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PubMed2000

Isolated hypercalciuria with mutation in CLCN5: relevance to idiopathic hypercalciuria.

UNLABELLED: Isolated hypercalciuria with mutation in CLCN5: Relevance to idiopathic hypercalciuria. BACKGROUND: Idiopathic hypercalciuria (IH) is the most common risk factor for kidney stones and often has a genetic component. Dent's disease (X-linked nephrolithiasis) is associated with mutations in the CLCN5 chloride channel gene, and low molecular weight (LMW) proteinuria was universally observed in affected males. We sought to identify mutations in CLCN5 or abnormalities in LMW protein excretion in a large group of patients with IH and in a rat model of genetic hypercalciuria. METHODS: One hundred and seven patients with IH (82 adults and 25 children) and one asymptomatic hypercalciuric man with a known inactivating mutation in CLCN5 were studied. Secondary causes of hypercalciuria were excluded in all. The excretion of retinol-binding protein and beta2-microglobulin was measured by immunoassay in 101 patients with IH. Mutation analysis of the CLCN5 gene was performed in 32 patients with IH and in the genetic hypercalciuric stone-forming (GHS) rat strain. RESULTS: LMW protein excretion was normal in 92 patients with IH, and only slight abnormalities were found in the other nine, none of whom had a mutation in CLCN5. One 27-year-old man who had a CLCN5 mutation was found to have isolated hypercalciuria without LMW proteinuria, renal failure, or other evidence of renal disease. Mutation analysis was normal in 32 patients with IH. The CLCN5 sequence was normal in the GHS rat. CONCLUSIONS: Inactivation of CLCN5 can be found in the setting of hypercalciuria without other features of X-linked nephrolithiasis. However, mutations in CLCN5 do not represent a common cause of IH.

Adolescent↗
PubMed1985

Exaggerated natriuretic and calciuric responses to hydrochlorothiazide in renal hypercalciuria but not in absorptive hypercalciuria.

Patients with hypercalciuria have been reported to have an exaggerated response to hydrochlorothiazide (HCTZ), implying a renal tubular defect in solute reabsorption. To determine whether this disturbance is generalized or unique to a particular pathogenetic type of hypercalciuria, we measured the increments in urinary sodium (delta Na), calcium (delta Ca), and magnesium after a 100-mg dose of oral HCTZ in 10 normal subjects and 31 patients with different types of hypercalciuric nephrolithiasis. Eleven patients with renal hypercalciuria had significantly greater delta Na (P less than 0.005) and delta Ca (P less than 0.005) than the normal subjects. Ten patients with absorptive hypercalciuria and 10 patients with fasting hypercalciuria without parathyroid stimulation had delta Na and delta Ca indistinguishable from those of normal subjects. In all groups, urinary HCTZ and basal 24-h urinary Na did not differ. The results suggest that the unique natriuretic and calciuric responses to HCTZ occur only in renal hypercalciuric patients with secondary hyperparathyroidism. The data support a renal tubular defect in renal hypercalciuric in contrast to other diagnostic categories of hypercalciuric nephrolithiasis.

Absorption↗
PubMed1985

Families of children with idiopathic hypercalciuria. Evidence for the hormonal basis of familial hypercalciuria.

Six children with idiopathic hypercalciuria and their families were examined with an oral calcium loading test. Family members were divided into two clinical categories: group 1 consisted of the six index children and their parents and siblings with urolithiasis or unexplained hematuria; group 2 comprised the remaining parents and siblings without signs or symptoms associated with hypercalciuria. The results revealed that fasting urinary excretion of calcium was similar in both groups, but group 1 displayed a greater calciuric response to an oral calcium load. Serum concentrations of calcitriol (1,25-dihydroxyvitamin D3) and calcium were higher in group 1 than in group 2, while parathyroid activity was lower in group 1 patients. Urinary excretion of sodium, phosphorus, and magnesium, urine pH, serum levels of calcifediol (25-hydroxyvitamin D3) and phosphorus, and the renal tubular threshold for phosphate were not significantly different in the two groups. These findings suggest that idiopathic hypercalciuria may arise from a disturbance in the regulation of vitamin D metabolism that mediates enhanced intestinal absorption of calcium.

Adult↗
PubMed1992

[Hypercalciuria and primary hyperparathyroidism in patients with kidney calculi. I. Hypercalciuria].

