Database : MEDLINE
Search on : Hypercalciuria [Words]
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[PMID]: 29376607
[Au] Autor:Olefir YV; Yavorskii AN; Butnaru DV; Shatalova OV; Gorbatenko VS; Gerasimenko AS
[Ad] Address:I.M. Sechenov First MSMU, Moscow, Russia.
[Ti] Title:[Idiopathic hypercalciuria. Diagnosis and treatment].
[So] Source:Urologiia;(6):112-119, 2017 Dec.
[Is] ISSN:1728-2985
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:Most patients with idiopathic hypercalciuria and calcium nephrolithiasis have a family history of the disease. Idiopathic hypercalciuria is a metabolic abnormality with various causes and developmental pathways. The systematic review describes specific mutations associated with idiopathic hypercalciuria and nephrolithiasis. Detection of these mutations may provide a better understanding of the pathogenesis of this heterogeneous disease and personalize patient management depending on the detected polymorphisms. A promising treatment option for a mutation in the vitamin D receptor gene is thiazide diuretics in combination with bisphosphonates. Among bisphosphonates, the drug of choice which has been most strongly supported by research evidence is alendronate.
[Mh] MeSH terms primary: Alendronate/therapeutic use
Mutation
Nephrolithiasis
Receptors, Calcitriol
[Mh] MeSH terms secundary: Female
Humans
Hypercalciuria/diagnosis
Hypercalciuria/drug therapy
Hypercalciuria/genetics
Hypercalciuria/metabolism
Male
Nephrolithiasis/diagnosis
Nephrolithiasis/drug therapy
Nephrolithiasis/genetics
Nephrolithiasis/metabolism
Receptors, Calcitriol/genetics
Receptors, Calcitriol/metabolism
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Receptors, Calcitriol); X1J18R4W8P (Alendronate)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180130
[St] Status:MEDLINE

  2 / 3760 MEDLINE  
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[PMID]: 29504582
[Au] Autor:Trejo P; Rauch F; Ward L
[Ad] Address:Shriners Hospital for Children and McGill University, Montreal, Quebec, Canada.
[Ti] Title:Hypercalcemia and hypercalciuria during denosumab treatment in children with osteogenesis imperfecta type VI.
[So] Source:J Musculoskelet Neuronal Interact;18(1):76-80, 2018 Mar 01.
[Is] ISSN:1108-7161
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Children with osteogenesis imperfecta (OI) type VI often have high fracture rates despite the current standard treatment with bisphosphonates. Subcutaneous injections of denosumab have been proposed as an alternative treatment approach, but safety data on denosumab in children are limited. Here we describe fluctuations in bone and mineral metabolism during denosumab treatment in four children with OI type VI who started denosumab (basic protocol: 1 mg per kg body mass every 3 months) between 1.9 and 9.0 years of age, after having received intravenous bisphosphonates previously. All four children developed hypercalciuria during active denosumab therapy. In two children aged 3.9 and 4.6 years, episodes of hypercalcemia were observed between 7 and 12 weeks after the preceding denosumab injection. During times when the interval between denosumab injections was increased to 6 months for clinical reasons, lumbar spine bone mineral density z-scores decreased rapidly. It appears that the duration of action of denosumab is short and variable in children with OI type VI. These observations call into question the concept that denosumab can be used as a stand-alone alternative to bisphosphonates to treat children with OI.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:In-Data-Review

  3 / 3760 MEDLINE  
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[PMID]: 29368300
[Au] Autor:Moe OW; Xu LHR
[Ad] Address:Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, 75390-8885, USA. orson.moe@utsouthwestern.edu.
[Ti] Title:Hyperuricosuric calcium urolithiasis.
[So] Source:J Nephrol;31(2):189-196, 2018 Apr.
[Is] ISSN:1724-6059
[Cp] Country of publication:Italy
[La] Language:eng
[Ab] Abstract:Hyperuricosuric calcium urolithiasis is a condition of mixed calcium oxalate stones characterized by hyperuricosuria either in isolation or in conjunction with other risk factors for calcium oxalate stones such as hypercalciuria, hyperoxaluria, and hypocitraturia. There are three proposed physicochemical models of pathogenesis where urate in its crystalline phase via heterogeneous nucleation, in its colloidal phase via removal of crystallization inhibitors, and in solution via precipitation crystallization, can all increase propensity to calcium oxalate precipitation. Regardless of the model, the phenomenologic observation of urate increasing calcium oxalate precipitation appears solid. Another supporting factor are retrospective data analysis and prospective trials showing uric acid lowering reduces stones events in hyperuricosuric calcium stone formers. Due to the heterogeneity of pathogenesis of calcium oxalate stones in the unselected stone-formers, association cannot be demonstrated between uric acid excretion rate and risk of kidney stone the general population. In calcium oxalate stoners with isolated hyperuricosuria or hyperuricosuria in combination with other calcium stone risks where treatment of these traditional risks fails to reduce stone formation, urate acid lowering should be cautiously attempted. More refinement of pathogenic models and prospective controlled trials in phenotypically defined subgroups of subjects with calcium oxalate urolithiasis will be informative.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1801
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:In-Data-Review
[do] DOI:10.1007/s40620-018-0469-3

