 2.1 years) with idiopathic hypercalciuria (24-hour urinary calcium excretion greater than or equal to 0.1 mmol per kilogram of body weight) and a history of multiple calcium oxalate kidney stones. As compared with 41 healthy controls, the patients with hypercalciuria had increased erythrocyte-membrane calcium-magnesium-ATPase activity (64.2 +/- 2.19 vs. 51.6 +/- 1.91 nmol of ATP split per milligram per minute; P less than 0.01) and increased sodium-potassium pump activity (6866 +/- 233 vs. 6096 +/- 228 mumol of sodium per liter of red cells per hour; P less than 0.05). No significant difference between the two groups was found in erythrocyte sodium-potassium cotransport, sodium-lithium countertransport, or potassium content. In 66 patients with kidney stones (38 with hypercalciuria and 28 with normal calcium excretion), 24-hour urinary calcium excretion correlated with calcium-magnesium-ATPase activity (r = 0.46, P less than 0.001). Erythrocyte calcium-magnesium-ATPase activity remained unchanged in eight subjects studied after four months on a low-calcium diet. A study of 30 healthy families found significant correlations between mean values in parents and those in offspring for calcium-magnesium-ATPase (r = 0.68, P less than 0.001) and urinary calcium excretion (r = 0.45, P less than 0.02), with no significant correlations between parents with respect to these measures (r = 0.27 and r = 0.08, respectively). We conclude that abnormalities in erythrocyte calcium-magnesium-ATPase activity may represent an inherited defect in calcium transport related to the cause of idiopathic hypercalciuria.

Adult↗
PubMed1999

Diet-dependent hypercalciuria in transgenic mice with reduced CLC5 chloride channel expression.

Dent's disease is an X-linked inherited disorder characterized by hypercalciuria, nephrocalcinosis, nephrolithiasis, low molecular weight proteinuria, Fanconi's syndrome, and renal failure. It is caused by inactivating mutations in CLC5, a member of the CLC voltage-gated chloride channel family. CLC5 is known to be expressed in the endosomal compartment of the renal proximal tubule, where it may be required for endosomal acidification and trafficking. Although the Fanconi's syndrome and low molecular weight proteinuria in Dent's disease can be explained by disruption of endosomal function in this nephron segment, the pathogenesis of the hypercalciuria in this disease is unknown. We have generated transgenic mice (RZ) with reduced CLC5 expression by introduction of an antisense ribozyme targeted against CLC5. RZ mice are markedly hypercalciuric compared with nontransgenic control mice, at a time when their serum electrolytes and renal function are otherwise normal. This suggests that hypercalciuria in Dent's disease is a direct consequence of CLC5 hypofunction and is not attributable to a gain of function by mutant CLC5, an effect of modifier genes, or a secondary result of nonspecific renal injury. Surprisingly, hypercalciuria in RZ mice is abolished by dietary calcium deprivation, suggesting that the hypercalciuria may be attributable to gastrointestinal hyperabsorption of calcium rather than a renal calcium leak.

Age Factors↗
PubMed2002

Extremely high prevalence of hypercalciuria in children living in the Aral Sea region.

UNLABELLED: The Aral Sea region is a natural area seriously polluted by human activities. In addition to the increased prevalence of diverse chronic diseases in children, the risk of developing urolithiasis is reported to be high in this region. This study was undertaken to clarify the prevalence of hypercalciuria in children of the Aral Sea region. A group of 205 children living in Kazalinsk, close to the Aral Sea, and a group of 187 children living in Zhanakorgan, far from the Aral Sea, were screened for hypercalciuria. Urinary sodium excretion (sodium per creatinine, uNa/Cr) in addition to calcium excretion (calcium per creatinine, uCa/Cr) was also calculated for each subject. Mean uCa/Cr (mmol/mmol) and uNa/Cr (mmol/mmol) excretions were significantly higher in Kazalinsk than in Zhanakorgan (uCa/Cr: 0.75 +/- 0.74 and 0.33 +/- 0.30; uNa/Cr: 3.54 +/- 2.27 and 2.89 +/- 1.69, respectively, mean +/- SD, p < 0.01). Hypercalciuria regarded as an uCa/Cr of more than 0.703 was observed in 79 out of 205 Kazalinsk children (38.6%) while this was seen in only 24 out of 187 Zhanakorgan children (12.8%). Linear regression analysis revealed a direct positive correlation between urinary calcium and sodium excretion (p < 0.01) in Kazalinsk children. CONCLUSION: The prevalence of hypercalciuria in children around the Aral Sea region is extremely high. This may be associated with excessive intake of calcium and sodium, or due to impaired renal tubular function caused by toxic chemicals. Therefore, hypercalciuria that may lead to urolithiasis should be taken into account when considering the health problems of this area.

