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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Idiopathic hypercalciuria is known to cause many nonstone urinary tract disorders in childhood. In addition to being the most common cause of microhematuria in children, our study demonstrates that idiopathic hypercalciuria is also frequently associated with urinary incontinence of all types. Of 124 children evaluated for idiopathic hypercalciuria 28 (23%) had urinary incontinence. Of the 28 children 15 (54%) had nocturnal, 6 (21%) diurnal, and 7 (25%) nocturnal and diurnal incontinence. The random urinary calcium-creatinine ratio, which was used to screen for hypercalciuria, should be part of the initial evaluation for urinary incontinence in children. Diagnosis may be confirmed by quantitative urinary calcium excretion. Most urinary incontinence in children that is due to idiopathic hypercalciuria responds to a combination of general treatment for hypercalciuria or thiazide diuretics.
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PMID:Urinary incontinence due to idiopathic hypercalciuria in children. 786 18

Primary renal glucosuria is a benign condition in which serum glucose level is normal. Idiopathic hypercalciuria is defined as increased urinary calcium excretion of more than 4 mg/kg/day in normocalcemic individuals in whom all known causes of hypercalciuria have been excluded. In this paper, we report on a case who has both renal glucosuria and hypercalciuria.
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PMID:Hypercalciuria in renal glucosuria. 899 66

Hypercalciuria is a rare biological symptom with multiple possible etiologies in children. Normal calcium excretion rate in children is defined as lower than 4 mg/kg per day, significantly higher values being observed in infants. When using urinary calcium: creatinine ratio, normal values are below 0.22 mg/mg in children, and below 0.6 to 0.8 mg/mg in infants. In our experience half patients with hypercalciuria have idiopathic hypercalciuria. Idiopathic hypercalciuria can be hereditary with a dominant autosomal mode of inheritance. Its pathophysiology is unclear, increased calcium intestinal absorption and impaired renal tubular calcium reabsorption being the two main underlying anomalies. Patients with hypercalciuria should be informed about the risk of urolithiasis and its possible prevention by a high water intake. In those patients with nephrocalcinosis or recurrent episodes of lithiasis, hydrochlorothiazide can be effective in reducing hypercalciuria. However, adverse effects of hydrochlorothiazide on serum lipids have been recently reported and make this treatment questionable in the long term.
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PMID:[Hypercalciuria: etiologies and treatment]. 918 9

Idiopathic hypercalciuria (IH) associated with nephrocalcinosis was found in three of six siblings. After the three affected children were maintained on a low-calcium diet, they demonstrated increasing hypercalciuria, parathyroid hormone, and vitamin D3 levels. An oral calcium loading test was not necessary to diagnose renal IH. During treatment with hydrochlorothiazide, the calcium excretion was normalized. These patients are remarkable because nephrocalcinosis is generally regarded as a rare complication of renal IH. Moreover, the fact that three of six siblings are affected raises the question of whether the renal form of IH is genetically distinct from other forms of IH.
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PMID:Nephrocalcinosis in three siblings with idiopathic hypercalciuria. 954 76

Genetic factors are important determinants for kidney stone formation. Cystinuria, primary hyperoxaluria, and X-linked nephrolithiasis (Dent's disease) are monogenic kidney stone diseases for which responsible genes have been identified. Familial stone disease with hyperuricosuria or renal tubular acidosis has been described in several clinical settings. Idiopathic hypercalciuria is the most common stone risk factor, and evidence in humans and in a rat model indicates that hypercalciuria is a complex, polygenic trait. Some candidate genes for idiopathic hypercalciuria are suggested by the known physiology, including those encoding the vitamin D receptor, the 1 alpha-hydroxylase of vitamin D, the calcium-sensing receptor, the renal sodium-dependent phosphate transporter, and chloride channels, but others remain to be identified. The multifaceted physiology of hypercalciuria may reflect the combined effects of polymorphisms in several genes.
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PMID:Nephrolithiasis. 1043 76

Nephrolithiasis is one of the most frequent pathologies of the urinary tract. Its prevalence in the city of Buenos Aires is 4%. Different biochemical and physiological disturbances may create an environment conductive to renal stone formation. We present the results of an ambulatory evaluation in 2612 patients for the purpose of updating the classification of nephrolithiasis. An abnormal urinary biochemistry was observed in 2423 patients (92.8%) that could be classified in 15 categories. A single diagnosis was documented in 61.5% of the patients, and the remaining 31.2% had more than one diagnosis (concurrent abnormalities). No abnormality was found in 189 stone formers (7.2%). Idiopathic hypercalciuria was the most frequent abnormality, it was encountered in 31.2%; hyperuricosuria and gouty diathesis (presence of urine pH < 5.5, with normal or high uricemia) accounted for 9.4% and 5.4% of patients, respectively. On the other hand, hypomagnesuria affected 6.7% of the stone formers and hypocitraturia was observed in 4.5%. Primary hyperparathiriodism, hyperoxaluria and cystinuria were seen less frequently in 2.6%, 1.3 and 0.45% of patients. Low urine volume was found in 12% of the patients. Among those patients with more than one abnormality, we found that hypercalciuria together with hyperuricosuria and hypocitraturia (12%) was the prevalent association followed by hypercalciuria with hyperuricosuria (9.1%). Our results show the importance of studying nephrolithiasis patients from a biochemical point of view, since this is the only way to achieve a diagnosis of the metabolic abnormality and introduce a specific therapy to prevent recurrence.
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PMID:[Metabolic changes in 2612 patients with nephrolithiasis]. 1068 59