  4 / 3760 MEDLINE  
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[PMID]: 29328898
[Au] Autor:Ryan LE; Ing SW
[Ad] Address:Clinical Associate Professor of Medicine, Center for Women's Health, Division of Endocrinology, Diabetes, and Metabolism, The Ohio State University, Columbus, OH, USA. laura.ryan@osumc.edu.
[Ti] Title:Idiopathic hypercalciuria: Can we prevent stones and protect bones?
[So] Source:Cleve Clin J Med;85(1):47-54, 2018 Jan.
[Is] ISSN:1939-2869
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Idiopathic hypercalciuria increases the risk of urinary stones and osteoporosis. The aim of this review is to delineate our current understanding of idiopathic hypercalciuria in the context of bone health, specifically its definition, causes, epidemiology, laboratory evaluation, and potential treatments.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1801
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Process
[do] DOI:10.3949/ccjm.85a.16090

  5 / 3760 MEDLINE  
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[PMID]: 29482694
[Au] Autor:Sethar GH; Almoghawi A; Khan N; Altourah W; Ashour NM
[Ad] Address:Department of Medicine, Al-Amiri Hospital, Kuwait.
[Ti] Title:Pseudohypoaldosteronism Type II: A Young Girl Presented with Hypertension, Hyperkalemia and Metabolic Acidosis.
[So] Source:J Coll Physicians Surg Pak;28(3):S21-S22, 2018 Mar.
[Is] ISSN:1681-7168
[Cp] Country of publication:Pakistan
[La] Language:eng
[Ab] Abstract:Pseudohypoaldosteronism (PHA) type II is an extremely rare disorder which presents with hypertension, hyperkalemia, and normal anion gap metabolic acidosis. PHA II is also known as familial hyperkalemic hypertension, Gordon syndrome, and chloride shunt syndrome. PHA II is an autosomal dominant disorder and is caused by mutation in WNK1, WNK4, CULLIN3, KLHL3, OSR, SPAK gene. The expression of these proteins is limited to the distal convoluted tube and collecting duct of the kidney. PHA II usually responds to salt restriction and thiazide diuretics. We are reporting here a case of 16-year girl who presented with generalised fatigue and shortness of breath, and blood pressure (BP) of 220/110 mmHg. Laboratory investigation showed hyperkalemia, normal anion gap metabolic acidosis, and hypercalciuria. Workup for secondary causes of hypertension was negative. She responded to thiazide diuretics and her BP is well controlled, and acidosis and hyperkalemia are corrected.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:In-Process
[do] DOI:10.29271/jcpsp.2018.03.S21

  6 / 3760 MEDLINE  
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[PMID]: 29457024
[Au] Autor:Moreira Guimarães Penido MG; de Sousa Tavares M; Saggie Alon U
[Ad] Address:Pediatric Nephrology Unit, Clinics Hospital, School of Medicine, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
[Ti] Title:Role of FGF23 in Pediatric Hypercalciuria.
[So] Source:Biomed Res Int;2017:3781525, 2017.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Background: This study explored the possible role of FGF23 in pediatric hypercalciuria. Methods: Plasma FGF23 was measured in 29 controls and 58 children and adolescents with hypercalciuria: 24 before treatment (Pre-Treated) and 34 after 6 months of treatment (Treated). Hypercalciuric patients also measured serum PTH hormone, 25(OH)vitD, phosphate, calcium, creatinine, and 24 h urine calcium, phosphate, and creatinine. Results: There were no differences in age, gender, ethnicity, or body mass index either between controls and patients, or between Pre-Treated and Treated patients. Median plasma FGF23 in controls was 72 compared with all patients, 58 RU/mL ( = 0.0019). However, whereas FGF23 in Pre-Treated patients, 73 RU/mL, was not different from controls, in Treated patients it was 50 RU/mL, significantly lower than in both controls ( < 0.0001) and Pre-Treated patients ( = 0.02). In all patients, there was a correlation between FGF23 and urinary calcium ( = 0.325; = 0.0014). Treated patients had significantly lower urinary calcium ( < 0.0001), higher TP/GFR ( < 0.001), and higher serum phosphate ( = 0.007) versus Pre-Treated patients. Conclusions: Pharmacological treatment of hypercalciuric patients resulted in significantly lower urinary calcium excretion, lower serum FGF23, and elevated TP/GFR and serum phosphate concentration, without significant changes in PTH. Further studies are indicated. This trial is registered with Clinical Registration Number RBR 8W27X5.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180221
[Lr] Last revision date:180221
[St] Status:In-Process
[do] DOI:10.1155/2017/3781525