Asia, Central↗
PubMed2005

Bone disease in primary hypercalciuria.

Primary hypercalciuria (PH) is very often accompanied by some degree of bone demineralization. The most frequent clinical condition in which this association has been observed is calcium nephrolithiasis. In patients affected by this disorder, bone density is very frequently low, and increased susceptibility to fragility fractures is reported. The very poor definition of this bone disease from a histomorphometric point of view is a crucial aspect. At present, the most common finding seems to be a low bone turnover condition. Many factors are involved in the complex relationships between bone loss and PH. Since bone loss was mainly reported in patients with fasting hypercalciuria, a primary alteration in bone metabolism was proposed as a cause of both hypercalciuria and bone demineralization. This hypothesis was strengthened by the observation that some bone resorbing-cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor nechrosis factor-alpha (TNF-alpha), are high in hypercalciuric patients. An excessive response to the acid load induced by dietary protein intake seems to be an additional factor explaining a primitive alteration of bone. The intestine plays a major role in the clinical course of bone disease in PH. Patients with absorptive hypercalciuria less frequently show bone disease, and a reduction in dietary calcium greatly increases the probability of bone loss in PH subjects. It has recently been reported that greater bone loss is associated with a larger increase in intestinal calcium absorption in PH patients. Considering the absence of parathyroid hormone (PTH) alterations, it was proposed that this is not a compensatory phenomenon, but probably the marker of disturbed cell calcium transport, involving both intestinal and bone tissues. While renal hypercalciuria is rather uncommon, the kidney still seems to play a role in the pathogenesis of bone loss in PH patients, possibly via the effect of mild-to-moderate urinary phosphate loss with secondary hypophosphatemia. In conclusion, bone loss is very common in PH patients. Even if most of the factors involved in this process have been identified, many aspects of this intriguing clinical condition remain to be elucidated.

Animals↗
PubMed2001

No evidence for point mutations of the calcium-sensing receptor in familial idiopathic hypercalciuria.

BACKGROUND: Idiopathic hypercalciuria (IH) is frequently associated with nephrolithiasis. As 40% of patients have a positive familial history of IH, an autosomal dominant mode of inheritance has been suggested. Numerous genes have been studied in this regard but none have been found to be linked to IH. Mutation of the calcium-sensing receptor (CaR) has never been studied. Therefore, we conducted a study to detect such mutations. METHODS: Seven families with IH and nephrolithiasis were recruited in a prospective study. Forty-two family members underwent 24-h urine calcium measurement. Twenty-five of them with 24-h hypercalciuria also underwent extensive metabolic evaluation. Blood samples were collected in one or two affected family members in each family and exons 2-7 of the CaR gene were sequenced. RESULTS: In the seven families, at least one parent and more than half of the children had hypercalciuria (21/30), consistent with autosomal dominant inheritance. Among the nine affected family members whose CaR gene has been studied, all nine had absorptive hypercalciuria, three also had fasting hypercalciuria, and one had renal phosphorous leak. No mutation of the CaR gene was detected in these seven families. Two previously reported polymorphisms were detected, each of them in five families: A986S and C-to-T change at -60 in intron 5. CONCLUSION: In these seven families, IH is not related to the CaR gene mutation. Although we cannot exclude that point mutations can be found in other families, familial IH does not seem to be generally associated with CaR mutation.

Adult↗
PubMed2000

The role of hypercalciuria in a subgroup of dysfunctional voiding syndromes of childhood.