In 1819 patients with active or non active respectively nephrolithiasis the following parameters were assessed: plasma level of calcium, phosphate, and uric acid and urinary excretion of calcium, phosphate, oxalate, uric acid and creatinine. These parameters were estimated after 5 days of diet containing 400 mg of calcium, 800 mg of phosphate, 100 mg of purines and 40 g of proteins. In 3/4 of all examined patients at least one lithogenic factor was present. More than 40% of patients showed presence of hypercalciuria. Among these patients in 68% renal in 17% absorptive and in 15% undefined hypercalciuria was diagnosed. Patients with active nephrolithiasis showed a similar frequency of hypercalciuria but more profound abnormalities of Ca P metabolism than patients with non active renal stone disease.

Adolescent↗
PubMed1979

[Idiopathic hypercalciuria due to primary decrease in the renal tubular reabsorption of calcium. Hypercalciuria type 2 according to Bordier (author's transl)].

A persistent hypercalciuria and normal serum levels of calcium were measured in a 5-year-old boy suffering from recurrent macro- and microhaematuria and bilateral nephrolithiasis (stone analysis was positive for calcium-oxalate). No growth retardation or any other relevant clinical parameters concerning hypercalciuria e.g. vitamin D-intoxication or renal tubular acidosis could be observed. A slight secondary hyperparathyroidism and increased calcium excretion during fasting or calcium depleted diet indicates a primary failure of calcium reabsorption as previously described by Bordier (hypercalciuria type 2). Treatment with a combination of hydrochlorothiazide (Esidrix) and sodium chloride depleted diet resulted in a long-lasting normalization of calcium excretion and thus disappearance of symptoms in the child.

Calcium↗
PubMed1979

Physiological basis for absorptive and renal hypercalciurias.

Idiopathic hypercalciuria constitutes two major variants-absorptive hypercalciuria, characterized by a primary intestinal hyperabsorption of calcium, and renal hypercalciuria, in which renal tubular reabsorption of calcium is primarily impaired. The two forms of hypercalciuria may be distinguished from each other, since a) parathyroid function is stimualted in renal hypercalciuria, but normal or suppressed in absorptive hypercalciuria, b) the renal leak of calcium is present in renal hypercalciuria, but not in absorptive hypercalciuria, c) intestinal calcium absorption is probably increased primarily in absorptive hypercalciuria, and secondarily in renal hypercalciuria (from parathyroid hormone excess), d) the increased calcium absorption in renal hypercalciuria probably results from the parathyroid hormone-dependent stimulation of 1,25-dihydroxyvitamin D synthesis, whereas that in absorptive hypercalciuria may be vitamin D-independent, e) the response of the two conditions to certain treatments is unique, and f) the sequelae of parathyroid hormone excess, such as low bone density and negative calcium balance, may be present in renal hypercalciuria, but not in absorptive hypercalciuria. These findings provide a physiological basis for the consideration of absorptive and renal hypercalciurias as distinct and separate entities.

Benzothiadiazines↗
PubMed1974

The hypercalciurias. Causes, parathyroid functions, and diagnostic criteria.

The causes for the hypercalciuria and diagnostic criteria for the various forms of hypercalciuria were sought in 56 patients with hypercalcemia or nephrolithiasis (Ca stones), by a careful assessment of parathyroid function and calcium metabolism. A study protocol for the evaluation of hypercalciuria, based on a constant liquid synthetic diet, was developed. In 26 cases of primary hyperparathyroidism, characteristic features were: hypercalcemia, high urinary cyclic AMP (cAMP, 8.58+/-3.63 SD mumol/g creatinine; normal, 4.02+/-0.70 mumol/g creatinine), high immunoreactive serum parathyroid hormone (PTH), hypercalciuria, the urinary Ca exceeding absorbed Ca from intestinal tract (Ca(A)), high fasting urinary Ca (0.2 mg/mg creatinine or greater), and low bone density by (125)I photon absorption. The results suggest that hypercalciuria is partly secondary to an excessive skeletal resorption (resorptive hypercalciuria). The 22 cases with renal stones had normocalcemia, hypercalciuria, intestinal hyperabsorption of calcium, normal or low serum PTH and urinary cAMP, normal fasting urinary Ca, and normal bone density. Since their Ca(A) exceeded urinary Ca, the hypercalciuria probably resulted from an intestinal hyperabsorption of Ca (absorptive hypercalciuria). The primacy of intestinal Ca hyperabsorption was confirmed by responses to Ca load and deprivation under a metabolic dietary regimen. During a Ca load of 1,700 mg/day, there was an exaggerated increase in the renal excretion of Ca and a suppression of cAMP excretion. The urinary Ca of 453+/-154 SD mg/day was significantly higher than the control group's 211+/-42 mg/day. The urinary cAMP of 2.26+/-0.56 mumol/g creatinine was significantly lower than in the control group. In contrast, when the intestinal absorption of calcium was limited by cellulose phosphate, the hypercalciuria was corrected and the suppressed renal excretion of cAMP returned towards normal. Two cases with renal stones had normocalcemia, hypercalciuria, and high urinary cAMP or serum PTH. Since Ca(A) was less than urinary Ca, the hypercalciuria may have been secondary to an impaired renal tubular reabsorption of Ca (renal hypercalciuria). Six cases with renal stones had normal values of serum Ca, urinary Ca, urinary cAMP, and serum PTH (normocalciuric nephrolithiasis). Their Ca(A) exceeded urinary Ca, and fasting urinary Ca and bone density were normal. The results support the proposed mechanisms for the hypercalciuria and provide reliable diagnostic criteria for the various forms of hypercalciuria.