  7 / 3760 MEDLINE  
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[PMID]: 29391272
[Au] Autor:Günthner R; Wagner M; Thurm T; Ponsel S; Höfele J; Lange-Sperandio B
[Ad] Address:Institute of Human Genetics, Technical University of Munich, Munich, Germany; Department of Nephrology, Klinikum rechts der Isar, Technical University Munich, Munich, Germany. Electronic address: roman.guenthner@mri.tum.de.
[Ti] Title:Identification of co-occurrence in a patient with Dent's disease and ADA2-deficiency by exome sequencing.
[So] Source:Gene;649:23-26, 2018 Apr 05.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Patients with co-occurrence of two independent pathologies pose a challenge for clinicians as the phenotype often presents as an unclear syndrome. In these cases, exome sequencing serves as a powerful instrument to determine the underlying genetic causes. Here, we present the case of a 4-year old boy with proteinuria, microhematuria, hypercalciuria, nephrocalcinosis, livedo-like rash, recurrent abdominal pain, anemia and continuously elevated CRP. Single exome sequencing revealed the pathogenic nonsense mutation p.(Arg98*) in the CLCN5 gene causing the X-linked inherited, renal tubular disorder Dent's disease. Furthermore, the two pathogenic and compound heterozygous missense variants p.(Gly47Ala) and p.(Pro251Leu) in the CECR1 gene could be identified. Mutations in the CECR1 gene are associated with a hereditary form of polyarteritis nodosa, called ADA2-deficiency. Both parents were carriers of a single heterozygous variant in CECR1 and the mother was carrier of the CLCN5 variant. This case evidently demonstrates the advantage of whole exome sequencing compared to single gene testing as the pathology in the CECR1 gene might have only been diagnosed after the occurrence of signs of systemic vasculitis like strokes or hemorrhages. Therefore, treatment and prevention can now start early to improve the outcome of these patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[St] Status:In-Process

  8 / 3760 MEDLINE  
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[PMID]: 29266368
[Au] Autor:Lv F; Guan Y; Ma D; Xu X; Song Y; Li L; Jiang Y; Wang O; Xia W; Xing X; Li M
[Ad] Address:Department of Endocrinology, Key Laboratory of Endocrinology, National Health and Family Planning Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
[Ti] Title:Effects of alendronate and alfacalcidol on bone in patients with myasthenia gravis initiating glucocorticoids treatment.
[So] Source:Clin Endocrinol (Oxf);88(3):380-387, 2018 Mar.
[Is] ISSN:1365-2265
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Glucocorticoids (GCs) are the first-line treatment for myasthenia gravis (MG) and act as long-term immunosuppressants. However, GCs can induce osteoporosis and bone fractures. In this study, we evaluate the effects of oral alendronate and alfacalcidol, or alfacalcidol alone on the bone of Chinese patients with MG who will initiate treatment with GCs. DESIGN AND METHODS: A total of 75 patients were included in this 12-month prospective, open-label, single-centre study. Patients with bone mineral density (BMD) T-score less than -1.0 at baseline were treated with 70 mg of alendronate per week. Patients with BMD T-score greater than -1.0 at baseline were included in the alfacalcidol-alone group. Patients in two groups were treated with 0.25 µg of alfacalcidol every other day and 600 mg of calcium daily. RESULTS: After 12 months of treatment, the mean BMD of lumbar spine, femoral neck and total hip increased by 3.4% (P = .002), 1.8% (P = .21) and 2.6% (P = .02), respectively, in alendronate group. In alfacalcidol-alone group, the mean BMD of lumbar spine, femoral neck and total hip decreased by 6.1%, 3.2% and 3.3%, respectively (all P < .001 vs baseline). CONCLUSIONS: We demonstrated for the first time that treatment with alendronate combined with alfacalcidol significantly increased BMD, decreased bone turnover biomarker levels and reduced the occurrence of hypercalciuria in a large cohort of Chinese patients with MG who initiated treatment with glucocorticoids. However, treatment with alfacalcidol alone failed to prevent bone loss in patients with MG receiving glucocorticoid therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180215
[Lr] Last revision date:180215
[St] Status:In-Data-Review
[do] DOI:10.1111/cen.13537