Idiopathic hypercalciuria (IHC) has been reported mainly in children with hematuria in the 1980s and early 1990s, when renal sonography was just becoming routine. The presence of microcalculi, i.e., of hyperechogenic spots < 3 mm in diameter in renal calyces, was not taken into account in those studies. We attempted to outline clinical presentation and natural course of IHC not only in children with hematuria, but also in those with dysuria and/or recurrent abdominal/flank pain and a family history of nephrolithiasis, taking into account the finding of microcalculi. We analyzed retrospectively the data at diagnosis from 74 consecutive children aged 2.4-18 years (mean 8.6) with IHC (calciuria 4.1-15.1 mg kg-1 24 h-1, mean 6.1) and the outcome of 30 of them who were followed > or = 1 years (mean 3.2) with no specific therapy. At diagnosis, 38 patients (51%) had no hematuria, 42 (57%) had microcalculi and four (5%) had calculi. Of the patients with normal urinalysis, 71% had microcalculi or stones. The subjects with microcalculi and those with stones were significantly older than those without microcalculi and stones (P = 0.004 and 0.007). A normal urinalysis at our evaluation and a history of abdominal/flank pain were significantly more frequent in patients with microcalculi than in those without (P = 0.02 and 0.0001, respectively). During the follow-up, four of 30 patients formed stones 1-3 years after first diagnosis of IHC. More than half of children with IHC have microcalculi. The risk of formation of microcalculi or stones increases with age. The lack of hematuria does not exclude the presence of microcalculi or calculi. Hypercalciuria has to be suspected in children with dysuria and/or recurrent abdominal flank pain and a family history of nephrolithiasis, even when they have no hematuria.
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PMID:Clinical presentation and natural course of idiopathic hypercalciuria in children. 1114 13

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.
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PMID:Hypercalciuria. 1119 13

Idiopathic hypercalciuria is a common metabolic abnormality in children of all ages. There is evidence of an association of idiopathic hypercalciuria with nephrolithiasis, hematuria, and osteoporosis. However, much of this evidence is anecdotal and the precise role of hypercalciuria in the pathogenesis of these conditions is far from clear. Furthermore, the precise definition of idiopathic hypercalciuria has not yet been established. The methodologies for quantitating urinary calcium excretion have also not been standardized, adding another potential confounding factor to the accurate interpretation of urinary calcium excretion. Long-term studies on the natural history of unselected children with idiopathic hypercalciuria are needed to establish the true clinical significance of this condition. The focus of this review is to critically evaluate the methods currently being used to measure urinary calcium excretion in children and to assess the validity of existing criteria for diagnosing idiopathic hypercalciuria.
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PMID:Idiopathic hypercalciuria in children--how valid are the existing diagnostic criteria? 1505 48

Idiopathic hypercalciuria is a complex disease resulting from an interaction between environmental and genetic factors. Recently, the relationship between vitamin D receptor ( VDR) alleles and calcium homeostasis has been investigated. This study was conducted to explore the association of VDR gene polymorphism with the risk of absorptive hypercalciuria (AH). We investigated the VDR gene polymorphisms, ApaI, BsmI, and TaqI, in relation to intact parathormone (PTH), osteocalcin, and 25-hydroxyvitamin D in 80 children (42 males, 38 girls) with AH and in 86 healthy children without hypercalciuria. A significant difference in the ApaI genotype was observed between the AH group and the control group ( chi(2)=7.21, P=0.027). The AA genotype was associated with a 3.5-fold increased risk for idiopathic hypercalciuria compared with the Aa/aa genotype (odds ratio 3.5, 95% confidence interval 1.1-11). The BsmI and TaqI polymorphisms did not show any significant association with AH. Serum osteocalcin levels were significantly higher in the group with the AA genotype compared with those with the Aa or aa genotype ( P=0.02, P=0.05, respectively). The results indicate that the ApaI AA genotype of the VDR gene is not only associated with AH but is also related to differences in serum osteocalcin.
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PMID:Vitamin D receptor gene polymorphism in hypercalciuric children. 1514 45


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