PURPOSE: Idiopathic hypercalciuria is believed to be the cause of a variety of urinary tract complaints in clinical pediatrics, including urinary frequency, urgency, and/or dysuria, often associated with gross or microscopic hematuria. In children noncalculous manifestations of idiopathic hypercalciuria are reportedly more common than urolithiasis. We determine the use of the calcium-to-creatinine ratio for the evaluation of different subsets of functional voiding disorders. MATERIALS AND METHODS: We retrospectively evaluated 288 patients with functional voiding disorders during the last 8 years. Patients presenting with isolated urinary tract infection were not included in the study. A thorough history with emphasis on voiding patterns was elicited and a routine urinalysis was performed in all patients. Patients were divided into 5 groups of 22 with total gross hematuria and dysfunctional voiding pattern, 102 with microhematuria and dysfunctional voiding pattern, 66 with isolated childhood daytime frequency, 45 with the isolated dysuria syndrome and 53 with combined childhood frequency-urgency-dysuria syndrome. The season at presentation was noted to determine a seasonal pattern. In 149 patients urine was evaluated for a spot calcium-to-creatinine ratio. RESULTS: Mean age of the 95 (33%) males and 193 (67%) females was 6.1 years (range 2 to 14) and mean duration of symptoms was 10 months (1 week to 10 years). The incidence of idiopathic hypercalciuria was 28% in cases with gross hematuria and dysfunctional voiding, 30% with microscopic hematuria and dysfunctional voiding, 21% with pure childhood daytime frequency, 22% with pure dysuria, and 28% with frequency, urgency and dysuria. The patients were treated predominantly with behavioral therapy, correction of faulty voiding habits, anticholinergics and minor diet modification in some. Mean followup of 6.5 months (range 1 month to 10 years) was available for 153 patients (53%). Resolution of symptoms along with marked improvement in voiding habits was noted in 136 (89%) patients, moderate improvement in 10 (6.5%) and persistent symptoms with minimal improvement in 7 (4.5%). Treatment with thiazides was used in only 6 (2%) patients who had intractable symptoms and a markedly elevated urine calcium-to-creatinine ratio of whom 5 responded favorably. CONCLUSIONS: Idiopathic hypercalciuria may have a significant role in cases of functional voiding disorders. It affects the different subsets of voiding disorders with remarkable consistency but the exact mechanism remains unknown. Although a significant number of patients with voiding dysfunction have an elevated calcium-to-creatinine ratio, the majority respond to standard behavioral therapy and pharmacotherapy in the form of anticholinergics, and treatment directed toward hypercalciuria is not required in most cases.

Adolescent↗
PubMed1990

Screening for hypercalciuria.

Reference values for the urinary calcium/creatinine ratio (Ca/Cr ratio) in the first morning urine were established in 361 healthy children aged 5 to 15 years, on unrestricted diets. The urinary Ca/Cr ratio in the urine upon arising was independent of sex but dependent upon age. The measurement of the urinary Ca/Cr ratio in the urine upon arising while on unrestricted diets may be a reasonable screening test for elevated calcium excretion. On the basis of the urinary Ca/Cr ratios in the urine upon arising during unrestricted diets and the calciuric response to calcium restricted diets and the oral calcium loading test, idiopathic hypercalciuria (IH) was subclassified into three groups: (1) absorptive hypercalciuria; (2) renal hypercalciuria; (3) dietary hypercalciuria. The pathogenesis of IH is controversial. Our data suggest that disordered 1,25 (OH)2 vitamin D metabolism with excessive urinary phosphate excretion occurs in absorptive hypercalciuria.

Adolescent↗
PubMedDate not supplied

Nephrocalcinosis, hypercalciuria and elevated serum levels of 1,25-dihydroxyvitamin D in children. Possible link to vitamin D toxicity.

Ten children age 1 1/2 to 14 years, had bilateral nephrocalcinosis and hypercalciuria, but normal serum calcium (Ca) and phosphate (P) concentrations. Patients with hypercalciuria were divided into absorptive (n = 4) and renal (n = 6) subgroups, and in the latter four patients had a primary Ca-leak and two had a P-leak. All the children had received intermittent high dose vitamin D prophylaxis during infancy. At the time of investigation all had normal serum levels of 25-hydroxyvitamin D, yet all but one had elevated values of 1,25-(OH)2D. Although the hypercalciuria was indistinguishable from the various known forms of idiopathic hypercalciuria, the previous clinical course and the pattern of bone mineral homeostasis suggest that both clinical features, namely nephrocalcinosis and hypercalciuria were related to vitamin D toxicity through various pathogenetic pathways.

Adolescent↗
PubMed1986

Chronic DOCA treatment increases Ca absorption: role of hypercalciuria and vitamin D.