Adult↗
PubMed2000

Hypercalciuria.

Hypercalciuria is a biological syndrome defined as excretion in the urine of more than 0.1 mmol/kg/24 hours of calcium in the absence of dietary manipulation. A number of endocrine, renal, and bone diseases can cause hypercalciuria. Urinary calcium excretion is substantially influenced by dietary intakes of calcium, sodium, protein, carbohydrates, alcohol, and potassium: a poorly balanced diet can result in hypercalciuria. Recently, there has been a burst of interest in the molecular underpinnings of rare nephrolithiasis syndromes, which have been shown to result from mutations in the CLCN5 chloride channel gene. Mutations affecting the calcium-sensing receptor (CaSR) have been identified in other forms of hypercalciuria. Idiopathic hypercalciuria is defined as hypercalciuria that persists after correction of dietary imbalances and has no detectable cause. The classification suggested by Pak ("absorptive" hypercalciuria [with three types] and "renal" hypercalciuria) is controversial and of little assistance in clinical practice. Three mechanisms can be incriminated in idiopathic hypercalciuria: increased intestinal absorption of calcium, defective reabsorption of calcium by the renal tubule, and increased bone resorption. Overexpression of the vitamin D receptor (VDR) and deficiencies in renal tubule enzymes may also be involved. Bone mineral density is moderately decreased in idiopathic hypercalciuria, particularly in the renal type. The risk of vertebral fracture seems increased, however. Overproduction of calcitriol and cytokines that stimulate bone resorption have been incriminated in the bone loss. Treatment of the cause is essential in secondary hypercalciuria (dietary advice, treatment of an underlying disease, etc.). A diet low in sodium and meat and containing no more than 800 mg of calcium per day is advocated in idiopathic hypercalciuria. Hydrochlorothiazide therapy is warranted in patients with osteopenia and an inadequate response to dietary therapy.

Calcium↗
PubMedDate not supplied

[Renal tubular function in children with hypercalciuria].

INTRODUCTION: Renal stone disease is commonly due to hypercalciuria [1, 2], which may be assessed either from a 24-hour urinary collection or from the fasting first morning urine. Hypercalciuria during childhood has been defined by a 24-hour calcium excretion greater than 3.5 mg/kg per day and/or calcium to creatinine ratio greater than 0.20 [3]. The alteration in the calcium transporting systems plays a pathogenetic role in promoting hypercalciuria [4, 5]. Since calcium reabsorption along the nephron is intimately related to that of other electrolytes and substances, it can be hypothesized that patients with hypercalciuria may have other renal tubular defects. The aim of the study was to investigate proximal tubular function (tubular reabsorption of sodium, potassium, phosphate and glucose) and distal tubular function (urinary concentrating capacity and acidifying capacity) in children with hypercalciuria. PATIENTS AND METHODS: Two groups of children were studied: hypercalciuric group included 23 children with hypercalciuria (10 males, aged 11.9 +/- 4.1 years), of whom 6 with nephrolithiasis, and control group included 42 healthy children (20 males, aged 11.2 +/- 3.8 years). All subjects had normal serum values for calcium, sodium, potassium, phosphate and glucose, as well as normal renal function. The urinary excretion of calcium, sodium, potassium, phosphate, glucose and creatinine was measured in a 24-hour urine specimen by standard laboratory methods. Urine osmolality and urinary specific gravity were measured following 12-hour water-deprivation test. A short ammonium chloride loading test was performed in 3 patients with urinary pH above 5.5. The fractional excretion of sodium, tubular phosphate reabsorption and renal threshold phosphate concentration were calculated according to standard formula. Statistical analysis was performed using the t-test and analysis of variance (ANOVA). Kruskal-Wallis method was used to compare urinary phosphate excretion between two groups. RESULTS: Table 1 summarizes urinary excretion of electrolytes in children with hypercalciuria compared with healthy controls. We found that urinary sodium excretion was significantly increased in patients with hypercalciuria when compared with controls (p < 0.05). Urinary phosphate excretion was significantly higher in patients with hypercalciuria in comparison to controls, and this was accompanied by a significant lowering of the tubular phosphate reabsorptive threshold (p < 0.05). Urinary potassium excretion tended to be lower, although not significantly, in the hypercalciuric children than in normal subjects. Table 2 shows the mean values +/- standard deviation of urinary specific gravity, urinary osmolality and urinary pH. Urinary specific gravity mean value was significantly lower in patients with hypercalciuria in comparison to controls (p < 0.05). Urinary pH was found below 5.5 in all patients. Glycosuria was detected in 3 patients (13.3%). As shown in Graph. 1, a significant correlation between the urinary excretion of calcium and sodium was demonstrated in both groups of children (r = 0.29; p < 0.01). DISCUSSION: The present study shows that children with hypercalciuria have significantly higher urinary sodium and urinary phosphate excretion in comparison to controls, while urinary potassium excretion is normal in both groups of children. According to some recent reports [6-9], these findings may indicated defects of the renal tubular transport of sodium and phosphate which may be interpreted as a cause or a consequence of the alteration of the calcium transporting system. Defects in both proximal and distal renal tubular functions have been demonstrated in patients with nephrolithiasis, particularly those with hypercalciuria. Proximal renal tubular defects include defects in sodium, fluid, phosphate and glucose reabsorption, which were evident also in our patients. (ABSTRACT TRUNCATED)