  9 / 3760 MEDLINE  
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[PMID]: 29442351
[Au] Autor:Skwarek A; Pachucki J; Bednarczuk T; Zurecka Z; Popow M
[Ad] Address:Warsaw University of Medicine. agathaskwarek@yahoo.com.
[Ti] Title:MILK-ALKALI SYNDROME (MAS) as a complication of the treatment of hypoparathyroidism.
[So] Source:Endokrynol Pol;, 2018 Feb 14.
[Is] ISSN:2299-8306
[Cp] Country of publication:Poland
[La] Language:eng
[Ab] Abstract:Milk-alkali syndrome (MAS), characterized by renal failure, metabolic alkalosis and hypercalcemia, is a severe and life-threatening complication of the treatment of hypoparathyroidism. The clinical course is often sudden and is not preceded by any prodromal symptoms. Occurrence does not depend on the duration of hypoparathyroidism treatment, although it is closely related to the applied therapy, especially the dose of calcium carbonate and active vitamin D preparations. Drugs influencing the glomerular filtration rate (angiotensin receptor blockers, sartans, aldosterone receptor antagonists, thiazide diuretics), lack of adequate routine control, changing the calcium carbonate supplementation, dehydration, a diet rich in pH-basic foods (i.e. vegetarian diet), pregnancy and other associated conditions are listed among the factors triggering MAS. A higher calcium carbonate dose is directly associated with an increased risk of milk-alkali syndrome. In case of a high calcium demand it is necessary to control renal function and monitor the level of calcium in the serum more frequently, aiming for the lower end of the reference range. If MAS has been confirmed or if there are alarming neurological symptoms suggestive of hypercalcemia, the patient must be sent to the hospital immediately. Treatment of MAS involves: discontinuation of calcium and vitamin D supplementation, and intravenous infusion of normal saline solution to eliminate volume deficiencies and to achieve forced diuresis while maintaining proper fluid balance. As soon as there is improvement in the patient's clinical condition, it is necessary to begin the treatment of comorbidities increasing the risk of renal failure or alkalosis (i.e. vomiting, diarrhea).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180214
[Lr] Last revision date:180214
[St] Status:Publisher
[do] DOI:10.5603/EP.a2018.0015

  10 / 3760 MEDLINE  
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[PMID]: 29257214
[Au] Autor:Ma Y; Yang H; Huang J
[Ad] Address:Department of Orthopaedics, The Second Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, Henan 450002, P.R. China.
[Ti] Title:Icariin ameliorates dexamethasone­induced bone deterioration in an experimental mouse model via activation of microRNA­186 inhibition of cathepsin K.
[So] Source:Mol Med Rep;17(1):1633-1641, 2018 Jan.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:The present study aimed to investigate bone deterioration in glucocorticoid­induced osteoporosis (GIOP) mice, and the anti­osteoporosis effect and underlying molecular mechanism of icariin. Dexamethasone (DSM) treatment was demonstrated to facilitate the induction of hypercalciuria in GIOP mice. Icariin treatment reversed the dexamethasone (DXM)­induced disequilibrium of calcium homeostasis and bone resorption, and increased serum alkaline phosphatase, tartrate resistant acid phosphatase, osteocalcin and deoxypyridinoline. Haematoxylin and eosin staining revealed an increase in disconnections and separation in the trabecular bone network of the tibial proximal metaphysis, in the GIOP group. Icariin treatment reversed the DXM­induced trabecular deleterious effects, and stimulated bone remodeling in GIOP mice. Furthermore, the results demonstrated that the mRNA and protein expression of cathepsin K were significantly increased in GIOP mice, compared with the control group. Icariin treatment may suppress the expression of cathepsin K in the tibia of GIOP mice. The levels of microRNA (miR)­186 were markedly reduced in the tibia of GIOP mice compared with control group; however, this was inhibited by icariin treatment. Bioinformatics analysis demonstrated that miR­186 regulates cathepsin K via binding to the upstream 3'­untranslated region. Furthermore, transfection with miR­186 mimics resulted in inhibition of cathepsin K expression, whereas miR­186 inhibitors facilitated cathepsin K expression in osteoclasts. In conclusion, the present study demonstrated the protective effects of icariin against bone deteriorations in the experimental GIOP mice, and the underlying mechanism was mediated, at least partially, via activation of miR­186­mediated suppression of cathepsin K. These results provide evidence to support the use of icariin as a therapeutic approach in the management of glucocorticoid­induced bone loss, and the disequilibrium of calcium homeostasis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180214
[Lr] Last revision date:180214
[St] Status:In-Process
[do] DOI:10.3892/mmr.2017.8065


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