To examine the effects of mineralocorticoidism on calcium (Ca) absorption and to define the mechanism, rats received a high-salt diet and injections of vehicle or deoxycorticosterone acetate (DOCA). Net (44.2 vs. 31.4 mg/day) and percent Ca absorption (28.1 vs. 20.1%) was increased after 5 days of DOCA. This was associated with increased duodenal 45Ca uptake. Thus despite the hypercalciuria, Ca balance was similar. Although the hypercalciuria persisted chronically, the gut effects were sustained, which maintained normal ionized Ca, bone Ca, and Ca balance. Urinary cyclic adenosine monophosphate was elevated by DOCA. Compared with appropriate controls, neither DOCA alone nor polydipsia (elicited by dextrose) produced similar magnitudes of hypercalciuria as DOCA plus high-salt diet. These maneuvers also failed to increase Ca absorption. Neutralization of the metabolic alkalosis neither attenuated the DOCA-induced hypercalciuria nor abolished the Ca hyperabsorption. In vitamin D-deprived rats, the hypercalciuria but not the intestinal effects of DOCA were reproduced. Serum 1,25-dihydroxyvitamin D3 levels were increased during chronic DOCA treatment (224 vs. 139 pg/ml). These data best fit the hypothesis that increased Ca absorption is secondary to the calciuric effects of DOCA and high-salt diet and is mediated via the increased parathyroid hormone and 1,25-dihydroxyvitamin D3 activities.

Alkalosis↗
PubMed1984

Hypercalciuria in clinical pediatrics. A review.

Idiopathic hypercalciuria is a cause of a variety of urinary tract complaints in clinical pediatrics. These include gross or microscopic hematuria, enuresis, urinary frequency or urgency, dysuria, sterile pyuria, and proteinuria in addition to renal calculi. A random urine calcium-creatinine concentration ratio can be used to initially screen for hypercalciuria. Patients with indeterminate results should have the test repeated, while those with abnormal values should receive a complete metabolic workup to determine the cause of hypercalciuria. Identifiable causes of hypercalciuria should be treated specifically, and thiazide diuretics are the preferred treatment for uncomplicated renal calculi. Pharmacotherapy in children with idiopathic hypercalciuria and symptomatology other than renal stones is controversial and should be limited to patients with severe clinical manifestations.

Adolescent↗
PubMed1984

An experimental human model of 1,25-dihydroxyvitamin D-mediated hypercalciuria.

An increase in fasting calcium excretion occurs in hypercalciuric patients and has been interpreted by many investigators as evidence for a primary renal tubular leak of calcium. In a recent series of 50 patients with absorptive hypercalciuria, we found a mean increase in fasting fractional calcium excretion (calcium clearance) and provided data suggesting that this leak of calcium was secondary to intestinal hyperabsorption of calcium and suppression of parathyroid secretion. To examine this question, a model of 1,25-dihydroxyvitamin D [1,25-(OH)2D]-mediated hypercalciuria was created by administering a large dose of 1,25-(OH)2D to normal subjects. In addition to the expected features of absorptive hypercalciuria during 1,25-(OH)2D administration, the subjects had an increase in fasting calcium excretion and a marked increase in calcium excretion during a restricted calcium diet, points that might be interpreted as favoring a resorptive and/or renal component to the net hypercalciuria. However, total hydroxyproline excretion remained unchanged (18.0 vs. 19.0 mg/g creatinine), and the increase in fasting calcium excretion was found to reflect an increase in calcium clearance; the latter was inversely correlated with parathyroid function, as determined by fasting measurements of nephrogenous cAMP excretion (r = -0.77; P less than 0.01). We conclude that measurements of calcium excretion in the fasting state or on a restricted calcium diet do not represent valid criteria for differential diagnosis of the hypercalciurias.

Adult↗
PubMed1989

[The effect of oral calcium loading on the serum magnesium concentration and its urinary excretion in patients with recurrent calcium nephrolithiasis and hypercalciuria--differential diagnostic potentials].

The study deals with 13 healthy controls with normal basic indices for calcium-phosphorus metabolism and 25 patients with recurrent calcium nephrolithiasis and hypercalciuria, 13 of them with renal hypercalciuria and 12 patients with absorptive hypercalciuria. The oral calcium-tolerance test was carried out in all persons. The changes in the serum and urine calcium and magnesium concentrations following the calcium loading are recorder. A statistically significant increase of magnesium urine excretion was found in all persons examined, the highest being in the patients with renal hypercalciuria, considerably higher than in the healthy controls. The conclusion is reached that the magnesium urine excretion gives valuable information for the diagnosis of patients with renal hypercalciuria.

Administration, Oral↗