Calcium↗
PubMed1987

Eventual attenuation of hypocalciuric response to hydrochlorothiazide in absorptive hypercalciuria.

The effect of long-term hydrochlorothiazide therapy on renal calcium excretion was measured in 12 well defined cases of absorptive hypercalciuria and 10 of renal hypercalciuria. Patients were studied during a control phase, at 3 to 6 months of therapy and after long-term treatment with hydrochlorothiazide (mean 61 months for absorptive hypercalciuria and 71 months for renal hypercalciuria). Evaluation comprised measurement of urinary calcium and fractional (intestinal) calcium absorption while patients were maintained on a constant metabolic diet (400 mg. calcium per day) for 3 days. In patients with absorptive hypercalciuria urinary calcium decreased significantly at 3 months of treatment (from 266 to 137 mg. per day, p less than 0.001). However, with continued treatment urinary calcium rebounded to 197 mg. per day. Of the patients with absorptive hypercalciuria 50 per cent were hypercalciuric (greater than 200 mg. per day) on long-term treatment, whereas none was hypercalciuric at 3 months. In contrast, urinary calcium in the patients with renal hypercalciuria decreased from 299 to 104 mg. per day (p less than 0.001) at 3 months of treatment and remained reduced (116 mg. per day) during long-term treatment. Intestinal calcium absorption was increased initially and remained unchanged throughout treatment in the patients with absorptive hypercalciuria. In patients with renal hypercalciuria intestinal calcium absorption decreased significantly after short-term treatment with hydrochlorothiazide and remained so after long-term therapy. The results suggest that, unlike patients with renal hypercalciuria, some with absorptive hypercalciuria lose the hypocalciuric effect of hydrochlorothiazide during long-term treatment.

Adult↗
PubMed1990

[Incidence of different types of hypercalciuria in the Madrid area. Demographic features].

A study to determine the incidence of idiopathic hypercalciuria was performed in 110 patients (59 females, 51 males). Classification of this metabolic disorder according to its different types revealed the following incidence: 50% for absorptive hypercalciuria, 14.5% for hypercalciuria from loss of renal phosphates, and 30% for renal hypercalciuria. Insufficient biochemical data with a significant value did not permit classification of 6.3%. Analysis of distribution according to sex revealed a similar incidence (50%) for males and females for absorptive hypercalciuria, a prevalence in men (71%) for hypercalciuria due to loss of renal phosphates, and a prevalence in females (64.7%) for renal hypercalciuria. However, correction of these data according to the male to female ratio of our study population revealed renal hypercalciuria to be more prevalent in females whereas absorptive hypercalciuria and hypercalciuria from loss of renal phosphates were more prevalent in men. Analysis of distribution according to age revealed a direct relationship between the increased incidence of renal hypercalciuria and patient age.

Absorption↗
PubMed1992

Increased urinary excretion of prostaglandin E2 in patients with idiopathic hypercalciuria is a primary phenomenon.

1. Urinary excretion of prostaglandin E2 is increased in patients with idiopathic hypercalciuria, but in order to conclude that hyperprostaglandinuria is a primary phenomenon, it must be demonstrated that high levels of urinary prostaglandin E2 can be dissociated from other factors, such as urine volume and natriuresis, and from the hypercalciuria itself. 2. We studied 10 patients with idiopathic hypercalciuria and 10 control subjects on high and low calcium diets providing daily calcium intakes of 30-35 mmol and 7.5-10 mmol, respectively, and similar sodium intakes. In addition, patients with idiopathic hypercalciuria and control subjects were studied during water restriction and water diuresis. 3. Urinary prostaglandin E2 excretion was more than twice as high in patients with idiopathic hypercalciuria than in control subjects on the low and high calcium diets as well as during water restriction and water diuresis (P less than 0.01). 4. Urinary prostaglandin E2 excretion was not affected by changes in urinary calcium excretion in patients with idiopathic hypercalciuria and in control subjects. Patients with idiopathic hypercalciuria on the low calcium diet and control subjects on the high calcium diet had similar levels of calciuria and natriuresis, yet urinary prostaglandin E2 excretion (mean +/- SEM) was 11.62 +/- 1.71 nmol/day in the patients with idiopathic hypercalciuria and 3.26 +/- 0.48 nmol/day in the control subjects (P = 0.0006). 5. These results indicate that increased urinary prostaglandin E2 excretion is a cardinal characteristic of patients with idiopathic hypercalciuria.

Adolescent↗
PubMed1996

Osteocalcin response to calcium-restricted diet: a helpful tool for the workup of hypercalciuria.

OBJECTIVES: The treatment of hypercalciuria is controversial. This study investigated whether the osteocalcin response (OCR) to a calcium-restricted diet is a potential tool for the differential therapy of hypercalciuria. 56 patients with calcium urolithiasis were investigated. METHODS: Osteocalcin (OC) was measured on a free diet (OC 1) and after a calcium-restricted diet (400 mg/24 h for 1 week, OC 2). The OCR was expressed as 100 x (OC 2 - OC 1)/OC 1. A calcium load test and vertebral mineral density measurements (L2-L4) were performed additionally. RESULTS: 27 patients showed diet-dependent hypercalciuria, 15 of them being classified as absorptive hypercalciuria type II (AH II). 12 were normocalciuric (NC). 29 patients had diet-independent hypercalciuria, 22 being classified as renal hypercalciuria (RH), 7 as absorptive hypercalciuria type I (AH I). 22 patients (42%) showed a positive OCR, indicating an increased bone turnover. Vertebral mineral density was lower in patients with positive than with negative OCR. Generally patients with RH or NC showed a positive OCR, patients with AH a negative or no OCR. 2 patients with AH, however, showed highly positive OCR, indicating negative calcium balance. Long-term follow-up on a low calcium diet showed a steady decrease in bone mineral density. CONCLUSIONS: This demonstrates that the OCR is more reliable to determine the appropriate management of hypercalciuria than calcium load tests. For practical purposes, we suggest treating hypercalciuric patients with positive OCR with thiazides; diet-dependent hypercalciuria with negative OCR should be treated with a low calcium diet.

Absorptiometry, Photon↗
PubMed1995

[Incidence of the different types of hypercalciuria in Spain].

OBJECTIVE: To carry out a comparative biochemical study of primary hyperparathyroidism, the different types of hypercalciuria and a healthy population. METHODS: Fourteen patients with primary hyperparathyroidism and 103 patients with idiopathic hypercalciuria were studied under conditions of restricted calcium intake and following a calcium load; the results were compared to those of 18 healthy controls. RESULTS: The patients with hyperparathyroidism showed high parathormone concentrations. Sixty-nine patients with idiopathic hypercalciuria had normal parathormone levels and were considered suffering from absorptive hypercalciuria. Those patients with high urinary calcium excretion under restricted calcium intake and normal urinary phosphate threshold were considered as being absorptive hypercalciuria type I, those with normal urinary calcium as absorptive hypercalciuria type II, and those with low urinary phosphate threshold constituted a renal phosphate leakage group. Thirty-four patients had normal serum calcium, elevated parathormone, hypophosphatemia and high calcium excretion under all dietary conditions, and were considered undergoing renal hypercalciuria. Patients with renal hypercalciuria had increased urine hydroxyproline and low serum calcium compared with the controls after an oral calcium load. This biochemical behaviour is compatible with secondary hyperparathyroidism caused by renal calcium leakage. CONCLUSIONS: In summary, the biochemical parameters: parathormone, urinary phosphate threshold and urinary calcium excretion, measured in fasting conditions, allowed classification of patients with idiopathic hypercalciuria.

Adult↗
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↗